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Biomedical subjects

C A Muller

Publications and source records attributed to C A Muller.

At least 37 records · Page 2Linked to original sources
PubMed1983

Calcium antagonists and the acutely ischemic heart: experimental effects on ventricular fibrillation and enzyme release.

To investigate and to compare the protective action of verapamil, nifedipine and diltiazem on the acutely infarcting myocardium, we studied effects on cellular damage and mechanical function in the isolated working rat heart preparation subjected to left main coronary artery ligation. First, the fall in the ventricular fibrillation threshold (VFT) was diminished by all three agents, but non-specific effects of these agents were operating at least in part. All three compounds afforded substantial dose-dependent reduction of lactate dehydrogenase release, which was taken as an index of cellular damage, and preserved ATP stores in the infarcting myocardium. The range of effective concentrations was small and close to doses which produced atrioventricular conduction disturbances (verapamil, diltiazem) or LV pump failure (nifedipine). It is argued that these concentrations may be therapeutically relevant, whereas the concentration of a beta-adrenoceptor antagonist agent required comparably to inhibit enzyme release was supra-therapeutic (metoprolol 10(-4) M). There are substantial differences between such animal models and the situation in acute myocardial infarction in man, where preliminary data show benefits both for beta-adrenergic blockade by sotalol and for calcium antagonism by nifedipine.

Adrenergic beta-Antagonists↗
PubMed1982

Cholinergic modulation of enhanced vulnerability to ventricular fibrillation evoked by adrenergic stimulation in the isolated rat heart.

We investigated whether acetylcholine could antagonize the enhanced vulnerability to ventricular fibrillation evoked by adrenergic stimulation. Epinephrine, 5 X 10(-7)M, caused an 80% reduction in the ventricular fibrillation threshold and a 130% increase in the tissue level of cAMP. Acetylcholine 1 X 10(-7)M, 5 X 10(-7)M, and 1 X 10(-6)M, reduced the epinephrine-induced fall in the ventricular fibrillation threshold by 42%, 100%, and 94%, respectively. This antifibrillatory effect of acetylcholine could not be related to tissue levels of cGMP but rather was associated with reduced tissue levels of cAMP. These results demonstrate cholinergic modulation of the epinephrine-enhanced vulnerability to ventricular fibrillation and suggest that reduced accumulation of cAMP may underlie this effect.

Acetylcholine↗
PubMed1981

Influence of propranolol isomers and atenolol on myocardial cyclic AMP, high energy phosphates and vulnerability to fibrillation after coronary artery ligation in the isolated rat heart.

The isolated rat heart with ligation of the left coronary artery was used to assess the role of the beta 1- adrenergic receptor-cyclic AMP mechanism in the genesis of vulnerability to ventricular fibrillation in early myocardial ischaemia. Coronary artery ligation was followed after 3 min by a reduction in ventricular fibrillation threshold which reached a minimum at 15 min. This was accompanied by reduction of ATP and phosphocreatine while cyclic AMP was significantly increased in ischaemic myocardium. The dl-, l- and d-isomers of propranolol attenuated the decrease in ventricular fibrillation threshold and the increase in ischaemic myocardial cyclic AMP, without altering the tissue depletion of ATP. Specific beta 1-adrenergic receptor antagonism with atenolol did not prevent either the increase of tissue cyclic AMP or the reduction in ventricular fibrillation threshold and high energy phosphates. These findings suggest that the mechanism whereby vulnerability to fibrillation is increased in very early myocardial ischaemia is linked to changes in cyclic AMP content of ischaemic myocardium and appears independent of depletion of myocardial high energy phosphates.

Adenosine Triphosphate↗
PubMed1979

Protective action of amiodarone against ventricular fibrillation in the isolated perfused rat heart.

The pretreatment of rats with amiodarone for 2 minutes to 3 weeks before the excision of their hearts caused a dose-related decrease in heart rate and an increase in the ventricular fibrillation threshold both before and after coronary arterial ligation. Similarly, amiodarone decreased the incidence of ventricular premature extrasystoles, ventricular tachycardia and fibrillation during the period of regional ischemia after coronary arterial ligation and also after reperfusion of the ischemic myocardium. There was no evidence of a metabolic protective effect on ischemic myocardium because tissue high energy phosphate content decreased to a similar extent in ischemic myocardium from control and amiodarone-treated rats. Instead, the protective effect of amiodarone against fibrillation was accompanied by attenuation of the increase in tissue cyclic adenosine monophosphate in ischemic myocardium after coronary arterial ligation. It is proposed that amiodarone exerts a potent antifibrillatory effect by decreasing tissue cyclic adenosine monophosphate in ischemic myocardium.

Amiodarone↗
PubMed1979

[Prevention of paralytic ileus after colonic surgery by continuous peridural sympathetic block. Preliminary report].

Gastrointestinal atony must be considered as a reflex response to surgical intervention, due to activation of sympathetic nerves. Following colonic surgery, the duration of this response may be notably extended and the ensuing intestinal distension becomes the paramount factor of a persisting ileus. Blocking the sympathetic fibers prevents intestinal distension. Introducing appropriate catheter into the peridural space up to the level of the 10th--11th thoracic vertebra makes it possible to realize a segmental continuous block between T6--L2, where gastrointestinal sympathetic innervation actually originates. Using bupivacaine at low concentration (0.125% with epinephrine 1/400,000) reduces untoward effect on circulation and may even prove beneficial if volaemia is effective. In addition, it produces a selective block on the visceromotor fibers which allows a differential diagnosis of the ileus, without risking to pass over a perforation of the gut whenever a coexisting mechanical factor is suspected.

Autonomic Nerve Block↗
PubMed1978

Cyclic A.M.P. and arrhythmias revisited.

Further evidence is presented for a hypothesis linking cyclic adenosine 3', 5' monophosphate (cyclic A.M.P.) and arrhythmias: in the isolated rat heart, changes in tissue cyclic A.M.P. are accompanied by changes in the ventricular-fibrillation threshold; and in the pig, large infarcts are associated with raised tissue cyclic A.M.P. and ventricular fibrillation, whereas small infarcts are not. Data showing that changes in the metabolism of potassium, glucose, fatty acids, and lactate can influence the action-potential duration are incorporated into a revised hypothesis which allows for multifactorial arrhythmogenic mechanisms in the early stages of acute myocardial infarction.

Action Potentials↗
PubMed1978

[Closed hemorrhoidectomy using Ferguson's technic].

The author describes the "closed" method of hemorrhoidectomy, as advised by J.A. Ferguson, about forty years ago. In retrospect, reviewing 237 cases operated with this method between 1963 and 1976, it appears that the closed hemorrhoidectomy induces less postoperative pain and is fraught with less postoperative complications. Hospitalization averages 5 days. The complete duration of treatment is 4 weeks with an average loss of work of 19.5 days. If our fellow-surgeons are really prepared to relinquish sectarism and to seek for "modern" techniques, they should consider closed hemorrhoidectomy as the treatment of choice for this untoward condition.

Hemorrhoids↗