Search PubMed⌕ Search

Biomedical subjects

M G Bogaert

Publications and source records attributed to M G Bogaert.

At least 145 records · Page 8Linked to original sources
PubMed1977

Influence of acute renal failure on the protein binding of drugs in animals and in man.

Serum protein binding of phenylbutazone has been measured in the rat, guinea pig, cat, rabbit and dog, and the influence on it of renal failure induced by uranyl nitrate injection has been studied. In all speciies a clearcut decrease in binding was observed after the occurrence of renal failure; the time course of the fall in binding correlated well with development of renal failure. In further experiments, serum protein binding of two acidic drugs (phenylbutazone, warfarin), two basic drugs (papaverine, quinidine) and one neutral drug (digitoxin) was studied in rabbits with experimental renal failure, and the results compared with those obtained in patients with acute renal failure. In the rabbits, a decrease in the binding of phenylbutazone, warfarin, papaverine and quinidine was found, whereas protein binding of digitoxin was unchanged. In man, there was a definite fall in protein binding of phenylbutazone and digitoxin, a small decrease for warfarin and papaverine, and a slight increase for quinidine.

Acute Kidney Injury↗
PubMed1977

Effect of beta-adrenergic blockade on blood pressure variation in patients with moderate hypertension.

The effect of beta-adrenergic blockade on blood pressure variation was studied in ten patients with moderate hypertension. Supine systolic and diastolic blood pressures were measured every 5 min during six hours sessions, using an ultrasonic method. Systolic and diastolic variation in each six hour session was defined as the standard deviation of the mean of systolic and diastolic readings made in that period. After 3 weeks of single-blind placebo, a 12 week double-blind randomized crossover study was initiated with placebo (6 weeks) and atenolol (100 mg b.i.d. for 3 weeks and 200 mg b.i.d. for 3 weeks). Systolic and diastolic blood pressure and heart rate decreased significantly (p less than 0.01) during atenolol treatment. Diastolic variation did not change significantly, whereas systolic variation decreased slightly but significantly (p less than 0.05) when expressed in absolute values, but not when expressed as a percentage of systolic blood pressure. It is concluded that beta-adrenergic blockade decreases blood pressure and heart rate without causing significant changes in spontaneous systolic or diastolic variation.

Atenolol↗
PubMed1977

Dopamine-induced neurogenic vaso-dilatation in the intact hindleg of the dog.

1 The dopamine-induced neurogenic vasodilation, previously described in the isolated perfused hindleg of the dog, has been studied in anaesthetized dogs with intact circulation in the hindleg. Dopamine was administered intravenously and/or intra-aortically, either as a bolus injection of 4 or 1l mug/kg, or as a continuous infusion of 4, 8, 16 or 32 mug kg-1 min-1. 2 Dopamine, given as a bolus injection or by infusion reversibly inhibited synaptic transmission in the paravertebral lumbar ganglia, studied with preganglionic stimulation at 1Hz. The inhibitory effect decreased gradually when the frequency of stimulation was increased to 16 Hz. The inhibition by dopamine was also present when spontaneous postganglionic activity was recorded. These effects were more pronounced on intra-aortic than on intravenous administration of dopamine. 3 In about half of the animals studied, injection or infusion of dopamine elicited a decrease of vascular resistance in the innervated femoral artery, whereas systemic blood pressure either did not change or decreased. In the denervated femoral artery, an increase in vascular resistance was alway observed. 4 The decrease in femoral vascular resistance was considered to correspond with neurogenic vasodilation caused by paravertebral ganglionic inhibition since (i) it only occurred in the innervated hindleg, (ii) blood pressure did not rise, (iii) this decrease was insensitive to atropine or propranolol and (iv) it was blocked by small doses of haloperidol. When hypovolemic shock was produced, the incidence of the neurogenic decrease of vascular resistance was smaller. 5 Dopamine also increased renal blood flow. This increase was not reduced by the occurrence of the neurogenic vasodilation in the inervated femoral artery. 6 These results are consistent with the idea that the dopamine-induced neurogenic vasodilation, originally described in the isolated perfused hindleg of the dog, also occurs when the circulation to the hindleg is intact. This suggests that, in the dog, also occurs when the circulation to the hindleg is intact. This suggests that, in the dog. the inhibitory effect of dopamine on sympathetic ganglia modulates its peripheral vasoconstrictor effects. In hypovolemic shock, where sympathetic nervous activity is high, the inhibitory effect of dopamine on sympathetic ganglia disappears and its direct vasoconstrictor effect on the vessels dominates.

Animals↗
PubMed1977

Vasodilatation produced by apomorphine in the hindleg of the dog.

Apomorphine, injected into the dog femoral artery in doses of 0.6 microng or higher, produced a marked increase in femoral blood flow, without a change in blood pressure. No increase in flow was produced by comparable doses of dopamine or morphine. After sympathetic denervation or administration of phenoxybenzamine, the apomorphine vasodilatation was either abolished or greatly reduced. When the vascular tone in the denervated hindleg was restored by sympathetic nerve stimulation, the vasodilatory effect of apomorphine often re-established itself; this was not the cases when the vascular tone was restored by an infusion of noradrenaline. The apomorphine vasodilatation was not antagonized by propranolol or atropine. Mepyramine, in doses that antagonize histamine, often inhibited the apomorphine vasodilatation. Haloperidol, injected i.a., antagonized the apomorphine effect without changing the responses to isopropylnoradrenaline, acetylcholine, histamine and and nitroglycerin. Haloperidol blockade was overcome by increasing the dose of apomorphine. These results suggest that apomorphine dilates the femoral vasculature by an action on a "dopamine receptor." The possibility that the receptor is located on sympathetic nerve endings is discussed.

