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N Acetyl L Cysteine
Amino Acid

Material Safety Data Sheet

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Results for your query on June 29, 1999:

Search all fields for: N-acetyl-L-cysteine And heart disease

Published in 1966 through 1999

Only select references with abstracts available

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Documents: 1 to 16 of 16

NLM database Documents

Record 1 from database: MEDLINE
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Title

Attempt to prevent doxorubicin-induced acute human myocardial morphologic damage with acetylcysteine.

Author

Unverferth DV; Jagadeesh JM; Unverferth BJ; Magorien RD; Leier CV; Balcerzak SP

Address

 

Source

J Natl Cancer Inst, 1983 Nov, 71:5, 917-20

Abstract

Doxorubicin induced acute as well as chronic myocardial morphologic alterations. Twenty patients with normal cardiovascular function were randomized to 2 groups based on age and dose of doxorubicin. Group I received placebo 1 hour before doxorubicin administration; group II received acetylcysteine (N-acetyl-L-cysteine) (Nac) 1 hour before doxorubicin. Endomyocardial biopsies were performed at base line at 4 and 24 hours after doxorubicin administration. Biopsy tissue was viewed by electron microscopy, and stereoscopic techniques were used to determine tubular and mitochondrial area. The change of the tubular area was similar in the 2 groups, was maximum at 4 hours, and was proportionately spread throughout the cell. The mitochondrial swelling was also similar in the 2 groups and proportionate throughout the cell but was maximum at 24 hours. This study demonstrated that the acute doxorubicin-induced damage was diffuse and not prevented by Nac.

Language of Publication

English

Unique Identifier

84065555

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MeSH Heading (Major)

Acetylcysteine|*PD; Doxorubicin|*AE; Myocardium|*UL

MeSH Heading

Adult; Aged; Biopsy; Drug Evaluation; Endocardium|DE/UL; Human; Microscopy, Electron; Middle Age; Mitochondria, Heart|DE/UL; Myocardial Diseases|CI; Support, Non-U.S. Gov't

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL

ISSN

0027-8874

Country of Publication

UNITED STATES

Record 2 from database: MEDLINE
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Title

Enantioselectivity in the metabolism of mexiletine by conjugation in female patients with the arrhythmic form of chronic Chagas' heart disease.

Author

Lanchote VL; Cesarino EJ; Santos VJ; Mere Júnior Y; Santos SR

Address

Faculdade de CiÈencias FarmacÈeuticas de RibeirÃao Preto, Universidade de SÃao Paulo, RibeirÃao Preto, Brazil.

Source

Chirality, 1999, 11:1, 29-32

Abstract

The phenomenon of enantioselectivity in the metabolism of mexiletine (MEX) conjugation was investigated in eight female patients with the arrhythmic form of chronic Chagas' heart disease treated with racemic mexiletine hydrochloride (two 100 mg capsules every 8 hr). Blood samples were collected up to 24 hr after the administration of the morning dose, with discontinuation of the subsequent doses during the study period. Plasma concentrations of N-hydroxymexiletine glucuronide were calculated as the difference between the concentrations of unchanged and total (unchanged + conjugated) MEX enantiomers. Total plasma MEX concentrations were analyzed by HPLC after enzymatic hydrolysis with beta-glucuronidase, the formation of diastereomeric derivatives with the chiral reagent N-acetyl-L-cysteine/o-phthalaldehyde, and fluorescence detection. The differences in the pharmacokinetic parameters of the enantiomers were evaluated by the paired t-test. The plasma concentrations of the (+)-(S)-MEX did not differ before and after enzymatic hydrolysis. The pharmacokinetic parameters calculated for (-)-(R)-N-hydroxymexiletine glucuronide are presented as means (95% confidence interval): maximum plasma concentration Cmax = 194.0 ng.ml-1 (154.3-233.7), time to maximum plasma concentration tmax = 1.4 hr (0.3-2.5), area under the plasma concentration versus time curve AUC0-24 = 2099.2 ng.h.ml-1 (1585.6-2612.6), elimination half-life t1/2 beta = 12.8 hr (9.9-15.6) and extent of conjugation of 31.6% (24.3-38.9%). The present data indicate stereospecific conjugation of (-)-(R)-N-hydroxymexiletine in the female patients with the arrhythmic form of Chagas' heart disease.

