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1. |
On the significance of significant |
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Clinical Pharmacology&Therapeutics,
Volume 30,
Issue 1,
1981,
Page 1-2
Walter Modell,
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摘要:
Clinical Pharmacology and Therapeutics(1981)30,1–2; doi:10.1038/clpt.1981.1
ISSN:0009-9236
DOI:10.1038/clpt.1981.120
年代:1981
数据来源: WILEY
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2. |
Suicide enzyme inhibitors as potential drugs |
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Clinical Pharmacology&Therapeutics,
Volume 30,
Issue 1,
1981,
Page 3-22
Albert Sjoerdsma,
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摘要:
Clinical Pharmacology and Therapeutics(1981)30,3–22; doi:10.1038/clpt.1981.1
ISSN:0009-9236
DOI:10.1038/clpt.1981.121
年代:1981
数据来源: WILEY
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3. |
Dynamic responses to continuous use of prazosin and hydralazine in patients with refractory heart failure |
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Clinical Pharmacology&Therapeutics,
Volume 30,
Issue 1,
1981,
Page 23-30
U Elkayam,
M Mathur,
W Frishman,
T LeJemtel,
J Strom,
E H Sonnenblick,
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摘要:
The hemodynamic effects of oral doses of prazosin and hydralazine were studied in the same group of patients with chronic congestive heart failure. Prazosin, 3 to 10 mg, and hydralazine, 75 to 100 mg, were given by mouth every 6 hr and the responses to the first and the fifth consecutive dose were compared. The first dose of prazosin was followed by a predominant effect on left ventricular filling pressure and concomitantly by reduction of left ventricular afterload. Hydralazine acted primarily on left ventricular afterload with no significant effect on the filling pressure. A marked difference was noted in respect to the dynamic responses to continuous therapy with these two drugs. While the initial hemodynamic effect of prazosin was markedly attenuated in most of the cases after the fifth consecutive oral dose, the response to hydralazine was augmented by continuous therapy. These findings suggest that the reported hemodynamic tachyphylaxis seen with prazosin does not occur with hydralazine when given to the same patients with chronic congestive heart failure. Our study also indicates the importance of prolonged monitoring for the assessment of the hemodynamic effect of prazosin and hydralazine in patients with severe chronic congestive heart failure.Clinical Pharmacology and Therapeutics(1981)30,23–30; doi:10.1038/clpt.1981.1
ISSN:0009-9236
DOI:10.1038/clpt.1981.122
年代:1981
数据来源: WILEY
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4. |
Reduction of first‐pass hepatic clearance of propranolol by food |
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Clinical Pharmacology&Therapeutics,
Volume 30,
Issue 1,
1981,
Page 31-34
Allan J McLean,
Cheryl Isbister,
Alex Bobik,
Francis J Dudley,
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摘要:
Exposure to drugs, chemicals, and hormones from the gut depends on initial (first‐pass) liver extraction and subsequent removal from the general circulation. We show that food decreases first‐pass liver extraction of a marker drug, propranolol, during first‐pass transit. This effect may apply to other drugs, environmental chemicals, and nutritional and gut‐hormone balance.Clinical Pharmacology and Therapeutics(1981)30,31–34; doi:10.1038/clp
ISSN:0009-9236
DOI:10.1038/clpt.1981.123
年代:1981
数据来源: WILEY
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5. |
Effects of diuretic and propranolol on plasma lipoprotein lipids |
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Clinical Pharmacology&Therapeutics,
Volume 30,
Issue 1,
1981,
Page 35-43
John H Bauer,
Charles S Brooks,
Ira Weinstein,
Henry H Wilcox,
Murray Heimberg,
Rebecca N Burch,
Rachael Barkley,
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摘要:
Ticrynafen (TCNF), a nonthiazide diuretic, has been reported to be nonhyperlipidemic. To define the effects of these drugs on plasma lipoproteins, experiments were performed in hypertensive subjects after placebo therapy, 4 wk after therapy with either hydrochlorothiazide (HCTZ) or TCNF, 3 mo after diuretic with propranolol, and 1 mo after therapy with propranolol alone. Plasma lipoproteins were separated by ultracentrifugation and the lipid fractions isolated by extraction and silicic acid thin‐layer chromatography. Plasma low‐density lipoprotein (LDL) total cholesterol fell and high‐density lipoprotein (HDL) total cholesterol rose in subjects receiving TCNF. TCNF had no effect on plasma very low‐density lipoprotein (VLDL) triglyceride or phospholipid. There were no significant changes in LDL or HDL total cholesterol in subjects on HCTZ. HCTZ tended to increase plasma VLDL triglyceride and phospholipid. The addition of propranolol to either diuretic had no effect on LDL or HDL total cholesterol but increased VLDL triglyceride, especially in subjects on HCTZ. Propranolol alone had no effect on any of the lipids measured.Clinical Pharmacology and Therapeutics(1981)30,35–43; doi:10.1038/clp
