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M Chaignon

Publications and source records attributed to M Chaignon.

65 records · Page 4Linked to original sources
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Clinical pharmacology of prazosin in hypertensive patients with chronic renal failure.

The clinical pharmacology of prazosin was studied in 10 hypertensive patients with chronic renal failure (group I) and in 9 hypertensive patients with normal renal function (group II). Prazosin, 2 mg, was given orally and blood samples were drawn at intervals for spectrofluorimetric assay. Blood pressure and heart rate were obtained at the same time. In the renal failure group, prazosin induced a significant decrease in systolic and diastolic blood pressures (-19 and -23%, respectively) at 90 min after intake, and these alterations were more rapid and marked than in the normal renal function group. Peak plasma concentration (Cmax) was higher (33.5 +/- 3.7 vs. 20.04 +/- 1.7 micrograms/liter, p < 0.01) and occurred earlier (1.3 +/- 0.2 vs. 2.7 +/- 0.3 hr, p < 0.005) in group I than in group II. The area under the plasma concentration-time curve (AUC0 infinity) was increased in the renal failure group (206.1 +/- 31.1 vs. 112.4 +/- 9.4 micrograms/hr/liter, p < 0.01). Apparent plasma elimination half-life (t 1/2) was not significantly different in the two groups (3.6 +/- 0.4 vs. 2.9 +/- 0.3 hr. ns). The mean blood pressure change (delta MBP%) was significantly correlated with the plasma level of prazosin in the renal failure group (n = 97, r = 0.489, p < 0.001) but not in patients with normal renal function (n = 74, r = 0.297, ns). The hypotensive action of prazosin is greater in patients with chronic renal failure, and the bioavailability or distribution of the drug is altered. Therefore, prazosin dosages should be modified in patients with impaired renal function.

Adult↗
PubMedDate not supplied

Clinical pharmacology and pharmacokinetics of prizidilol in hypertensive patients.

We evaluated the clinical pharmacology of prizidilol, a compound with vasodilator and beta-blocking properties, in 12 hypertensive patients with normal renal function. A single dose of 600 mg prizidilol was given orally and blood samples were withdrawn at intervals for high-performance liquid chromatography assay. Blood pressure and heart rate were recorded every hour in supine and standing positions. A nitroglycerin test was performed at the 2nd, 4th, and 6th h for evaluation of cardiac beta-adrenoceptor activity. Results were compared with those after placebo intake the day before. Prizidilol produced a significant decrease in supine systolic and diastolic blood pressures (-22 and -24%, respectively), with a maximum effect 5 h after intake. Blood pressure changes were not different in slow and fast acetylators, suggesting that the acetylated metabolites were active. Heart rate decreased slightly but significantly during the first 2 h, but was similar to control levels thereafter. However, the nitroglycerin test data suggested a prolonged blockade of beta-adrenoceptor activity. Pharmacokinetics showed large variations among patients; several peaks were observed on the curves, indicating irregular absorption. The apparent plasma elimination half-life was 4.4 +/- 0.4 h. Total body clearance was high despite a very low renal clearance, indicating that the drug was eliminated mainly by the metabolic or intestinal route. No significant correlations were found among plasma concentration, blood pressure, and heart rate. In conclusion, prizidilol is a potent antihypertensive drug having equilibrated vasodilator and beta-blocking effects. The pharmacokinetic data suggest a first-pass effect and elimination by extra-renal routes.

Adrenergic beta-Antagonists↗
PubMedDate not supplied

Acute and chronic effects of a new calcium inhibitor, nicardipine, on renal hemodynamics in hypertension.

