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Biomedical subjects

H Grobecker

Publications and source records attributed to H Grobecker.

At least 55 records · Page 3Linked to original sources
PubMed1983

Ceftazidime: pharmacokinetics in young volunteers versus elderly patients and therapeutic efficacy with complicated urinary tract infections.

Thirty-six urological patients (21 male, 15 female) aged 21 to 83 years with complicated and/or hospital-acquired urinary tract infections due to sensitive bacteria were treated with ceftazidime intravenously with a daily dose of 2 g bd over 5 to 17 days. Twenty-seven patients were followed for 1 to 4 weeks after therapy. Cure was observed in 41%, reinfection in 33% and relapse in 26% of the patients. Eradication of the original pathogen occurred in 74%. Five patients showed minor side effects: diarrhoea (2), nausea (1), rash (1), headache (1). No signs of renal, hepatic or haematological toxicity were observed. A pharmacokinetic study was performed in 13 elderly patients aged 63 to 83 years on day 1 of treatment and in 6 volunteers aged 24 to 32 years following administration of 2 g of ceftazidime as short intravenous infusion. The mean serum half life in 12 patients 2.9 h significantly higher than in volunteers (1.75 h). Serum concentrations in patients on day 7 of treatment, however, showed no accumulation when treated with a dosage of 2 g bd.

Adult↗
PubMed1983

Transmitter-peptide coexistence in the central nervous system.

In this minireview about transmitter coexistence situations in central nervous system and peripheral sympathetically innervated tissues, the classical transmitters, dopamine, noradrenaline, adrenaline and serotonin, together with peptides such as substance P, cholecystokinin and avian pancreatic polypeptide, have been considered. The specificity of an immunohistochemical reaction for the identification of peptides and functional aspects of central transmitter peptide coexistence are discussed. In conclusion, in several experimental models it has been demonstrated that peptides, which are known to coexist with monoamines, exert specific effects in those regions where coexistence situations have been reported. In general, the effect of the co-stored peptides seems to be enhancement of the response caused by monoamines, indicating that two coexisting neuroactive substances cooperate in causing a certain physiological response.

Adrenal Medulla↗
PubMed1982

Induction of anesthesia with halothane increases plasma norepinephrine concentrations.

In seven unstimulated, unmedicated patients given halothane/O2 via face mask, plasma norepinephrine concentration increased 15 min after induction and returned to control at 45 to 60 min. Changes in plasma norepinephrine levels did not correlate with changes in cardiovascular variables. In 10 additional awake, unpremedicated patients, plasma norepinephrine concentration did not change during 5 min of application of 100 per cent oxygen via face mask, but rose with subsequent administration of halothane and nitrous oxide. Again, changes in plasma norepinephrine did not correlate with changes in cardiovascular variables. The authors perfused seven isolated cat spleens with a Krebs-Ringer's lactate solution. Addition of 0.01 atm halothane to the perfusate initially increased release of norepinephrine into the effluent. The authors conclude that halothane or halothane-nitrous oxide initially increases plasma norepinephrine during induction of anesthesia. This increase is not due to the placement of a face mask, but may relate to an effect of halothane at sympathetic nerve endings.

Adolescent↗
PubMed1981

Plasma noradrenaline correlates to sympathetic muscle nerve activity in normotensive man.

Recordings of multiunit sympathetic activity were made in muscle branches of the peroneal nerve in 22 healthy subjects at rest in recumbent position. Nerve activity was quantitated in terms of burst incidence (number of pulse synchronous sympathetic bursts per 100 heart beats or per min). In a separate session, 4-45 months later, blood was drawn from an antecubital vein for noradrenaline analysis. Both sympathetic activity and plasma concentrations of noradrenaline varied widely between subjects and both parameters increased with age. There was a significant positive correlation between a subject's level of sympathetic activity and his plasma concentration of noradrenaline. It is suggested that overflow of transmitter from sympathetic terminals in muscles contributes significantly to plasma levels of noradrenaline at rest.

Adult↗
PubMed1981

Comparative determination of cefotaxime and desacetyl cefotaxime in serum and bile by bioassay and high-performance liquid chromatography.