ISSN:0009-9236
DOI:10.1038/clpt.1981.124
年代:1981
数据来源: WILEY
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6. |
Verapamil disposition kinetics in chronic atrial fibrillation |
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Clinical Pharmacology&Therapeutics,
Volume 30,
Issue 1,
1981,
Page 44-51
Robert E Kates,
Deborah L D Keefe,
Janice Schwartz,
Sandra Harapat,
Edward B Kirsten,
Donald C Harrison,
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摘要:
Verapamil disposition was studied in 12 patients with chronic atrial fibrillation. After an intravenous bolus of 15 mg plasma concentration was determined and the data fit to a three‐compartment model. Model independent parameters were calculated and values for half‐life (t½), clearance, and steady‐state distribution volume were 6.3 ± 4 hr, 13.3 ± 7.7 ml/min/kg, and 4.3 ± 1.9 l/kg. The model was used to design a multistep infusion scheme, which was employed successfully to acheive predetermined plasma concentrations. Following single oral doses of 120 mg, plasma levels of verapamil and norverapamil were determined. The elimination t½ for verapamil and norverapamil were 8.2 ±6.1 and 10.5 ± 5.6 hr, respectively. The bioavailability of oral verapamil was 35 ± 16%. During long‐term oral therapy the mean verapamil plasma concentration was twice the value predicted from the single‐dose studies. This suggests that verapamil may have reduced clearance during long‐term oral use.Clinical Pharmacology and Therapeutics(1981)30,44–51; doi
ISSN:0009-9236
DOI:10.1038/clpt.1981.125
年代:1981
数据来源: WILEY
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7. |
Direct determination of hepatic extraction of verapamil in cardiac patients |
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Clinical Pharmacology&Therapeutics,
Volume 30,
Issue 1,
1981,
Page 52-56
Barry G Woodcock,
Wolfgang Schulz,
Gisbert Kober,
Norbert Rietbrock,
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摘要:
Hepatic extraction of verapamil was determined directly in cardiac patients undergoing diagnostic catheterization and receiving 10 mg verapamil intravenously or intra‐arterially. The extraction curves of verapamil concentrations in blood from the ascending aorta and hepatic vein were similar to those reported after single intravenous doses of indocyanine green. The rectilinear fall in concentration lasted 10 to 15 min. Mean hepatic extraction of verapamil in four patients who received intravenous doses was 0.86 (range 0.84 to 0.89) and in four who received intra‐arterial doses was 0.87 (range 0.83 to 0.89). These estimates are the same as those for hepatic first‐pass extraction determined by indirect methods based on areas under plasma concentration‐time curves and requiring calculation of apparent hepatic blood flow. The results are considered to be proof that the first‐pass effect of verapamil after oral doses is attributable mainly, if not entirely, to hepatic elimination.Clinical Pharmacology and Therapeutics(1981)30,52–56; doi:10.1038/c
ISSN:0009-9236
DOI:10.1038/clpt.1981.126
年代:1981
数据来源: WILEY
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8. |
Effects of labetalol and methyldopa on renal function |
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Clinical Pharmacology&Therapeutics,
Volume 30,
Issue 1,
1981,
Page 57-63
Frank Cruz,
William M O'Neill,
Gil Clifton,
John D Wallin,
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摘要:
Renal function studies were performed in subjects with mild hypertension treated with labetalol (n = 5) and moderate to moderately severe hypertension treated in a random double‐blind fashion with either labetalol (n = 6) or methyldopa (n = 6). Drugs were given in doses sufficient to reduce standing diastolic blood pressure to<90 mm Hg. This was achieved in all subjects without significant side effects. Inulin clearance, para‐aminohippurate clearance, filtration fraction, free‐water clearance, and maximal concentrating ability were assessed before and after 15 days of drug. No alterations in any parameter were noted with labetalol. Inulin clearance fell by 13% (p<0.05), and filtration fraction fell from 0.23 to 0.18 (p<0.02), but other parameters of renal function did not change with methyldopa.Clinical Pharmacology and Therapeutics(1981)30,57–63; doi:10.1038/clpt.
