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Biomedical subjects

J Brachmann

Publications and source records attributed to J Brachmann.

148 records · Page 9Linked to original sources

Effect of brief periods of paced ventricular tachycardia on coronary blood flow in dogs before and after graded coronary stenosis.

The effect of short bouts (1 min) of electrically induced ventricular tachycardias (VT) of increasing rates (160-240/min) was studied in 8 anesthetized dogs before and after graded constrictions of the left anterior descending (LAD) and the circumflex (CCA) coronary arteries. In the absence of coronary stenosis, paroxysmal VT caused a significant decrease in tension-time index (TTI), coronary blood flow (CBF) and coronary vascular resistance (CVR). Single and combined coronary stenosis caused relatively small alterations of the VT-induced depression of the systemic hemodynamics but reversed the effect of paroxysmal VT on the CVR. In the presence of single 90% LAD stenosis, VT resulted in an increase in CVR-LAD and a decrease in F-LAD associated with a fall in CVR-CCA and a rise in F-CCA. Combination of 90% LAD plus 70% CCA stenosis abolished the compensatory fall of CVR-CCA resulting in a pronounced reduction of F-CCA during VT. The results support the concept that in the presence of severe coronary stenosis brief paroxysmal ventricular tachycardias do increase myocardial nutritional demand but rather decrease nutritional supply.

Animals↗

Role of some components of ischemia in the genesis of spontaneous ventricular arrhythmias.

The importance of single components of ischemia including hypoxia, lactic acidosis, high potassium, and sympathetic stimulation to the spontaneous occurrence of ventricular arrhythmias was studied in chloralose-anesthetized cats using systemic and local intracoronary administration. Hypoxia and acidosis provoked no spontaneous arrhythmias regardless of systemic or regional administration. Systemic or local hyperpotassemia induced regularly ventricular ectopic activity including recurrent ventricular tachycardias that were characterized by a sudden onset and termination and by a stable rate. Stimulation of the left, right or bilateral stellate ganglia failed to provoke ventricular arrhythmias during hypoxia or acidosis and had also no influence on the initiation or rate of K+-induced ventricular tachycardias. The results indicate that high extracellular K+ may be the predominant arrhythmogenic factor of the components of ischemia we studied and that sympathetic ganglia stimulation does not affect K+-induced ventricular tachycardia.

Acidosis↗