Language of Publication

English

Unique Identifier

99113079

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MeSH Heading (Major)

Anti-Arrhythmia Agents|CH/*PK; Chagas Cardiomyopathy|*ME/PP; Mexiletine|CH/*PK

MeSH Heading

Adult; Aged; Area Under Curve; Arrhythmia|ME/PP; Biotransformation; Chronic Disease; Female; Glucuronates|ME; Human; Hydroxylation; Middle Age; Stereoisomerism

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE

ISSN

0899-0042

Country of Publication

UNITED STATES

Record 3 from database: MEDLINE
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Title

Enantioselective analysis of N-hydroxymexiletine glucuronide in human plasma for pharmacokinetic studies.

Author

Lanchote VL; Santos VJ; Cesarino EJ; Dreossi SA; Mere Júnior Y; Santos SR

Address

Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Brazil.

Source

Chirality, 1999, 11:2, 85-90

Abstract

Enzymatic hydrolysis with beta-glucuronidase/sulfatase was used for the enantioselective determination of N-hydroxymexiletine glucuronide in plasma for pharmacokinetic studies. N-Hydroxymexiletine glucuronide was determined as the quantity of mexiletine released by hydrolysis (difference between the enantiomeric concentrations of mexiletine obtained with and without hydrolysis). Plasma samples (100 microliters) were treated at pH 5.0 with 10 mg of the enzyme (Limpet Acetone Powder type I) for 16 hr at 37 degrees C and extracted at pH 10.4 with diisopropyl ether. Chiral mexiletine discrimination was obtained by reaction with o-phthalaldehyde/N-acetyl-L-cysteine, separation of the resulting diastereomers on a C-18 reversed-phase column with a mobile phase of methanol-0.05 N acetate buffer, pH 5.5 (6.5:3.5, v/v), and fluorescence detection (lambda ex 350 nm, lambda em 455 nm). The performance characteristics for the enantioselective analysis of mexiletine preceded by enzymatic hydrolysis were recovery approximately 90%, quantification limit 1 ng/ml, and linearity up to 1000 ng/ml plasma for both enantiomers. The coefficients of variation obtained in the study of intra- and inter-day precision were respectively 5% and 7% for both enantiomers. The assay was shown to be suitable for a pharmacokinetic study performed in a patient with the arrhythmic form of chronic Chagas' heart disease treated with 200 mg t.i.d. of racemic mexiletine hydrochloride. The high sensitivity of the method allows analysis of only 100 microliters plasma.

Language of Publication

English

Unique Identifier

99136551

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MeSH Heading (Major)

Anti-Arrhythmia Agents|*BL; Mexiletine|*AA/BL

MeSH Heading

Calibration; Chromatography, High Pressure Liquid; Human; Hydrolysis; Reproducibility of Results; Stereoisomerism; Substrate Specificity

Publication Type

JOURNAL ARTICLE

ISSN

0899-0042

Country of Publication

UNITED STATES

CAS Registry/EC Number

0 (Anti-Arrhythmia Agents); 151636-18-9 (N-hydroxymexiletine glucuronide); 31828-71-4 (Mexiletine)

 

Record 4 from database: MEDLINE
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Title

Chronic obstructive pulmonary disease.

Author

Wynne JW

Address

 

Source

Compr Ther, 1975 Dec, 1:8, 26-30

Abstract

The diagnosis of COPD can easily be made on the basis of history, physical findings, and simple laboratory procedures. Treatment is aimed at symptoms and is individualized to the patient's needs. Therapy must be given on a long-term basis. The patient should be educated in the basic nature of his disease and encouraged to return to as normal a life as possible. Patients with COPD often are severely restricted in their earning ability, and treatment can cause a severe financial drain. Thus the physician should carefully consider costs--especially the cost of medications. Finally, the correct choice and use of the many therapeutic measures available can yield marked symptomatic relief and improvement in lifestyle--often allowing the patient to return to productive employment.

Language of Publication

English

Unique Identifier

76164325

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MeSH Heading (Major)

Lung Diseases, Obstructive|CO/*DT/RH

MeSH Heading

Acetylcysteine|TU; Aerosols; Antibiotics|TU; Bronchodilator Agents|TU; Chronic Disease; Expectorants|TU; Guaiacol Glyceryl Ether|TU; Heart Failure, Congestive|DT; Human; Humidity; Patient Education; Patients|ED; Physical Therapy; Prednisone|TU

Publication Type

JOURNAL ARTICLE

Country of Publication

UNITED STATES

Record 5 from database: MEDLINE
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Title

Early changes in human myocardial nuclei after doxorubicin.

