Acute global ischemia elevated left ventricular end-diastolic pressure due to a marked decrease in systolic performance (stroke work decreased from 21.0 to 3.5 gm-m) rather than an altered pressure-volume relationship.
Does acute global ischemia elevate left ventricular end-diastolic pressure through a decrease in contractility or an alteration of the pressure-volume relationship in a canine model?
The elevation of left ventricular end-diastolic pressure during acute global ischemia is due to decreased systolic performance rather than altered pressure-volume relationships.
The mechanism of elevation of left ventricular end-diastolic pressure during acute global ischemia was evaluated by examiniation of the relative contributions of a decrease in contractility and an alteration of the pressure-volume relationship. The external circumference (mercury-in-silastic gauge) pressure relationship, as an index of the pressure-volume relationship, was studied in beta adrenergic and ganglionic blocked, open chest dogs on right heart bypass at constant heart rate ane aortic pressure. Ischemia of one and two hours' duration was produced by reducing total coronary blood flow in cannulated left and right coronary arteries until left ventricular end-diastolic pressure rose significantly. At a constant stroke work, left ventricular end-diastolic pressure rose from 5.0 +/- 0.5 to 15.0 +/- 0.5 cm H2O in the experiments of one hour of ischemia, and from 7.0 +/- 1.0 to 17.0 +/- 1.0 cm H2O in experiments of two hours of ischemia. Ischemia was followed by one hour of restoration of coronary blood flow. Ischemia produced a marked depression of ventricular function: stroke work, considered at a left ventricular end-diastolic pressure of 15 cm H2O, decreased from 21.0 +/- 3.0 to 3.5 +/- 0.5 gm-m, and from 15.0 +/- 2.0 to 2.5 +/- 0.5 gm-m, in the experiments of one and two hours, respectively. Neither ischemia nor reflow changed the pressure-volume relationship. Thus, the elevation of left ventricular end-diastolic pressure during ischemia in an otherwise normal canine myocardium is due to a decrease in systolic performance of the heart rather than to an alteration of the pressure-volume relationship.
Palacios et al. (1976) studied Acute global ischemia. Acute global ischemia vs. Baseline (pre-ischemia) was evaluated on Left ventricular end-diastolic pressure and pressure-volume relationship. Acute global ischemia elevated left ventricular end-diastolic pressure due to a marked decrease in systolic performance (stroke work decreased from 21.0 to 3.5 gm-m) rather than an altered pressure-volume relationship.