Search PubMed⌕ Search

Biomedical subjects

W J Gamble

Publications and source records attributed to W J Gamble.

At least 37 records · Page 2Linked to original sources
PubMed1972

The Anrep effect reconsidered.

Evidence is presented supporting the hypothesis that the positive inotropic effect after an abrupt increase in systolic pressure (Anrep effect) is the recovery from subendocardial ischemia induced by the increase and subsequently corrected by vascular autoregulation of the coronary bed. Major evidence consists of data obtained from an isolated heart preparation showing that the Anrep effect can be abolished with coronary vasodilation, and that with an abrupt increase in systolic pressure there is a significant reduction in the distribution of coronary flow to subendocardial layers of the ventricle. Furthermore, the intracardiac electrocardiogram shows S-T segment and T wave changes after an abrupt increase in ventricular pressure similar to that noted after coronary constriction. Major implications are that normally there may be ischemia of the subendocardial layers tending to reduce myocardial contractility which may account, in part, for the positive inotropic effect of various coronary vasodilators; that with an abrupt increase in ventricular pressure the subendocardium is rendered temporarily ischemic, placing the heart in jeopardy from arrhythmias until this is corrected; and that end-diastolic pressure and the intracardiac electrocardiogram may provide a means of evaluating the adequacy of circulation to subendocardial layers in diseased ventricles when systolic pressure is abruptly increased.

Adenosine Triphosphate↗
PubMed1971

Left ventricular performance and coronary flow after coronary embolization with plastic microspheres.

Coronary flow, left ventricular circumference, and left ventricular pressure were observed in the isovolumically contracting, isolated canine heart supported with arterial blood from a donor. Systolic pressure, heart rate, and coronary perfusion pressure were held constant while the coronary bed was progressively embolized with either large (average 865 mu) or small (average 10 mu) polystyrene microspheres. During embolization with large microspheres, coronary flow diminished progressively. After sufficient embolization, decreased ventricular performance was indicated by a rise in end-diastolic pressure. During embolization with small microspheres, coronary flow initially increased, which suggests the effective release of a vasodilator substance. Return of coronary flow to control levels occurred only after the end-diastolic pressure rose, on the average, to above 30 mm Hg. After embolization with both sizes of microspheres, ventricular diastolic pressure-volume relationships showed decreased ventricular compliance. This was attributed, in part, to edema of the ventricular wall and, in part, to focal shortening of the sarcomeres where the circulation was compromised. Embolization with both sizes of microspheres ultimately caused a decrease in ventricular performance, although when the systolic pressure was increased the usual relationship between peak developed wall stress, and end-diastolic pressure showed less of a descending limb than that found in the nonembolized, isolated heart. It is felt that the data summarized above have bearing on ventricular performance and coronary flow in clinical situations where hearts are perfused through pump oxygenator systems and are thereby subject to embolization from aggregated clumps of platelets and fibrin.

Animals↗