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Biomedical subjects

M Chaignon

Publications and source records attributed to M Chaignon.

At least 37 records · Page 2Linked to original sources
PubMed1986

[Clinical pharmacology of enalapril in hypertension with chronic renal failure].

The effects of a single oral dose of enalapril (20 mg) on blood pressure (BP), heart rate (HR) plasma renin activity (PRA) aldosterone (PA), converting enzyme inhibition (CEI) and enalaprilat (E, active metabolite) were investigated during 96 h in 3 groups of 5 hypertensive patients with (1) normal renal function (creatinine clearance: Clcr greater than 80 ml.min-1); (2) moderate chronic renal failure: 80 greater than or equal to Clcr greater than 30 ml.min-1; (3) severe chronic renal failure: 30 greater than or equal to Clcr greater than 10 ml.min-1. Results are as follows (mean +/- SEM): (Table: see text) CEmax: maximal plasma concentration; TEmax: delay corresponding to CEmax; TE 1/2: plasma elimination half-life; AUCE: area under plasma level versus time curve. a: p less than 0.01; b: p less than 0.001; versus (1). In the 3 groups, CEI reached 87-94% as early as the 3rd h; however, at 96 h, CE1 was higher in (3) than in (1) and (2): 77.6 +/- 3.3% versus 6.0 +/- 1.6 and 17.7 +/- 4.8 (p less than 0.001 respectively). In (3). PRA increased at the 1st h and remained elevated: at 96 h, delta PRA was + 3.0 +/- 2.9 ng.ml-1 -.h-1 in (3) versus + 0.10 +/- 0.06 and + 0.25 +/- 0.17 ng.ml-1.h-1 .n (1) and (2) [(3) versus (1): p less than 0.01]; delta PA was lower in (3): -4.56 +/- 2.01 ng. 100 ml-1 versus -0.54 +/- 0.31 and -2.50 +/- 0.38 ng. 100 ml-1 [(3) versus (1): p less than 0.05].(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1985

Comparative study of muzolimine and acebutolol in the treatment of moderate hypertension.

In a controlled double-blind study the effect of muzolimine (20 mg o.d.) and acebutolol (400 mg o.d.) were investigated in outpatients suffering from moderate essential hypertension. After a three week placebo run-in period, 49 patients were recruited and followed by a cooperative group of general practitioners over a period of 3 months. Blood pressure decreased to the same extent in both groups. With regard to clinical and biological tolerance, no differences appeared between the two drugs.

Acebutolol↗
PubMed1985

[Comparative effects of nifedipine and indapamide in the treatment of arterial hypertension].

A controlled multicentre trial was organised to compare the effects of 20 mg Nifedipine tablets (N) and 2,5 mg Indapamide tablets (I) during a 4 months' treatment period after a placebo period, in 59 patients with moderate essential hypertension (n = 59). The results of blood pressure measurements of 18 patients treated by nifedipine (1 tablet twice daily) and 22 patients treated by indapamide (1 tablet every morning) were compared. The systolic blood pressure, after 10 minutes recumbency, fell from 165 +/- 10 mmHg to 148 +/- 13 mmHg (p less than 0.01), and the diastolic pressure from 104 +/- 6 mmHg to 86 +/- 7 mmHg (p less than 0.01) in the patients treated with nifedipine. In the indapamide group, the SBP fell from 164 +/- 13 mmHg to 152 +/- 15 mmHg (p less than 0.01) and the DBP from 100 +/- 4 mmHg to 87 +/- 6 mmHg (p less than 0.01). There were no significant changes of heart rate with either drug; plasma creatinine, potassium and uric acid concentrations were also unchanged. There was a higher incidence of headaches and tiredness in the nifedipine group, whilst patients treated with indapamide complained more often of muscular cramps. Flushing was observed in nearly a quarter of the patients in both groups. These results confirm that both nifedipine and indapamide induce significant and persistant falls in systolic and diastolic blood pressure. Although the fall was greater with nifedipine than with indapamide, the difference was not statistically significant. The tolerance was satisfactory in both groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

[Acute and chronic effects of a new calcium blocker, nicardipine, on renal hemodynamics in arterial hypertension].

Renal hemodynamics and natriuresis were studied in 9 hypertensive patients without renal failure, 2 hours and 4 hours after oral intake of Nicardipine 30 mg; sodium intake was kept constant during the study (100 mmol per day). 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 hours after the morning dose). Renal blood flow (RBF) and glomerular filtration rate (GFR) were measured by the clearance methods using 131I-hippuran and 125I-iothalamate respectively. Results are as follows: (Table: see text). These results confirm the potent renal vasodilatory effect of Nicardipine; GFR was not significantly altered while RBF and FF 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.

Calcium Channel Blockers↗
PubMed1984

[Malignant arterial hypertension, symptomatic and prognostic aspects. Retrospective study of 140 cases].

