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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hemodynamic responses to ventricular defibrillation were studied in anesthetized dogs. Observations were made on arterial, right atrial and left ventricular end-diastolic pressures, on cardiac output (dye dilution), heart rate, and right atrial electrocardiogram. Ventricular fibrillation was induced electrically with a bipolar electrode catheter placed in the right ventricle. Fibrillation was maintained for 15 or 30 sec and terminated with a 400 w sec capacitor discharge across the thoracic cage. Responses lasted 1-10 min after conversion and included a cholinergic and an adrenergic component. The cholinergic component was characterized by sinus bradycardia, periods of sinus arrest, atrioventricular block, and ventricular premature beats. The adrenergic component included increases in arterial pressure, in cardiac output, and in left ventricular stroke work at a time when left ventricular end-diastolic pressure was normal; there was no change in total peripheral resistance. The pH of arterial blood decreased slightly and pCO(2) increased but pO(2) and the concentration of lactate were unchanged. Bilateral vagotomy and intravenous administration of atropine blocked the cholinergic component, unmasked a sinus tachycardia, and accentuated the adrenergic component of the response. The latter was blocked by intravenous administration of propranolol and phenoxybenzamine.THESE RESPONSES WERE RELATED PRIMARILY TO CONVERSION OF VENTRICULAR FIBRILLATION RATHER THAN TO THE ELECTRICAL DISCHARGE OF COUNTERSHOCK BECAUSE COUNTERSHOCK WITHOUT VENTRICULAR FIBRILLATION CAUSED MORE TRANSIENT AND SMALLER RESPONSES THAN THOSE OBSERVED WITH DEFIBRILLATION: furthermore, the hemodynamic effects of defibrillation were augmented by prolongation of the duration of fibrillation. The results suggest that the cholinergic component of the response may be detrimental in that it favors spontaneous recurrence of fibrillation; on the other hand, the adrenergic component may be essential for conversion since only one of six dogs depleted of endogenous catecholamines with reserpine survived ventricular defibrillation.
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PMID:Hemodynamic effects of ventricular defibrillation. 490 40

To analyze the hemodynamic parameters during prosthetic circulation as an entity, non linear mathematical techniques were used. To compare natural and prosthetic circulation, two pneumatically actuated ventricular assist devices were implanted as biventricular bypasses in chronic animal experiments using adult goats to consitute the biventricular bypass complete prosthetic circulation model with ventricular fibrillation. After implantation, these goats were placed in a cage and extubated after waking. All hemodynamic parameters with the natural circulation without biventricular bypass pumping, and the artificial circulation with biventricular bypass pumping under ventricular fibrillation were recorded under awake conditions. By the use of a non linear mathematical technique, the arterial blood pressure waveform was embedded into a four dimensional phase space and projected into three dimensional phase space. The Lyapunov numeric method is used as an adjunct to the graphic analysis of the state space. A phase portrait of the attractor showed a high dimension complex structure, with three dimensional solid torus suggesting deterministic chaos during natural circulation. However, a simple attractor, such as a limit cycle attractor, was observed during artificial circulation. Positive Lyapunov exponents during artificial circulation suggest the lower dimensional chaotic system. Thus, hemodynamic parameters during prosthetic circulation must be carefully controlled when unexpected stimuli are fed from outside.
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PMID:Deterministic chaos in the hemodynamics of an artificial heart. 772 27

Seven conscious dogs documented to be at high risk by the occurrence of ventricular fibrillation (VF) during acute myocardial ischemia were randomly assigned to 6 weeks of either daily exercise training or cage rest followed by exercise training. After 6 weeks of daily treadmill training, heart rate variability, a marker of vagal tone, increased by 74% (P < .001); baroreflex sensitivity, a marker of the capability to reflexly augment vagal activity, increased by 69% (P < .01); the repetitive extrasystole threshold, a marker of ventricular electrical stability, increased by 44% (P < .05). After exercise training, the incidence of ventricular fibrillation during acute myocardial ischemia decreased by 100%, as all animals survived. Neither passage of time nor heart rate level during ischemia contributed to the outcome. The most likely mechanism to explain the striking change in risk status is the shift in autonomic balance characterized by increased cardiac vagal activity, which was previously shown to have an antifibrillatory effect. These results suggest that exercise training in healthy individuals may decrease their likelihood of developing lethal arrhythmias during acute myocardial ischemia.
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PMID:Exercise training confers anticipatory protection from sudden death during acute myocardial ischemia. 808 69