L Maxwell1, J B Gavin. 1. Department of Pathology, University of Auckland, New Zealand.
Abstract
STUDY OBJECTIVE: The aim was to determine the contribution of ischaemia per se to the development of microvascular incompetence in the myocardium. DESIGN: Isolated, buffer perfused rat hearts were made globally ischaemic for 0-60 min, then fixed with nitrogen bubbled glutaraldehyde and perfused with nuclear track emulsion to identify and quantify competent blood vessels in scanning and transmission electron micrographs. SUBJECTS: Adult Male Wistar rats weighing between 275 and 350 g were used. MEASUREMENTS AND MAIN RESULTS: Thirty or more min ischaemia significantly (p less than 0.05) reduced the density of competent capillaries in the subendocardial third of the myocardium, as did 45 or more min in the subepicardial third and 60 min in the middle third. Following 60 min ischaemia virtually all vessels in the subendocardial third were not perfusable. Severely ischaemic myocardium showed relatively normal, open, unobstructed capillaries and an absence of the endothelial, myocyte and mitochondrial swelling which have previously been attributed to ischaemia. CONCLUSIONS: In severely ischaemic myocardium microvascular incompetence shows a transmural gradient in severity. It develops progressively, starting near the endocardium. These findings suggest that postischaemic reoxygenation may accelerate the development of microvascular incompetence.
STUDY OBJECTIVE: The aim was to determine the contribution of ischaemia per se to the development of microvascular incompetence in the myocardium. DESIGN: Isolated, buffer perfused rat hearts were made globally ischaemic for 0-60 min, then fixed with nitrogen bubbled glutaraldehyde and perfused with nuclear track emulsion to identify and quantify competent blood vessels in scanning and transmission electron micrographs. SUBJECTS: Adult Male Wistar rats weighing between 275 and 350 g were used. MEASUREMENTS AND MAIN RESULTS: Thirty or more min ischaemia significantly (p less than 0.05) reduced the density of competent capillaries in the subendocardial third of the myocardium, as did 45 or more min in the subepicardial third and 60 min in the middle third. Following 60 min ischaemia virtually all vessels in the subendocardial third were not perfusable. Severely ischaemic myocardium showed relatively normal, open, unobstructed capillaries and an absence of the endothelial, myocyte and mitochondrial swelling which have previously been attributed to ischaemia. CONCLUSIONS: In severely ischaemic myocardium microvascular incompetence shows a transmural gradient in severity. It develops progressively, starting near the endocardium. These findings suggest that postischaemic reoxygenation may accelerate the development of microvascular incompetence.