PubMed Health⌕ Search

Biomedical subjects

C Richer

Publications and source records attributed to C Richer.

At least 109 records · Page 6Linked to original sources
PubMed1980

Beta-adrenoceptor blocking effects and pharmacokinetics of betaxolol (SL 75212) in man.

1 The pharmacological effects and the pharmacokinetics of betaxolol (SL 75212), a new beta-adrenoceptor blocking agent, were compared with those of propranolol and a placebo in a double-blind trial involving six healthy volunteers. 2 Heart rate (HR), myocardial contractile force (MCF), systolic blood pressure (SBP) and peak expiratory flow rate (PEFR) were measured at rest and during vigorous exercise before and at intervals up to 25 h after oral administration of the drugs. In addition, plasma renin activity (PRA) at rest and blood levels of betaxolol and propranolol were determined. 3. Betaxolol proved to be a potent and long-lasting beta-adrenoceptor blocking drug, devoid of intrinsic beta-sympathomimetic activity. Its beta-adrenoceptor blocking action was shown to four-fold that of propranolol at the cardiac and renal levels and to last at least 25 h after drug intake. 4 The peak blood level of betaxolol was reached 2 to 4 hr after its administration, the first-pass loss is likely to be low and the half-life is 12.3 h. These pharmacokinetic data are perfectly consistent with the long duration of the pharmacological effects of betaxolol in man.

Adrenergic beta-Antagonists↗
PubMed1980

Captopril and hypertension development in the SHR.

Captopril (100mg/kg) administered daily by gavage to young spontaneously hypertensive rats (SHRs) from their 6th to 20th weeks of age almost completely inhibited genetic hypertension development (GHD). This effect was correlated with an early and long-lasting limitation of the progressive increase in peripheral resistance which normally develops in SHRs during their growth. Heart rate, cardiac and systolic indexes remained unchanged, plasma renin concentration was significantly increased and heart weight/body weight ratio was significantly decreased. At last, captopril's GHD preventive effect persisted up to 12 weeks after treatment discontinuation.

Angiotensin II↗
PubMed1980

beta-Adrenoreceptor blockage and genetic hypertension development in rats.

The effects of propranolol (100 mg/kg), atenolol (200 mg/kg) and acebutolol (1000 mg/kg) administered daily by gavage to spontaneously hypertensive rats (SHRs) from their 6th to 20th weeks of age were investigated on genetic hypertension development (GHD) and at regular intervals on heart rate (HR), cardiac output (CO), stroke volume (SV), peripheral resistence (PR), plasma renin concentration (PRC) and heart weight/body weight ratio (HW/BW). Treatment with propranolol and especially atenolol markedly inhibited GHD while acebutolol was ineffective. No correlation was found between GHD prevention and (1) the degree of beta-adrenergic blockade (2) the reductions in HR and CO and (3) the decrease in PRC induced by the three treatments. Although none of the three drugs prevented the progressive increase in PR which develops in SHRs during their growth, propranolol and atenolol opposed GHD mainly by reducing CO, this effect being however partly counterbalanced for atenolol by a secondary potentiation of PR increase. With acebutolol, a similar reinforcement of PR increase occurred which completely neutralized the reduction in CO, resulting in the drug's ineffectiveness against GHD. These differential effects of the three drugs probably reflect different early induced structural modifications at cardiac and/or vascular levels.

Acebutolol↗
PubMed1980

[Antihypertensives and the prevention of development of genetic hypertension in the hypertensive SHR rat].

1. The preventive effects against genetic hypertension development (GHD) of seven antihypertensive drugs chronically administered to the young SHRs from their 5th to their 13th week of age have been investigated. 2. While prazosin (20 mg/kg) and hydrochlorothiazide (6,5 and 25 mg/kg) are ineffective and while YC 93, a calcium-antagonist (10, 30, 100 mg/kg) exerts only a slight protective effect, captopril (30 and 100 mg/kg), dihydralazine (25 mg/kg) and atenolol (200 mg/kg) strongly prevent GHD. 3. Captopril and dihydralazine oppose GHD by inhibiting the progressive increase in peripheral resistance (PR) which normally occurs with ageing in SHRs. Simultaneously, these two drugs do not affect the cardiac output (CO) but increase plasma renin concentration (PRC). On the other hand, atenolol opposes GHD mainly by reducing CO and PRC while it simultaneously reinforces the progressive increase of PR with age. Captopril and atenolol, unlike dihydralazine, limit SHRs' myocardial hypertrophy. 4. After 14 weeks of treatment, arterial blood pressure (BP) of dihydralazine - and atenolol-treated animals meets control animals BP within 4 weeks whereas captopril preventive effects are still present up to 12 weeks after treatment discontinuation. Wit atenolol and captopril ther is after treatment discontinuation a good correlation between the evolution of heart weight/body weight and BP, which suggests that captopril could temporarily oppose the myocardial structural alterations which usually accompany GHD.

Animals↗
PubMed1980

Pulmonary tuberculosis in children.

A major change has occurred in the incidence and management of pulmonary tuberculosis in patients of all ages. This review emphasizes the effectiveness of drug therapy and the declining role of surgical management of pulmonary tuberculosis in children. Surgical intervention was necessary in only two of 140 children (1.4%) with proved tuberculosis, one for a large tuberculoma and the other for refractory involvement of the chest wall. The remaining 138 children were treated successfully with anti-tuberculous drugs. Pulmonary tuberculosis in children is primarily a medical disease and only rarely is surgical intervention indicated.

Adolescent↗
PubMed1978

Chronic atenolol treatment and hypertension development in spontaneously hypertensive rats.