Author

Unverferth BJ; Magorien RD; Balcerzak SP; Leier CV; Unverferth DV

Address

 

Source

Cancer, 1983 Jul, 52:2, 215-21

Abstract

Ten nuclei from the endomyocardial biopsies for each of the following 32 patients were examined by electron microscopy: seven patients before and then four and 24 hours after treatment with first-dose doxorubicin; seven patients before and four and 24 hours after treatment with first-dose doxorubicin plus N-acetyl cysteine; nine patients with doxorubicin induced cardiomyopathy; and nine patients with idiopathic congestive cardiomyopathy. Five criteria were used to semiquantitatively compare nuclei and nucleoli from each group. The most dramatic changes in nuclear and nucleolar morphology were seen four hours after doxorubicin administration. Nucleoli were smaller, contracted or segregated and contained fewer fibrillar centers and a collapsed or fragmented nucleolonema. The addition of N-acetylcysteine to treatment did not alter these results. By 24 hours, nuclei had returned to the pre-treatment status. Long-term doxorubicin therapy produced increased chromatin clumping and slightly contracted nucleoli. The idiopathic congestive cardiomyopathic nuclei differed significantly from these doxorubicin cardiomyopathic nuclei in the decreased amount of chromatin clumping and the increase in fibrillar centers and nucleonema pattern. It is concluded from this study that: (1) doxorubicin markedly alters the morphology of the human myocardial nucleus and nucleolus four hours after treatment, but these changes diminish by 24 hours; (2) N-acetylcysteine treatment fails to prevent these changes; and (3) the nuclei and nucleoli of chronic doxorubicin-induced cardiomyopathy differ significantly from other congestive cardiomyopathies, but do resemble changes seen four hours after the first dose of doxorubicin.

Language of Publication

English

Unique Identifier

83232573

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MeSH Heading (Major)

Cell Nucleus|*DE/UL; Doxorubicin|AE/*PD; Heart|*DE

MeSH Heading

Acetylcysteine|PD; Cell Nucleolus|DE/UL; Chronic Disease; Dose-Response Relationship, Drug; Human; Myocardial Diseases|CI/PA; Myocardium|UL; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0008-543X

Country of Publication

UNITED STATES

Record 6 from database: MEDLINE
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Title

Prospective randomized study of the role of N-acetyl cysteine in reversing doxorubicin-induced cardiomyopathy.

Author

Dresdale AR; Barr LH; Bonow RO; Mathisen DJ; Myers CE; Schwartz DE; dAngelo T; Rosenberg SA

Address

 

Source

Am J Clin Oncol, 1982 Dec, 5:6, 657-63

Abstract

We conducted a randomized prospective trial in 19 disease-free soft tissue sarcoma patients with doxorubicin-induced cardiomyopathy identified by ECG radionuclide angiography at rest and during exercise to determine the efficacy of the free radical scavenger, N-Acetyl Cysteine (NAC), in reversing the drug's cardiotoxic effect. Of the 19 patients, 11 received oral NAC (5.5 gm/m2 daily for 30 days) and eight patients served as controls. Patients were stratified for age less than greater than 45 years, time from final dose of doxorubicin to randomization less than greater than 8 months, and history of treatment with mediastinal irradiation. The two groups were well-matched for all parameters. Cumulative mean doxorubicin dose (523 mg/m2 and 532 mg/m2) and range 500-600 mg/m2 was comparable. Left ventricular (LV) ejection fraction before randomization was not significantly different between the two groups either at rest (39 +/- 10% control, 38 +/- 13% NAC) or during exercise (38 +/- 12% control, 35 +/- 11% NAC). Neither rest nor exercise ejection fraction values changed significantly in either group between prerandomization and 1-month postrandomization studies. Late studies performed in seven NAC patients 3-5 months after randomization revealed no difference in LV ejection fraction compared to 1-month postrandomization values. Clinical course in patients with overt congestive heart failure was similar in both groups. LV function did not return to normal in any patient in either group. We conclude that N-Acetyl Cysteine has no effect in reversing long standing doxorubicin-induced cardiomyopathy.

