Incomplete coronary vasodilation during myocardial ischemia in swine

Abstract

To determine if endogenous (ENDG) vasodilation was maximum during myocardial ischemia, left anterior descending (LAD) mean pressure (P) was reduced for 20 min in 13 swine. At LAD P of 45 mmHg (LAD P45) flow fell during ENDG = 25 but rose to 44 ml/min during adenosine (AD) infusion (P less than 0.01). Flow increased to subendocardium (ENDG 0.65 vs. AD 1.04 ml X min-1 X g-1) and to subepicardium (ENDG 0.99 vs. AD 1.83 ml X min-1 X g-1; P less than 0.05). No significant change occurred in myocardial O2 consumption (MVO2; ENDG 2.91 vs. AD 3.18 ml X min-1 X g-1), lactate extraction (ENDG = -5 vs. AD-1%), and wall thickening (WTh; ENDG + 16 vs. AD + 17%). At LAD P35, flow during ENDG was 12 but rose to 19 ml/min during AD (P less than 0.01). Flow increased to subendocardium (ENDG 0.24 vs. AD 0.46 ml X min-1 X g-1; P less than 0.02) and subepicardium (ENDG 0.51 vs. AD 0.87 ml X min-1 X g-1; P less than 0.01). No significant change occurred in MVo2 (ENDG 1.38 vs. AD 1.59 ml/min), lactate extraction (ENDG -38 vs. AD -22%), WTh (ENDG -1 vs. AD + 1%). Thus endogenous vasodilation reserve was not used fully during ischemia. AD increased flow but did not improve abnormalities in myocardial function or metabolism.

Acidosis during ischemia promotes adenosine triphosphate resynthesis in postischemic rat heart. In vivo regulation of 5'-nucleotidase.

“…The delay in return to normal ATP levels may also delay return of cardiac function. It is relevant that increasing flow during ischemia by pharmacological interventions has been shown to improve function only slightly (42) or not at all (43).…”

The effect of hypertension and left ventricular hypertrophy on the lower range of coronary autoregulation.

“…This assumption may not be true because it has recently been found that vasodilator reserve to pharmacologic stimuli persists when coronary perfusion is reduced by a decrease in the perfusion pressure below the autoregulatory range. [16][17][18][19] Several technical limitations have made it difficult to study the effect of hypertension and left ventricular hypertrophy on coronary autoregulation. First, coronary autoregulation is difficult to demonstrate consistently in the anesthetized, open-chest animal.…”

Attenuation of exercise-induced myocardial ischemia in dogs with recruitment of coronary vasodilator reserve by nifedipine.

“…However, the effect on regional contractile function of the recruitment of persistent vasodilator reserve in these studies remains controversial.2. 3 Significant a2-adrenergic coronary vasoconstriction mediates the enhanced poststenotic myocardial ischemia observed in anesthetized dogs during cardiac sympathetic nerve stimulation.' A recent study from our laboratory suggests that coronary vasodilator reserve is also not exhausted when myocardial ischemia is induced in conscious dogs by production of a coronary stenosis during exercise, since ischemia is attenuated by intracoronary a2-blockade under these conditions.5…”