140 cases of malignant hypertension were diagnosed in our clinic from January 1966 to December 1982. On admission the mean blood pressure was 183 +/- 17 mm Hg, and all patients had grade III to IV retinopathy according to the Keith and Wagener classification; 84% of the patients had renal failure (10% of acute origin). 43% of the patients presented with clinical signs of left heart failure. Hypertension was associated with various renal diseases in 48%, was essential in 41%, and renovascular lesions were found in 9% of the cases. Headaches, asthenia and visual disorders were the 3 main symptoms of malignant hypertension, as classically described. Severe cerebral damage (including all the neurological manifestations present on admission) was found in 27% of the patients. Among the 122 patients available to follow-up, half died during the study period. The survival rate, calculated on a 5-year basis, has doubled compared with a similar patient population 17 years ago, increasing from 35% (period 1966 to 1970) to 72% (period 1977-1982). This remarkable achievement in survival rate is due to more intensive research and therapeutic progress (including, more recently, extrarenal epuration) reaching an increasingly large hypertensive population.

Adolescent↗
PubMed1984

Influence of chronic renal failure on captopril pharmacokinetics and clinical and biological effects in hypertensive patients.

The pharmacokinetic parameters of unchanged plasma captopril and the kinetics of the drug effects on plasma converting enzyme activity (PCEA), plasma renin activity (PRA), plasma aldosterone (PA) and mean blood pressure (MBP) were studied over 24 h after oral administration in three groups of hypertensive patients: with normal renal function (group 1, plasma creatinine less than 110 mumol/l, n = 10), with moderate chronic renal failure (group 2, 135 less than plasma creatinine less than 450 mumol/l, n = 10) and with severe chronic renal failure (group 3, plasma creatinine greater than 500 mumol/l, n = 10). Renal impairment had no effect on plasma captopril Cmax, CLtot and relative bioavailability (AUC). In contrast, captopril kel decreased while T1/2 increased progressively from group 1 to group 3. PCEA blockade (T1/2 and AUC) was increased significantly and proportionally to the degree of renal impairment. However, there were no differences between the three groups regarding captopril-induced modifications of PRA and PA. Although the maximal reduction in MBP was identical in the three groups, the overall antihypertensive effect (AUC) of captopril increased significantly and progressively from group 1 to group 3, especially in duration. There was no correlation between basal plasma creatinine values and unchanged captopril relative bioavailability (AUC) and between unchanged captopril relative bioavailability (AUC) and the drug effects (AUC) on PCEA, PRA, PA and MBP. However there was a correlation between basal plasma creatinine values and plasma captopril T1/2, PCEA blockade (AUC) and overall antihypertensive effect (AUC). The apparent discrepancy between the lack of effects of chronic renal failure on plasma unchanged captopril bioavailability and its potentiating effects on PCEA blockade and MBP reduction may be accounted for by the renal impairment-induced accumulation of captopril metabolites.

Adult↗
PubMed1984

[Effect of renal insufficiency on the pharmacokinetics of captopril and converting enzyme inhibition in the hypertensive patient].

The influence of renal insufficiency (RI) on the pharmacokinetics of captopril (1 mg/kg, orally) and on the kinetics of the induced converting enzyme inhibition (CEI) was investigated in three groups of hypertensive patients: without RI (n = 10, plasma creatinine less than 100 mumol/l), with moderate RI (MRI) (n = 10,200 less than creatinine less than 400 mumol/l) and with severe RI (SRI) (n = 8, creatinine greater than 500 mumol/l). Captopril pharmacokinetic parameters were not modified by RI, with the exception of elimination half-life which was lengthened, but relative bioavailability of the drug was not modified. In contrast, captopril-induced CEI was strongly potentiated in patients with RI, an effect correlated with plasma creatinine values. This apparent discrepancy between the lack of modification in captopril plasma bioavailability and the prolongation of its biological effects can probably be accounted for by a decreased elimination and/or an increased formation of captopril metabolites during RI.

Adult↗
PubMed1982

[Cardiovascular effects of prostacyclin].

Numerous studies have recently been devoted to the effects of prostaglandins on blood vessels. Prostacyclin (PGI2) produces relaxation of vascular smooth muscles, thereby contributing, with other vasoactive substances, to the regulation of general and local haemodynamics. Moreover, it would appear that the effects of some risk factors in atherosclerosis are mediated, at least partly, by changes in prostaglandin production. The potent vasodilator action of prostacyclin has been confirmed in man and has been investigated in some pathological conditions, such as lower limb arteriopathy, malignant arterial hypertension and coronary artery disease. The vascular effects of many therapeutic drugs are now known to be associated with their action on the biosynthesis of prostaglandins. Further studies are required to determine the role of prostaglandins, especially prostacyclin, in the pathophysiology, prevention and treatment of vascular diseases.

