Protective effects of cardioplegia on diastolic function of hypertrophied rat hearts after hypothermic ischaemic arrest

Abstract

This study was undertaken to assess the effects of hypothermia and chemical cardioplegia on the functional recovery of hypertrophied non-failing rat hearts subjected to an extended period of global ischaemia. Left ventricular hypertrophy was produced by constriction of the abdominal aorta. Hearts were studied an average of 8 weeks following this procedure. Sham-operated animals served as controls. Twenty-nine isolated isovolumic perfused rat heart preparations were then subjected to 2 h of ischaemic arrest at 15-18 degrees C followed by 45 min of normothermic reperfusion. In one series of hearts (8 sham, 8 hypertrophied), myocardial protection consisted of hypothermia alone. In another series (6 sham, 7 hypertrophied), repeated infusions of cardioplegic solution at 30-min intervals throughout arrest were added to hypothermia. Hypothermia alone resulted in a similar preservation of contractility as evidenced by the recovery of dp/dtmax/left ventricular (LV) systolic pressure after 45 min of reperfusion (91.6 +/- 5.9% of control values in sham vs 78.6 +/- 6.5% in hypertrophied hearts). Conversely, the recovery of compliance was much more impaired in hypertrophied hearts as indicated by a significantly higher percentage of increase in post-ischaemic LV diastolic pressure (DP) (at 45 min of reperfusion: 243.8 +/- 27.5% of control values vs 167.1 +/- 23.8% in sham, P less than 0.05). The addition of cardioplegia improved the preservation of contractility in both groups but its major effect was to normalize the recovery of compliance in hypertrophied hearts so that post-ischaemic LVDP values were no longer different from those recorded in normal hearts (at 45 min of reperfusion: 102.1 +/- 32.8% vs 98.5 +/- 14.2% of pre-ischaemic values respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of Heme Oxygenase-1 Upregulation on Blood Pressure and Cardiac Function in an Animal Model of Hypertensive Myocardial Infarction

“…Mainly hemodynamic determinants of −dp/dtmax are peak aortic systolic pressure and LVSP [39]. Additionally, several studies have adopted (−d p /d t max )/LVSP to evaluate left ventricular diastolic function [40,41]. Therefore, this study finally chose both −d p /d t max and (−d p /d t max )/LVSP to discuss the influence of HO-1 upregulation on diastolic function more precisely.…”

Monoamine oxidase-A is an important source of oxidative stress and promotes cardiac dysfunction, apoptosis, and fibrosis in diabetic cardiomyopathy

“…-dp/dt, a cardiac diastolic index is widely used to assess diastolic function. Since LVSP was demonstrated to be a hemodynamic determinant of -dp/dt min, several studies have implemented (-dp/dt min )/LVSP to evaluate left ventricular diastolic function more accurately (33,34,35,36). Thus we selected both -dp/dt min and (−dp/dt min )/LVSP to determine whether MAO A inhibition could restore diastolic function in diabetic rats.…”