Reperfusion at reduced flow rates enhances postischemic contractile recovery of perfused heart

Abstract

The effects of reperfusion at reduced flow rates on postischemic cardiac contractile function were examined in perfused rat hearts. Isolated hearts were subjected to 35-min ischemia followed by reperfusion at the preischemic flow rate (9.0 ml.g-1.min-1; ordinary flow rate) or at reduced flow rates (0.9-8.1 ml.g-1.min-1). Reperfusion at ordinary flow rate did not generate any left ventricular developed pressure (LVDP), whereas reperfusion at reduced flow rates (0.9-7.2 ml.g-1.min-1) elicited 13-57% of initial contractile force at reperfusion's end; optimal recovery occurred at 3.6 ml.g-1.min-1 (reduced flow rate). Reduced flow rate reperfusion attenuated ischemia-reperfusion-induced increase in left ventricular end-diastolic pressure (LVEDP) and perfusion pressure (PP), alteration in tissue Na+, K+, Ca2+, and Mg2+, release of creatine kinase and ATP metabolites, and development of triphenyltetrazolium chloride-unstained areas. Enhanced postischemic LVDP recovery was inversely related to higher coronary PP at the initial stage (4 min) of reperfusion (r = -0.763). The benefit of reduced flow rate reperfusion could not be attributed to rate of calcium delivery to the heart, formation of oxygen free radicals in myocardium, endothelium-dependent coronary artery dilation, or LVDEP reduction. Enhancement of postischemic LVDP recovery was associated with attenuation of ischemia-reperfusion-induced increases in myocardial sodium and calcium; failure of postischemic LVDP recovery was accompanied by an increase. Reduction in sodium and calcium overload may underlie the beneficial effects of reduced flow rate reperfusion in ischemic-reperfused heart.

Delayed low pressure at reperfusion: A new approach for cardioprotection

“…11 Another intervention called ''controlled or gentle reperfusion'' has been proposed to protect the ischemic heart and to attenuate postischemic contractile dysfunction. [12][13][14] Despite the experimental proofs accumulated over the years showing the importance for the use of controlled reperfusion methods after cardiac ischemia, these procedures are not widespread in the operating block. We have thus conceived a simple but reliable protocol of LPR aimed to be tested in the clinical setting.…”

Ischemia-Induced Norepinephrine Release, but not Norepinephrine-Derived Free Radicals, Contributes to Myocardial Ischemia - Reperfusion Injury

“…Reperfusion at reduced flow rates enhances postischemic contractile recovery. 42 Brunvand et al demonstrated that -adrenoceptor blockade inhibited reperfusion hyperemia and reduced infarct size in feline hearts. 43 The reduction in the infarct by denervation in the present study may have been partially induced by suppression of reactive hyperemia, because NE release during ischemia and reperfusion was completely inhibited.…”

Oxygen Concentration during Reperfusion in Mitral Valve Surgery

“…The concept of reperfusion injury remains controversial with several proposed mechanisms, but it is mainly oxygen-derived free radicals and calcium overload that play an important role in the development of left ventricular dysfunction, stunning, reperfusion arrhythmias, vascular damage, and endothelial dysfunction [15]. Various strategy used to reduce ischemic-reperfusion injury include lowering blood pressure during reperfusion, reducing blood flow during reperfusion, but one of the most vigorously researched methods is controlling arterial oxygen tension in order to reduce reperfusion injury [16][17][18]. Maintaining normoxic cardiopulmonary bypass in children with cyanotic congenital heart disease resulted in dramatically reduced levels of conjugated diens, which represents the lipid peroxidation levels of the heart, compared with patients that maintained on hyperoxic cardiopulmonary bypass [19].…”