Animals↗
PubMed1975

Radioimmunoassay of digoxin in renal failure: a comparison of different commercial kits.

Six commercially available kits for radioimmunoassay of digoxin were compared. When serum from patients with chronic renal failure on maintenance digoxin therapy was analysed, important discrepancies in the results obtained with the 6 kits were found in some of these patients. However, recovery of digoxin added to serum of a healthy volunteer, was within acceptable limits and comparable for the 6 kits. In patients with renal failure not taking digoxin but several other medications, digoxin estimations gave results close to zero. The affinity of the antibodies for some metabolites of digoxin was also assessed: important differences between the kits were found.

Adult↗
PubMed1975

Dopamine-induced neurogenic vasodilatation in isolated perfused muscle preparation of the dog.

Dopamine, injected into the lumbar aorta of the dog in doses which produce a reversible inhibition of synaptic transmission in the lumbar paravertebral ganglia (0.5-64x10-8 moles), produces a neurogenic vasodilatation in the isolated perfused hindleg or gracilis muscle. This was abolished by acute preganglionic decentralization and by administration into the perfused preparation of alpha-adrenoceptor blocking agents, but not of atropine or diphenhydramine. After decentralization, preganglionic electrical stimulation restored the dopamine-induced indirect vasodilatation. The neurogenic vasodilatation was also seen with intra-aortic injections of epinine (2-32x10-8 moles) and apomorphine (1.2-19.2x10-8 moles) and was preferentially blocked by haloperidol (0.26x10-6 moles). (-)-Noradrenaline, injected into the lumbar aorta in baroreceptor-denervated dogs, was found to be equipotent with dopamine in eliciting the neurogenic vasodilatation; this (-)-noradrenaline-induced effect was preferentially blocked by phentolamine (8x10-6 moles). The possibility that the neurogenic vasodilatation, which occurs upon intra-aortic injection of dopamine in the dog, is due to its gnaglionic-inhibitory effect is discussed.

Acetylcholine↗
PubMed1975

The influence of imipramine on dopamine-induced ganglionic inhibition and neurogenic vasodilatation in the dog.

Imipramine potentiates the dopamine-induced inhibition in the paravertebral lumbar ganglia of the dog. Potentiation by imipramine of the dopamine-induced neurogenic vasodilatation in the isolated perfused gracilis muscle, is seen in cross-circulation preparations only, where imipramine is injected into the perfusion circuit of an isolated perfused gracilis muscle, it antagonizes the dopamine-induced neurogenic vasodilatation. When imipramine is injected intravenously into a dog with an autoperfused gracilis muscle, the peripheral antagonism masks the potentiating effect at the ganglionic level, and the dopamine-induced neurogenic vasodilatation is abolished.

Action Potentials↗
PubMed1975

Meptazinol (Wy 22811), a new analgesic: preliminary pharmacokinetic data.

The authors report on the pharmacokinetic profile of a new analgesic, meptazinol, from studies of plasma and urine levels after intravenous injection in 4 healthy volunteers. Conjugated product is formed very soon after injection and its concentration changes little over the period studied compared with the unchanged product where a fast, then a relatively slow phase of decline can easily be distinguished, suggesting a two compartment open system model. Meptazinol is predominantly eliminated in this conjugated form by urinary excretion of the metabolites. Excretion is very rapid in the first few hours after dosing and elimination is almost completed after 24 hours.

Analgesics↗
PubMed1975

Metabolism of papaverine. I. Identification of metabolites in rat bile.

1. After hydrolysis with glusulase of bile from rats treated with papaverine, four metabolites (A, B, C and D) were separated. 2. The structures A, B and C were established as monodemethylated compounds, 4'-desmethyl-, 7-desmethyl-, and 6-desmethylpapaverine, respectively. 3. D was formed from papaverine by bis-desmethylation. Since it was found in cat bile after administering either A or C, but not B, it was identified as 4', 6-desmethylpapaverine.

Animals↗
PubMed1975

Metabolism of papaverine. II. Species differences.

1. The urinary and biliary excretion of radioactive products in a 6 hr period after intravenous administration of [3H]papaverine was studied in rat, guinea-pig, rabbit, cat and dog. All species excreted metabolites extensively in the bile; only in rabbit and guinea-pig is urinary excretion important. 2. Metabolites in urine and bile of all species studied are mainly monophenolic compounds conjugated to glucuronic or sulphuric acid. Differences in the excretion patterns of the metabolites between different species are only quantitative. 3. Blood or plasma levels of papaverine after intravenous injection decreased with half-lives of approximately 12, 15, 22, 60 and 60 min for rabbit, rat, guinea-pig, cat and dog, respectively. The metabolites disappeared much more slowly than papaverine from the plasma. 4. Binding of papaverine to plasma proteins, as studied by equilibrium dialysis, was more than 90% in all species.

Animals↗