In rat serum as well as in human serum and bile after injection of cefotaxime (CTX), the parent compound and the active metabolite desacetyl cefotaxime (dCTX) have been demonstrated by quantitative analysis with high-performance liquid chromatography (HPLC). Simultaneous determination of CTX by bioassay using test organisms sensitive to both CTX and dCTX resulted in spuriously high concentration readings of CTX. Using dCTX insensitive test organisms concentrations of cefotaxime obtained by agar diffusion test and by assay with HPLC were highly correlated. In human serum and bile after i.v. injection of 2 g CTX, as may be administered therapeutically, high concentrations of dCTX were observed. dCTX has a longer elimination half-life than the parent molecule. It is concluded that the measurement of CTX in biological fluids should be performed by HPLC or by bioassay with a selective test organism in order to obtain correct pharmacokinetic parameters.

Adult↗
PubMed1980

Exercise induced changes of catecholamines and potassium in plasma of dogs after treatment with propranolol.

Previous studies in man have shown that during beta-adrenoceptor blockade physical exercise caused a significantly greater elevation of plasma catecholamines than without blockade. After blockade of beta-adrenoceptors, increased levels of circulating catecholamines should have an unopposed effect on adrenergic alpha-receptors. In order to elucidate such an effect, experiments were performed with 7 trained dogs before and after acute beta-adrenoceptor blockade (0.1 mg/kg (-)-propranolol i. v.). Exercise was performed on a conveyor (10 min, 10 km/h, slope 10%). Besides catecholamine concentrations in plasma, as an index of alpha-receptor-stimulation potassium concentrations in plasma were determined. Immediately after exercise, plasma noradrenaline was increased from 310 to 579 pg/ml, plasma adrenaline from 136 to 222 pg/ml and plasma potassium from 4.23 to 4.6 mmol/l. After beta-adrenoceptor blockade exercise caused a significantly higher increase in plasma noradrenaline from 352 to 755 pg/ml and plasma adrenaline from 172 to 260 pg/ml. Also plasma potassium concentrations were significantly elevated from 4.03 to 5.05 mmol/l. The results indicate an enhanced reflex activation of sympatho-neuronal and sympatho-adrenal mechanisms during exercise after beta-adrenoceptor blockade; the increased concentrations of noradrenaline at the adrenoceptors might reduce the efficiency of beta-blockade. Concomitantly, increased stimulation of alpha-adrenoceptors is elicited, which becomes obvious by an increase of potassium concentration in plasma.

Animals↗
PubMed1979

[Effects of acute beta-adrenoceptor blockage (metoprolol i.v.) on plasma norepinephrine concentration and hemodynamics in postmyocardial infarction patients].

The effect of acute beta-adrenoceptor blockage (Metoprolol) (M), 0.1 mg/kg i.v.) on left ventricular performance has been investigated at rest and during exercise in 15 patients with 2--3 months old transmural myocardial infarctions. Coronary venous and arterial norepinephrine (NE) concentrations were determined. There was no significant change in arterial and coronary venous NE concentrations (0.27 and 0.22 ng/ml, respectively) after blockage of beta-adrenoceptors (0.36 vs 0.26 ng/ml), which caused a fall of stroke volume from 79 to 68 ml, a reduction of ejection fraction from 62 to 55% and of circumferential fibre shortening form 1.2 to 0.9 circ/sec. During physical exercise the plasma NE concentration in the arterial (0.51 ng/ml) and coronary venous (0.6 ng/ml) blood increased significantly and increased even further to 0.65 and 0.76 ng/ml, respectively, following administration of Metoprolol. The arterio-coronary sinus difference in NE concentrations demonstrate a release of NE from the myocardium. As compared to control values, heart rate following Metoprolol was lower (116 vs 106/min), mean PCV pressure was slightly increased (from 21 to 23 mm Hg) and there was a fall of cardiac index from 6.3 to 5.2 l/min X m2. It is likely that the increased sympathetic activity after Metoprolol and during exercise is a compensatory reaction due to the hemodynamic effects of blockade of beta-adrenoceptors. Further studies are in preparation in order to find out if this is only a transient phenomenon during the early adaptation phase after blockade of beta-adrenoceptors.

Adult↗
PubMed1978

Changes in central catecholaminergic neurons in the spontaneously (genetic) hypertensive rat.