Renal hemodynamics and natriuresis were studied in 10 hypertensive patients without renal failure, 2 and 4 h after oral intake of 30 mg nicardipine; then, nicardipine was given at a dose of 30 mg three times a day and the hemodynamic study was repeated on the 6th day (2 h after the morning dose). The first dose of nicardipine produced an increase in renal blood flow (from 888 +/- 45 to 999 +/- 59 ml/min 1.73 m2, p less than 0.01) and a decrease in renal vascular resistances (from 0.16 +/- 0.01 to 0.12 +/- 0.01 arbitrary unit, p less than 0.05). Glomerular filtration rate did not change and the decrease in filtration fraction was not significant. Sodium excretion increased markedly during the first 2 h (from 0.17 +/- 0.04 to 0.29 +/- 0.06 mmol/min, p less than 0.05). On the 6th day renal vascular resistances and filtration fraction remained lowered whereas glomerular filtration rate was unchanged. Nicardipine did not produce any significant alteration in plasma renin activity and plasma aldosterone after acute or chronic administration. These results confirm the potent renal vasodilatory effect of nicardipine; glomerular filtration rate was not significantly altered whereas renal blood flow and filtration fraction returned to normal levels. An early and transient natriuretic effect was observed after the first dose of nicardipine, and body weight showed a significant decrease during the study indicating that no sodium retention was induced by nicardipine.

Adult↗
PubMedDate not supplied

Effect of hemodialysis on blood volume distribution and cardiac output.

Effects of hemodialysis on extracellular fluid volume distribution, left ventricular volumes, and cardiac output were determined in patients with end-stage renal disease (n = 19). Distribution of extracellular fluid loss from hemodialysis differed widely among patients, so that weight change correlated weakly with contraction of total blood volume (index of determination 29%, p less than 0.05). End-diastolic volume (EDV) decreased from 150 +/- 49 ml (mean +/- SD) to 118 +/- 42 ml, p less than 0.001; stroke volume (SV) decreased from 108 +/- 36 to 86 +/- 33 ml (p less than 0.001) without change in ejection fraction (from 0.73 +/- 0.09 to 0.74 +/- 0.11). A significant correlation was found between total blood volume (TBV) and EDV before (r = 0.66, p less than 0.005) and after dialysis (r = 0.61, p less than 0.001). The correlation between TBV and SV was highly significant before (r = 0.78, p less than 0.001) and after dialysis (r = 0.66, p less than 0.005), but there was no correlation between change in TBV and change in EDV or in SV. The ratio of EDV to TBV (EDV/TBV x 100) was reduced significantly from 3.49 +/- 0.92 to 3.06 +/- 0.97, p less than 0.001). There results suggest that, although intravascular volume was the major determinant of cardiac output in dialyzed patients, the postdialysis reduction in cardiac output might be related more to the relocation of blood volume than to the absolute degree of blood volume contraction.

Blood Volume↗
PubMedDate not supplied

Blood pressure response to hemodialysis.

Blood pressure response to hemodialysis was investigated in 15 patients with end-stage kidney disease; mean arterial pressure was unchanged in five (Group 1) and reduced 10 mm Hg in 10 (Group 2). The two groups did not differ significantly with regard to either biochemical values or hemodynamic indices before dialysis, and both sustained comparable reduction in body weight, total blood volume, and cardiac output following dialysis. Heart rate remained unchanged in both. The only significant difference between the two was the response of total peripheral resistance (TPR) to fluid depletion. TPR rose adequately in Group 1 but was unchanged in Group 2 (7.5 +/- 2.2 (SE) vs 0.7 +/- 1.1 units, p less than 0.025) despite equal fall in cardiac output in both (881 +/- 212 vs 890 +/- 173 ml/m, p less than 0.10). Thus, differences in arterial pressure response to fluid loss by hemodialysis could be due to impaired autonomic control of resistance vessels; this abnormality might not be revealed by tests of baroreceptor activity that depend only on heart rate responses to blood pressure variations.

Adult↗
PubMedDate not supplied

[Amyloidosis and polycythemia vera (author's transl)].

The authors report a case of systemic amyloidosis with predominantly hepatic, splenic and renal deposits and polycythemia vera with secondary myelofibrosis. The course of both diseases during a 9-year-follow-up and the late appearance of a monoclonal IgM lead the authors to examine a possible relationship between the two diseases.

Amyloidosis↗