Language of Publication

English

Unique Identifier

83149732

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MeSH Heading (Major)

Acetylcysteine|*TU; Doxorubicin|*AE; Myocardial Diseases|CI/*DT; Sarcoma|*DT; Soft Tissue Neoplasms|*DT

MeSH Heading

Adolescence; Adult; Child; Female; Heart Function Tests; Human; Male; Middle Age; Prospective Studies; Random Allocation

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL

ISSN

0277-3732

Country of Publication

UNITED STATES

Record 7 from database: MEDLINE
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Title

Potentiation of isosorbide dinitrate effects with N-acetylcysteine in patients with chronic heart failure.

Author

Mehra A; Shotan A; Ostrzega E; Hsueh W; Vasquez Johnson J; Elkayam U

Address

Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.

Source

Circulation, 1994 Jun, 89:6, 2595-600

Abstract

BACKGROUND: Supply of sulfhydryl groups with the administration of N-acetylcysteine (NAC) has been reported to reverse tolerance to nitroglycerin but not to isosorbide dinitrate (ISDN). Lack of interaction between NAC and ISDN was suggested as an explanation for these findings. The present study was therefore designed to further evaluate this hypothesis. For this purpose, we compared the hemodynamic and hormonal effects of ISDN when given alone and in combination with NAC. METHODS AND RESULTS: We performed a randomized, cross-over design evaluation of the hemodynamic and hormonal effects of ISDN and ISDN + NAC in 14 patients with chronic congestive heart failure due to left ventricular systolic dysfunction. The findings of this study demonstrated a substantial NAC-mediated potentiation of ISDN effect on mean right atrial pressure (-11 +/- 21% versus -38 +/- 27%, -17 +/- 20% versus -34 +/- 27%, and -7 +/- 20% versus -25 +/- 26% at 2, 3, and 4 hours, respectively; all P < .05), mean pulmonary artery wedge pressure (-18 +/- 16% versus -33 +/- 14%, -15 +/- 25% versus -33 +/- 19%, -14 +/- 22% versus -25 +/- 22%, and -16 +/- 16% versus -26 +/- 16% at 2, 3, 4, and 5 hours, respectively; all P < .05), mean pulmonary artery pressure (-8 +/- 11% versus -20 +/- 15% at 3 hours, P < .05), and cardiac output (an increase of 2 +/- 16% versus 25 +/- 20% at 4 hours, P < .05). Although there were no significant changes in serum catecholamine levels and plasma renin concentration with both regimens, ISDN + NAC resulted in a greater fall in plasma levels of atrial natriuretic peptide (296 +/- 251 pg/mL after ISDN versus 202 +/- 118 pg/mL after ISDN + NAC, P < .05). CONCLUSIONS: The results of this study provide strong evidence for the existence of an interaction between thiols and ISDN and further support the role of sulfhydryl groups in the activation and therapeutic action of organic nitrates. The discrepancy between the results of this study demonstrating NAC-induced potentiation of ISDN effects and a previous study showing failure to reverse ISDN tolerance with NAC may suggest that ISDN-NAC interaction requires normal intracellular levels of sulfhydryl groups and does not occur after intracellular sulfhydryl group depletion.

Language of Publication

English

Unique Identifier

94265312

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MeSH Heading (Major)

Acetylcysteine|*AD/PD; Heart Failure, Congestive|*DT/PP; Isosorbide Dinitrate|AD/PD/*TU

MeSH Heading

Adult; Aged; Atrial Natriuretic Factor|BL; Catecholamines|BL; Chronic Disease; Drug Synergism; Drug Therapy, Combination; Female; Human; Male; Middle Age; Renin|BL; Support, U.S. Gov't, P.H.S.

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL

ISSN

0009-7322

Country of Publication

UNITED STATES

Record 8 from database: MEDLINE
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Title

Cardioprotection in patients undergoing chemo- and/or radiotherapy for neoplastic disease. A pilot study.

Author

Wagdi P; Fluri M; Aeschbacher B; Fikrle A; Meier B

Address

Department of Cardiology, University Hospital, Bern, Switzerland.