Catecholamines and catecholamine-synthesizing enzymes have been examined in specific brain areas during the development of spontaneously (genetic) hypertensive (SH) rats. Changes in catecholamine metabolism were localized to regions of the brain implicated in the regulation of blood pressure. Norepinephrine levels and dopamine-beta-hydroxylase (DBH) activities were decreased in specific nuclei of the hypothalamus and in the nucleus interstitialis striae terminalis ventralis, in both young and adult rats. The decrease in the formation of norepinephrine can result in a reduced activation of central alpha-adrenergic receptors which may be related causally to the onset of hypertension. The activity of the epinephrine-forming enzyme, phenylethanolamine-N-methyltransferase (PNMT), was increased in the A1 and A2 areas of the brainstem in young SH rats, but it was normal in adult hypertensive animals. These results implicate adrenergic neurons in the brainstem and noradrenergic neurons in the hypothalamus in the development of spontaneous (genetic) hypertension in rats.

Animals↗
PubMed1977

Effect of prolonged treatment with adrenergic neuron blocking drugs on sympathoadrenal reactivity in rats.

The effects of repeated high doses of the adrenergic neuron blocking drug guanethidine or a hexahydropyrazinoindole compound (2-guanyl-1,2,3,10,10a, hexahydro-1,2,a-pyrazinoindole, EMD 21192) (30 mg/kg i.p., 21.5 mg/kg i.p. respectively, equimolar doses) on sympathoadrenal activity were investigated in normotensive adult rats. During treatment for 5 weeks with either guanethidine or EMD 21192 the systemic blood pressure fell steadily. Noradrenaline content in the heart and vas deferens were decreased markedly by guanethidine and to a much less degree by EMD 21192. EMD 21192 markedly lowers the catecholamine content of the adrenal medulla, presumably as a result of inhibition of dopamine-beta-hydroxylase. The plasma catecholamine concentrations reflected the different sites of action of the drugs in the sympathoadrenal system, i.e. guanethidine mainly reduced circulating norepinephrine and dopamine-beta-hydroxylase by more than 50%, whereas EMD 21192 decreased considerably by the total catecholamines (mainly epinephrine) without altering significantly in the plasma norepinephrine. Disappearance or reduction of fluorescent nerve endings in the iris and the heart and a decrease of the intensity of fluorescence in chromaffin cells of the adrenal gland caused by the drugs were consistent with the biochemical alteration. Whereas the repeated doses of guanethidine caused degeneration of sympathetic nerves, destruction of adrenergic neurons was not found after prolonged treatment with EMD 21192.

Adrenal Glands↗
PubMed1977

[Quantitative parameters of sympatho-neuronal and sympatho-adrenal activities in man. The influence of beta-receptor blocking agents (author's transl)].

Determination of both catecholamine concentrations (norepinephrine and epinephrine) and the activity of dopamine-beta-hydroxylase in the plasma of health volunteers and hypertensive patients leads to the conclusion that these parameters used together can be considered an index for sympathetic neuronal activity. However, highly specific and sensitive radiometric methods are necessary for the measurement of these biochemical parameters. In healthy volunteers and hypertensive patients after acute and chronic administration of beta-adrenergic blocking agents, e.g., propranolol, practolol or penbutolol, a significantly higher increase of catecholamine concentrations in the plasma has been observed during physical exercise. This pronounced increase in plasma catecholamine concentrations (mainly norepinephrine) is probably due to an enhanced compensatory sympathetic neuronal activity, accompanied by an increased peripheral resistance; this is obviously necessary in order to maintain a sufficient perfusion of peripheral tissues during work load under the influence of beta-adrenergic blocking agents, since an adequate cardiac output is prohibited by blockade of adrenergic beta-receptors. On the other hand, the pronounced increase in sympathetic tone after beta-blockade, especially after administration of high doses, could be responsible for certain reported side effects, such as hypertensive crisis in psychiatric patients or in patients with phaeochromocytoma.

Adrenal Medulla↗
PubMed1977

Biochemical and morphologic study of catecholamine metabolism in spontaneously hypertensive rats.

Catecholamines and catecholamine-synthesizing enzymes have been studied quantitatively in specific brain areas of spontaneously (genetically) hypertensive rats by means of a combination of sensitive enzymatic-isotopic methods and a microdissecting technique. Changes in catecholamine metabolism were found to be localized to regions of the brain implicated in the regulation of blood pressure. Noradrenaline levels were decreased in specific nuclei of the anterior hypothalamus and in the nucleus interstitialis striae terminalis ventralis. The activity of the adrenaline-forming enzyme, phenyl-ethanolamine-N-methyl transferase, was increased in the A1 and A2 areas of the brain stem. These results implicate catecholamine-forming neurons in the hypothalamus and brain stem in the development of spontaneous hypertension in rats.

Animals↗