Microvascular incompetence and the failure of hearts to recover contractile function after cardioplegia
Jenkins, D.P.; Yellon, D.M.
European Heart Journal 16(8): 1020-1021
1995
ISSN/ISBN: 0195-668X PMID: 8665959 Document Number: 452549
The relationship between the development of microvascular incompetence and the loss of potential for functional recovery following cardioplegia was investigated using St. Thomas' Hospital No. 2 solution (STH) in isolated working rat hearts. Cardiac function was measured prior to cardioplegia and again after 30 min of reperfusion at 37 degree C following 1, 2 or 4 h arrest at 30 degree C (n = 5). The hearts were then fixed by perfusion with 2.5% glutaraldehyde and then nuclear track emulsion was perfused as an intravascular marker of competent capillaries. Following cardioplegia for 1 h hearts showed 95.4% recovery of aortic flow in the working mode, and a high proportion of the capillaries in the subendocardial (84.6 +- 2.3%), middle (94.6 +- 3.0%) and subepicardial (89.1 +- 4.9%) thirds of the left ventricular myocardium transmitted perfusate. Two hours arrest resulted in significantly diminished recovery of left ventricular function (aortic flow: 56.6 +- 7.6% and aortic pressure: 64.4 +- 2.5% of pre-arrest values), but microvascular competence was not reduced. Hearts arrested for 4 h did not recover useful levels of left ventricular function (aortic flow 0%, aortic pressure 6 +- 2.5% and heart rate 56.0 +- 23.1%). This loss of the remaining two thirds of the potential for functional recovery was associated with significant (P lt 0.01) reductions in the proportions of competent capillaries (subendocardial, middle and subepicardial thirds to 10.9%, 19.2% and 14.2%, respectively). These non-functional capillaries had open lumina and showed no sign of structural alteration, obstruction or compression, although some focal collections of myocytes ( lt 30%) showed evidence of reperfusion damage including contraction band necrosis. Despite reductions in microvascular competence overall, coronary flow rates (non-working) did not decline, suggesting shunting via large arterio-venous channels. It seems likely that the loss of the first third of the potential for rapid functional recovery following cardioplegia is due to loss of high energy phosphates, whereas the loss of the remaining two-thirds is associated with endothelial cell mediated constriction of small arterial vessels which produces the capillary incompetence demonstrated in this study.