Source

Jpn Heart J, 1996 May, 37:3, 353-9

Abstract

OBJECTIVES: To assess the cardioprotective efficiency of an antioxidant regimen (vitamins E, C and N-acetylcysteine) in patients receiving high dose chemo- and/or radiotherapy for malignant disease. METHODS: Prospective, placebo controlled, randomized and double blinded pilot study involving 13 patients receiving chemotherapy and 12 patients receiving radiotherapy. RESULTS: In patients receiving antioxidants, left ventricular ejection fraction did not change (63 +/- 4% to 63 +/- 4%). In the placebo group, ejection fraction changed from 67 +/- 6% to 61 +/- 4% (p = 0.03). No patient in the antioxidant group and 6/13 (46%) patients in the placebo group showed a fall of > 10% in the left ventricular ejection fraction. In the chemotherapy group, the left ventricular ejection fraction changed from 62% (+/- 2) to 63% (+/- 2) in the patients treated with antioxidants (ns) and from 63% (+/- 5) to 61% (+/- 5) in patients treated with placebo (ns). No patient showed a significant fall in ejection fraction in the antioxidant group, whereas 2/7 (29%) in the placebo group showed a reduction > or = 10%. In the radiotherapy group, left ventricular ejection fraction did not change 64% (+/- 6) to 64% (+/- 5) in patients treated with antioxidants (ns) and changed from 70% (+/- 8) to 60% (+/- 4) in patients treated with placebo (p = 0.008). No patient in the antioxidant group, but 4/6 (66%) patients in the placebo group showed a fall of > or = 10% in ejection fraction. CONCLUSION: The small number of patients in the study precludes a definitive statement. The preliminary results however suggest efficient cardioprotection by this nontoxic and inexpensive antioxidant combination, so larger studies are warranted for confirmation.

Language of Publication

English

Unique Identifier

96370732

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MeSH Heading (Major)

Antioxidants|*AD; Heart|*DE/RE; Neoplasms|*TH

MeSH Heading

Acetylcysteine|AD; Antineoplastic Agents|AE; Ascorbic Acid|AD; Double-Blind Method; Human; Pilot Projects; Prospective Studies; Radionuclide Ventriculography; Radiotherapy|AE; Radiotherapy Dosage; Stroke Volume|DE; Support, Non-U.S. Gov't; Vitamin E|AD

Publication Type

CLINICAL TRIAL; JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL

ISSN

0021-4868

Country of Publication

JAPAN

Record 9 from database: MEDLINE
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Title

The anecdotal antidotes.

Author

Litovitz TL

Address

 

Source

Emerg Med Clin North Am, 1984 Feb, 2:1, 145-58

Abstract

The author reviews obscure or unusual antidote recommendations, emphasizing antidotes or antidote uses that are not generally acknowledged or that have little experimental or clinical confirmation of their efficacy. Also included are unusual uses of well known antidotes. Among the antidotes considered are naloxone, physostigmine, folate, Prussian blue, n-acetylcysteine, cimetidine, subcutaneous magnesium salts, nicotinamide, and thioctic acid.

Language of Publication

English

Unique Identifier

85101158

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MeSH Heading (Major)

Antidotes|*; Poisoning|*DT

MeSH Heading

Acetylcysteine|TU; Adult; Aged; Animal; Case Report; Child; Cimetidine|TU; Female; Ferrocyanides|TU; Folic Acid|TU; Heart Diseases|CI; Human; Magnesium|AD/TU; Male; Middle Age; Naloxone|AE/TU; Niacinamide|TU; Physostigmine|AE/TU; Pyridoxine|TU; Thioctic Acid|TU

Publication Type

JOURNAL ARTICLE; REVIEW

ISSN

0733-8627

Country of Publication

UNITED STATES

Record 10 from database: MEDLINE
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Title

Homocysteine redox receptor and regulation of extracellular matrix components in vascular cells.

Author

Tyagi SC

Address

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216, USA.