Animals↗
PubMed1982

Acute effects of hemodialysis on echographic-determined cardiac performance: improved contractility resulting from serum increased calcium with reduced potassium despite hypovolemic-reduced cardiac output.

The hemodialysis session leads to reduction in circulating blood volume (TBV) and arterial pressure (BP) plus correction of electrolyte imbalance. The effect of these alterations on cardiac performance was evaluated in 18 patients with end-stage renal disease. Hemodialysis for 5 hours led to significant reduction (p less than 0.001) in weight TBV, and BP. Neither ejection fraction nor percentage fiber shortening was altered, whereas mean velocity of circumferential fiber shortening (mean VCF) and mean systolic ejection rate (MSER) were both significantly increased (1.17 +/- 0.20 to 1.38 +/- 0.28 circ/sec and 2.38 +/- 0.27 to 2.80 +/- 0.40 EDV/sec, respectively; p less than 0.001 for each). Since both venous return and systolic BP were decreased, increase in velocity of ventricular contraction implies enhancement of cardiac performance beyond what would be expected from alterations in ventricular filling and resistance to ejection. This enhancement is possibly related to concomitant reduction in serum potassium (p less than 0.001) and increase in serum calcium (p less than 0.005) achieved by hemodialysis.

Blood Pressure↗
PubMed1982

Hemodynamic effects of hemodialysis and hemofiltration.

The hemodynamic effects (n = 8) of hemodialysis (HD) and hemofiltration (HF) were compared in the same group of dialyzed patients. The two procedures induced the same decrease in body weight, total blood volume, and blood pressure; however, hemodynamic alterations were different. Cardiac index and stroke index decreased markedly with HD and did not change significantly with HF, and peripheral resistance remained stable after HD and decreased significantly after HF. These results suggest that the maintenance of a high cardiac output may account for the lack of acute hypotensive episodes reported during HF. The reduction of blood pressure after HF is related to the decrease in total peripheral resistance. Thus, the arterial vasodilator effect induced by HF might explain the improvement of severe hypertension on long-term treatment with HF, as reported previously.

Adult↗
PubMed1982

[Acute effects of metoprolol on blood pressure and heart rate. Value of the nitroglycerin test].

The acute effects of Metoprolol on blood pressure and heart rate were studied with reference to the plasma level of the betablocker in 10 patients (6 male and 4 female) with permanent moderate uncomplicated hypertension. Each patient was given a single oral dose of 200 mg Metoprolol: blood samples were taken over a 12 hour period at given times for Metoprolol estimation. The blood pressure was measured with a mercury manometer; heart rate was measured lying and during a stress test (glyceryl trinitrate). The antihypertensive effect of Metoprolol was significant from the 4th hour; at the 8th hour the systolic pressure was reduced by 15% and the diastolic pressure by 17% (p less than 0.001). The blood pressure then rose progressively. The heart rate in the recumbent position fell 10 to 15% during the study. The heart rate during the trinitrin test varied linearly with time (r = 0.991, p less than 0.001). The variation in systolic and diastolic blood pressure did not correlate with the plasma Metoprolol level (r = 0.03, and 0.19); no correlation was found between the fall in lying heart rate and the plasma betablocker level. On the other hand, the trinitrin heart rate (at the end of the test) correlated negatively with the logarithm of the plasma Metoprolol (n = 56, r = 0.688, p less than 0.001). These results confirm that the antihypertensive effect of Metoprolol is not directly related to the plasma level of the betablocker. On the other hand, the betablocker effect assessed by the trinitrin test, correlated with the plasma Metoprolol level. This relationship is similar to those previously observed with other betablockers; atenolol and oxprenolol.

Adrenergic beta-Antagonists↗
PubMed1982

[Acute hemodynamic effects of prostacyclin in severe or malignant hypertension].

The antihypertensive effect of Prostacyclin (PGI2) was investigated in 7 patients with severe or malignant hypertension. Cardiac output (dilution method), arterial blood pressure and total blood volume (TBV, radio-albumin dilution method) were measured before and during a PGI2 infusion, the effective dose ranging from 10 to 20 ng/kg/min. Cardiac index(CI) rose from 2.8 to 3.9 1/min/m2 and heart rate (HR) from 75 to 94 beats/min (p less than 0.01) Mean blood pressure decreased from 154 to 120 mmHg (p less than 0.001) and total peripheral resistances from 4650 to 2540 dynes.s.cm-5 (p less than 0.001). The ratio: central blood volume/total blood volume increased from 0.21 to 0.26 (p less than 0.001). The results confirm that PGI2 produces a potent vasodilatation of the systemic compartment with a marked decrease in blood pressure; however the antihypertensive effect is blunted by the increase in CI mainly related to the increase in HR; significant central translocation of blood suggests that PGI2 does not produce dilatation of the capacitance vessels. Sympathetic nervous system is highly stimulated by PGI2 very likely through the baroreceptor system.

Antihypertensive Agents↗