ISSN:0009-9236
DOI:10.1038/clpt.1981.127
年代:1981
数据来源: WILEY
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9. |
Minoxidil and pericardial effusion: An idiosyncratic reaction |
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Clinical Pharmacology&Therapeutics,
Volume 30,
Issue 1,
1981,
Page 64-70
Michael J Reichgott,
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摘要:
Minoxidil is a new potent antihypertensive vasodilator. Although highly effective, its use is limited by the association of the drug with pericardial effusion. We examined possible relationships in 37 patients. There were two significant effusions identified by echocardiography in 22 patients under active treatment. Retrospective review of 15 additional patients no longer under treatment identified seven who had had effusion and one who had had transient pericarditis. Resolution of effusion accompanied withdrawal in five patients; rechallenge was followed by effusion in one patient. Ninety‐one episodes of pericardial disease have been reported in 1,869 experimental subjects (4.8%). Pericardial tamponade occurred in 21, with eight associated deaths. There are no specific patient characteristics that predict the likelihood of effusion. Since the reaction is both idiosyncratic and potentially fatal, it seems appropriate to continue to limit the use of minoxidil.Clinical Pharmacology and Therapeutics(1981)30,64–70; doi:10.1038/clpt.1981
ISSN:0009-9236
DOI:10.1038/clpt.1981.128
年代:1981
数据来源: WILEY
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10. |
Barbiturate and hypnosedative withdrawal by a multiple oral phenobarbital loading dose technique |
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Clinical Pharmacology&Therapeutics,
Volume 30,
Issue 1,
1981,
Page 71-76
Geoffrey M Robinson,
Edward M Sellers,
Eva Janecek,
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摘要:
Although intravenous phenobarbital loading is effective in barbiturate withdrawal, controlled infusions of drug are inconvenient. To develop a practical and more widely applicable method, oral loading doses of phenobarbital were given to 21 barbiturate addicts, whose estimated mean daily intake of barbiturates was 1 gm (range 0.5 to 4 gm). Twelve had a past or present history of barbiturate withdrawal seizures. Phenobarbital was given orally at a rate of 120 mglhr until a predetermined clinical end point of phenobarbital effect was achieved. This end point was the presence of at least three of the following: nystagmus, drowsiness, ataxia, dysarthria, or emotional lability. The total phenobarbital loading dose (x̄ ± SD) was 23.4 ±7.1 mg/kg, median phenobarbital concentration after loading was 35.9 mg/1 (range 13.2 to 71.6 mg/1), and median half‐life (t½) of phenobarbital was 90 hr (range 38 to 240 hr). One patient with t½ = 38 hr was given supplemental doses of phenobarbital. None developed seizures or other evidence of barbiturate withdrawal.Clinical Pharmacology and Therapeutics(1981)30,71–76; doi:10.1038/clpt
ISSN:0009-9236
DOI:10.1038/clpt.1981.129
年代:1981
数据来源: WILEY
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