Source

Am J Physiol, 1998 Feb, 274:2 Pt 1, C396-405

Abstract

Dynamic changes in the reduction-oxidation (redox) state of the tissue lead to the pathophysiological condition. Reduced homocysteine causes dysfunctions in endothelium. The proliferation of smooth muscle cells may lead to occlusive vascular disease, ischemia, and heart failure, but whether fibrosis and hypertension are a consequence of smooth muscle proliferation is unclear. Redox changes during hyper-homocyst(e)inemia may be one of the causes of premature atherosclerotic heart disease. To examine the effect of homocystine on human vascular smooth muscle cells (HVSMC), we isolated HVSMC from idiopathic dilated cardiomyopathic hearts. Coronaries in these hearts were apparently normal. HVSMC numbers in culture were measured by hemocytometer in the presence and absence of homocystine. Results show that homocystine induced cellular proliferation. This proliferation was reversed by the addition of the antioxidant N-acetylcysteine (NAC). Homocystine induces collagen expression in a dose- and time-dependent manner, as measured by Northern blot (mRNA) analysis. The 50% inhibitory concentration of 5 microM for collagen was estimated. The induction of collagen was reversed by the addition of NAC and reduced glutathione. To localize the receptor for homocystine on HVSMC, we synthesized fluorescamine-labeled homocystine conjugate. Incubation of labeled homocystine with HVSMC demonstrated membrane and cytosol localization of homocystine binding. The receptor-ligand binding was disrupted by NAC. Based on sodium dodecyl sulfate-polyacrylamide gel electrophoresis fluorography, we observed a 40- to 25-kDa homocystine redox receptor in HVSMC. Our results suggested that the redox homocysteine induces HVSMC proliferation by binding to the redox receptor and may exacerbate atherosclerotic lesion formation by inducing collagen expression.

Language of Publication

English

Unique Identifier

98147083

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MeSH Heading (Major)

Extracellular Matrix Proteins|*PH; Homocysteine|*PH; Homocystine|*PH; Muscle, Smooth, Vascular|DE/*PH; Receptors, Cell Surface|DE/*PH

MeSH Heading

Acetylcysteine|PD; Actins|BI; Amino Acid Sequence; Cell Division; Collagen|BI; Free Radical Scavengers|PD; Glutathione|ME; Human; Molecular Sequence Data; Oxidation-Reduction; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.

Publication Type

JOURNAL ARTICLE

ISSN

0002-9513

Country of Publication

UNITED STATES

Record 11 from database: MEDLINE
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Title

Six cases of pulmonary alveolar proteinosis: presentation of unusual associations.

Author

García Río F; Alvarez Sala R; Caballero P; Prados C; Pino JM; Villamor J

Address

Dept of Pulmonology, La Paz Hospital, School of Medicine, Autonoma University, Madrid, Spain.

Source

Monaldi Arch Chest Dis, 1995 Jan, 50:1, 12-5

Abstract

We report the cases of six patients with pulmonary alveolar proteinosis (PAP). Four of the patients were adults, two males and two females (mean age 39 +/- 19 yrs). The other two patients were children, both females, one aged 6 years and one 3 days old. The diagnosis was made by thoracotomy-lung biopsy in two subjects, autopsy in two, transbronchoscopic biopsy in one and bronchoalveolar lavage (BAL) in one. Some of our cases presented unusual associations that have not been described previously in the medical literature: renal tubular acidosis, Fanconi's disease, glioblastoma multiforme and atrioventricular septal defect. In two patients, treatment with acetylcysteine and ambroxol was unsuccessful. Therapeutic BAL improved the clinical, analytical, functional and radiological aspects of two cases. In one subject, three months after the diagnosis of PAP, pulmonary tuberculosis appeared. Both diseases disappeared with antituberculous treatment.

Language of Publication

English

Unique Identifier

95261370

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MeSH Heading (Major)

Pulmonary Alveolar Proteinosis|*/CO/DI/TH

MeSH Heading

Acetylcysteine|TU; Adult; Ambroxol|TU; Biopsy; Brain Neoplasms|CO; Bronchoalveolar Lavage Fluid; Case Report; Child; Fanconi Syndrome|CO; Female; Glioblastoma|CO; Heart Septal Defects|CO; Human; Infant, Newborn; Lung|PA; Male; Middle Age; Oxygen Inhalation Therapy; Respiratory Function Tests; Tuberculosis, Pulmonary|CO

Publication Type

JOURNAL ARTICLE

ISSN

1122-0643

Country of Publication

ITALY

Record 12 from database: MEDLINE
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Title

Different susceptibility to the development of nitroglycerin tolerance in the arterial and venous circulation in humans. Effects of N-acetylcysteine administration.

Author

Ghio S; de Servi S; Perotti R; Eleuteri E; Montemartini C; Specchia G

Address

Division of Cardiology, IRCCS S. Matteo Hospital, Pavia, Italy.

