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The adverse effect of systemic hypertension following myocardial reperfusion
Insights
Postoperative hypertension following coronary artery bypass surgery can worsen myocardial damage. This study found that hypertension during reperfusion impairs heart muscle function and increases tissue damage.
Area of Science:
- Cardiovascular Physiology
- Myocardial Ischemia and Reperfusion Injury
Background:
- Transient myocardial ischemia is common after coronary artery bypass surgery.
- Postoperative hypertension can exacerbate myocardial damage during reperfusion.
Purpose of the Study:
- To investigate the effects of hypertension during reperfusion on transiently ischemic myocardium.
- To determine if hypertension accentuates myocardial damage following ischemia.
Main Methods:
- An open-chest pig model with induced myocardial ischemia (30 min) and reperfusion (2 hr).
- Comparison of a normotensive control group with a hypertensive group (phenylephrine-induced).
- Evaluation of left ventricular wall thickness, mitochondrial function, sarcoplasmic reticulum Ca2+ uptake, tissue calcium, and hemorrhage.
Main Results:
- Hypertensive group showed loss of systolic wall thickening and increased diastolic wall thickness in the reperfused zone.
- Intramyocardial hemorrhage was observed in the reperfused area of hypertensive animals.
- Impaired mitochondrial oxidative phosphorylation and reduced sarcoplasmic reticulum Ca2+ uptake were noted.
- Increased ischemic tissue calcium levels were found in the hypertensive group.
Conclusions:
- Hypertension during reperfusion significantly worsens myocardial injury.
- Elevated blood pressure accentuates cellular damage, including mitochondrial dysfunction and calcium overload.
- These findings suggest that managing hypertension post-revascularization is crucial to limit myocardial damage.
Abstract:
Transient myocardial ischemia in postoperative hypertension is relatively common with coronary artery bypass surgery. This study examines the effect of hypertension during reperfusion of transiently ischemic myocardium. The animal model was open chest pigs with myocardial ischemia induced by the occlusion of the left anterior descending coronary artery for 30 min followed by 2 hr of reperfusion. A normotensive control group was compared with animals rendered hypertensive with phenylephrine during the ischemic and reperfusion times. In the hypertensive group, systolic blood pressure was raised from 106 to 161 mm Hg and peripheral vascular resistance from normal to 3600 dyn-sec-cm-5. Regional left ventricular wall thickness, mitochondrial function, sarcoplasmic reticulum Ca2+ uptake, tissue calcium, water content, and hemorrhage were evaluated. Compared to controls the hypertensive group had (1) loss of systolic wall thickening with increased diastolic wall thickness in the reperfused zone, (2) intramyocardial hemorrhage in the area of reperfusion, (3) significant impairment of oxidative phosphorylation by mitochondria isolated from the reperfused zone, (4) a marked reduction in the rate of Ca2+ uptake by sarcoplasmic reticulum vesicles, and (5) an increase in ischemic tissue calcium. Thus, hypertension associated with revascularization of acutely ischemic myocardium may accentuate myocardial damage.