Changes in systolic blood pressure (SBP), heart rate (HR), heart rate and plasma renin concentration (PRC) have been compared in three different groups of rats between the ages of 5 and 20 weeks. The groups were: spontaneously hypertensive rats (SHRs), atenolol-treated SHRs (200 mg/kg/day orally throughout the 15 weeks) and normotensive rats of the same strain (WKYs). Treatment with atenolol markedly inhibited the onset of genetic hypertension, reduced HR and PRC from the outset and diminished the heart weight/body weight ratio. Comparison of changes in these parameters in atenolol-treated SHRs, control SHRs and WKYs strongly suggests that the mechanism of atenolol's preventive action against hypertension development in SHRs primarily involves its effects on heart and on the renin--angiotensin system.

Animals↗
PubMed1978

Clazepam: pharmacokinetics and effects on performance.

1. The effects of clazepam, a new benzodiazepine (30 mg orally) on performance tests and the cardiovascular system have been compared to those of chlordiazepoxide (30 mg orally) and a placebo in a double-blind trial involving six healthy volunteers. Simultaneously, the pharmacokinetics of clazepam were investigated. 2. While clazepam itself could be detected neither in plasma nor in urine, it gave rise to two plasma metabolites, the former, an alcoholic derivative with a short half-life, and the second, desmethyldiazepam, with a long half-life. These two metabolites and oxazepam were excreted in urine and, within the 24 h period following drug intake, accounted for 73% of the ingested dose. 3. Seven hours after its administration, clazepam slightly improved performance and reduced anxiety. The kinetics of these effects and the metabolic data suggest that clazepam acts mainly through the formation of desmethyldiazepam. However, owing to the low blood levels of this metabolite, the activity of clazepam was very moderate.

Adult↗
PubMed1977

[Determination of plasma digoxin in newborn infants. Practical applications].

Measurement of plasma digoxin concentrations in infants after three increasing dosage levels shows that the optimal dose of this glycoside in 20 microgram/kg/day, i.e. a loading dose of 20 microgram/kg followed every 8 hours by a maintenance dose of 7 microgram/kg. The plateau concentration achieved is 3.0 +/- 0,5 ng/ml 8 hours after the last administration. When digoxin levels exceed 5 ng/ml (overdosage, renal failure or low body weight), toxic manifestations occur.

Digoxin↗
PubMed1977

Comparative beta-adrenoceptor blocking effects and pharmacokinetics of penbutolol and propranolol in man.

1 The beta-adrenoceptor blocking effects of penbutolol were compared with those of propranolol and a placebo in a double-blind trial involving six healthy volunteers. 2 Heart rate (HR), systolic blood pressure (SBP) and peak expiratory flow rate (PEFR) were measured at rest and during vigorous exercise before and at intervals up to 7 h after oral administration of the drugs. In addition, plasma renin activity (PRA) at rest and plasma levels of penbutolol and propranolol were determined. 3 Penbutolol proved to be a non-cardioselective beta-adrenoceptor blocking drug, antagonizing exercise-induced tachycardia, reducing exercise-induced increase in PEFR and decreasing PRA. The beta-adrenolytic potency of penbutolol was shown to be four-fold that of propranolol but the duration of its effect was similar. 4 The peak plasma level of penbutolol was reached 1 h after administration and its half-life was 4.5 h. 5 Comparison of plasma levels and biological activity of penbutolol revealed that after oral administration this drug is transformed into an active metabolite in man.

Adrenergic beta-Antagonists↗
PubMed1977

Plasma renin activity and its postnatal development in preterm infants. Preliminary report.

Immunoassayable plasma renin activity (PRA) was measured in 16 healthy preterm infants of different gestational ages. A total of 52 measurements have been performed between the second week of life and the date of the expected term. PRA was found markedly increased in preterm infants and a highly significative negative correlation with postmenstrual age was proved.

Female↗
PubMed1976

Influence of sex on the clinical pharmacology of flutiorex, a new anorectic drug.

The effects of flutiorex, a new anorectic agent, and of a placebo on food intake and the activity of the sympathetic and central nervous systems have been compared in a double blind trial in two groups of healthy volunteers, one of five males and the other of five females. Flutiorex 20 mg orally had a significant anorectic effect both in males and females, the observed reduction in food intake being 34.0 and 27.5%, respectively. It caused alpha-adrenergic stimulation (blood pressure and pupil diameter) and central nervous system excitation (critical flicker frequency), both of which were more marked in males than in females. Flutiorex was better tolerated by women than by men. Measurement of the blood level of flutiorex and its de-ethylated metabolite, norflutiorex, showed that both compounds were detectable in four of the five male subjects, but in only one of the five females. Sex-linked differences in the pharmacokinetics of flutiorex may explain the greater intensity of its effects in males.

Adult↗
PubMed1976

Preliminary assessment of flutiorex, a new anorectic drug, in man.

1 The effects of +/--flutiorex, a new anorectic agent, on food intake, the sympathetic nervous system and the central nervous system were compared to those of fenfluramine and a placebo in a double-blind trial involving six healthy volunteers. 2. Flutiorex exerts a singificant anorectic effect and was shown to be approximately twice as potent as fenfluramine in this regard. 3 Flutiorex induces a definite alpha-adrenergic sympathomimetic stimulation as was shown by a rise in systolic blood pressure and the development of marked mydriasis. 4 Flutiorex is a central nervous system stimulant producing an increase in critical flicker frequency. It does not, however, influence psychomotor coordination as reflected in the pursuit rotor test. 5 Serial determinations of blood and urine levels of flutiorex and its deethylated metabolite, norflutiorex, showed that flutiorex is rapidly absorbed and deethylated, accumulates in large quantities in the tissues and, like its metabolite, is excreted in the urine in very small quantities. Blood levels of norflutiorex appear to remain elevated longer than those fo flutiorex.

Adult↗