Source

Circulation, 1992 Sep, 86:3, 798-802

Abstract

BACKGROUND. Tolerance to the effects of organic nitrates develops rapidly during continuous exposure to these drugs; its main mechanism seems to be an intracellular sulfhydryl group depletion. However, the relative susceptibility to the development of nitroglycerin tolerance of the arterial or venous circulation in humans is still a matter of dispute. METHODS AND RESULTS. Twenty patients with coronary artery disease underwent a continuous 24-hour nitroglycerin infusion followed by a bolus administration of N-acetylcysteine. Forearm blood flow (ml/100 ml/min) and venous volume (ml/100 ml) were measured by strain gauge plethysmography under control conditions, at the end of nitroglycerin titration, after 24-hour infusion, and after N-acetylcysteine; vascular resistance was calculated as mean cuff blood pressure divided by flow. After 24 hours of nitroglycerin infusion, the initial increase in venous volume was reduced 48% (p less than 0.01), whereas the acute effects on vascular resistance were not attenuated in the whole group. N-Acetylcysteine completely restored nitroglycerin venodilator effects in all 10 patients in whom attenuation of the venous effects was observed during the infusion period. CONCLUSIONS. The data indicate that the susceptibility to the development of nitrate tolerance in humans is higher in the venous than in the arterial circulation, and that the sulfhydryl group donor N-acetylcysteine is extremely effective in reversing nitroglycerin tolerance in the venous circulation in humans.

Language of Publication

English

Unique Identifier

92386679

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MeSH Heading (Major)

Acetylcysteine|*PD; Arteries|*DE; Nitroglycerin|*PD; Veins|*DE

MeSH Heading

Blood Pressure|DE; Blood Volume|DE; Drug Tolerance; Female; Heart Rate|DE; Human; Infusions, Intravenous; Injections, Intra-Arterial; Male; Middle Age; Vascular Resistance|DE

Publication Type

JOURNAL ARTICLE

ISSN

0009-7322

Country of Publication

UNITED STATES

Record 13 from database: MEDLINE
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Title

Development of nitrate tolerance in human arteries and veins: comparison of nitroglycerin and SPM 5185.

Author

Arnet U; Yang Z; Siebenmann R; von Segesser LK; Turina M; Stulz P; Lüscher TF

Address

Department of Research, University Hospitals, Basel, Switzerland.

Source

J Cardiovasc Pharmacol, 1995 Sep, 26:3, 401-6

Abstract

Nitrate tolerance is a clinical problem in patients with coronary artery disease and heart failure. Human internal mammary arteries and saphenous veins obtained intraoperatively were suspended in organ chambers, and isometric tension was measured. In the artery, nitroglycerin elicited a potent relaxation, which was significantly diminished after prolonged incubation with nitroglycerin (10(-6) M, 1 h). In contrast, no tolerance occurred in saphenous vein under the same conditions. However, incubation with 10(-5) M nitroglycerin also developed tolerance. Compared to nitroglycerin, the new cysteine-containing mononitrate SPM 5185 exhibited a lower sensitivity but comparable maximal relaxation in arteries and veins. In nitroglycerin-tolerant arteries and veins, SPM 5185 caused relaxations similar to those under control conditions. Our results show that in isolated blood vessels, vascular nitrate tolerance occurs more readily in the mammary artery than in the saphenous vein. SPM 5185 seems to be less prone to the development of tolerance, which may be advantageous during chronic nitrate therapy.

Language of Publication

English

Unique Identifier

96058636

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MeSH Heading (Major)

Dipeptides|ME/*PD/TU; Muscle, Smooth, Vascular|*DE; Nitroglycerin|ME/*PD/TU; Vasodilator Agents|ME/*PD/TU

MeSH Heading

Acetylcysteine|PD/TU; Arginine|AA/PD/TU; Drug Tolerance; Free Radical Scavengers|PD/TU; Human; In Vitro; Isometric Contraction|DE; Mammary Arteries|DE/ME; Muscle Relaxation|DE; Myocardial Reperfusion Injury|DT; Nitric-Oxide Synthase|AI; Saphenous Vein|DE/ME; Support, Non-U.S. Gov't

Publication Type

JOURNAL ARTICLE

ISSN

0160-2446

Country of Publication

UNITED STATES

Record 14 from database: MEDLINE
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Title

Inhibition of NF-kappa B activation in vitro and in vivo: role of 26S proteasome.

Author

Grisham MB; Palombella VJ; Elliott PJ; Conner EM; Brand S; Wong HL; Pien C; Mazzola LM; Destree A; Parent L; Adams J

Address

Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport 71130-3932, USA.

Source

Methods Enzymol, 1999, 300:, 345-63

Abstract

It is becoming increasingly apparent that NF-kappa B plays a critical role in regulating the inflammatory response. Data obtained from studies in our laboratories demonstrate that the proteasome plays an important role in the inflammatory cascade by regulating the activation of NF-kappa B. Indeed, the availability of selective and orally active proteasome inhibitors should prove useful in delineating the roles of the proteasome and NF-kappa B in other pathophysiological conditions such as cancer and heart disease.

Language of Publication

English

Unique Identifier

99118181

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MeSH Heading (Major)

NF-kappa B|*ME; Peptide Hydrolases|*DE; Protease Inhibitors|*PD

MeSH Heading

Acetylcysteine|AA/PD; Animal; Arthritis|DT; Boronic Acids|PD; Cell Adhesion Molecules|BI; Cytokines|BI; Dipeptides|PD; Endothelium, Vascular|DE/ME; Female; Hela Cells; Human; Hypersensitivity, Delayed|DT; Jurkat Cells; Leupeptins|PD; Rats; Rats, Inbred Lew; T-Lymphocytes|DE

Publication Type

JOURNAL ARTICLE

ISSN

0076-6879

Country of Publication

UNITED STATES

Record 15 from database: MEDLINE
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Title

Clinical applications of N-acetylcysteine.

Author

Kelly GS

Address

Alternative Medicine Review, Greenwich, CT.

Source

Altern Med Rev, 1998 Apr, 3:2, 114-27

Abstract

N-acetylcysteine (NAC), the acetylated variant of the amino acid L-cysteine, is an excellent source of sulfhydryl (SH) groups, and is converted in the body into metabolites capable of stimulating glutathione (GSH) synthesis, promoting detoxification, and acting directly as free radical scavengers. Administration of NAC has historically been as a mucolytic agent in a variety of respiratory illnesses; however, it appears to also have beneficial effects in conditions characterized by decreased GSH or oxidative stress, such as HIV infection, cancer, heart disease, and cigarette smoking. An 18-dose oral course of NAC is currently the mainstay of treatment for acetaminophen-induced hepatotoxicity. N-acetylcysteine also appears to have some clinical usefulness as a chelating agent in the treatment of acute heavy metal poisoning, both as an agent capable of protecting the liver and kidney from damage and as an intervention to enhance elimination of the metals.

Language of Publication

English

Unique Identifier

98238108

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MeSH Heading (Major)

Acetylcysteine|AE/PD/*TU; Free Radical Scavengers|AE/PD/*TU

MeSH Heading

Antiviral Agents|TU; Expectorants|TU; Glutathione|BI; Human; Poisoning|DT

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

1089-5159

Country of Publication

UNITED STATES

Record 16 from database: MEDLINE
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Title

Managing patients with acute myocardial ischemia and reperfusion injury with N-acetylcysteine.

Author

Stewart S; Ryan C; Poropat S

Address

Department of Cardiology, Queen Elizabeth Hospital, Woodville, South Australia.

Source

Dimens Crit Care Nurs, 1997 May, 16:3, 122-31

Abstract

Previously administered in cases of acetaminophen toxicity, N-Acetylcysteine (NAC) is now also being used in the management of acute myocardial ischemia and reperfusion injury. NAC potentiates the beneficial effects of nitrates such as nitroglycerin and reduces oxidative stress on the heart. The critical care nurse plays an important role in optimizing the therapeutic benefits of NAC and minimizing its potential harmful effects.

Language of Publication

English

Unique Identifier

97332145

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MeSH Heading (Major)

Acetylcysteine|*TU; Free Radical Scavengers|*TU; Myocardial Ischemia|*DT; Myocardial Reperfusion Injury|*DT

MeSH Heading

Acute Disease; Aged; Case Report; Critical Care; Drug Monitoring; Human; Male; Nursing Assessment

Publication Type

JOURNAL ARTICLE; REVIEW; REVIEW, TUTORIAL

ISSN

0730-4625

Country of Publication

UNITED STATES

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