Effect of sodium suberogorgin on hemodynamics and myocardial ischemic-reperfused injury in isolated guinea pig working hearts
Abstract
AIM: To study the actions of sodium suberogorgin (Sub) on normal- and myocardial ischemic-reperfused-working hearts.
METHODS: The isolated guinea pig working hearts were perfused with edetic acid (0.2 mumol.L(-1))-Krebs-Henseleit solution by left pulmonary vein at 37 +/- 0.5 degrees C. The perfusing pressure of left atrium and the afterload of left ventricle were maintained at 1.0 and 7.2 kPa, respectively. During 50-min low-flow global ischemia, coronary flow was maintained at 4.7 +/- 0.2% of normal working hearts via retrograding perfusion. Reperfusion lasted 35 min following ischemia.
RESULTS: Before ischemia, the aortic pressure, left ventricular systolic pressure, the maximal rate of left ventricular pressure change (+ dp/dtmax and -dp/dtmax), cardiac output, stroke volume, left ventricular end-diastolic pressure, and heart rate of working hearts treated with Sub 10 mumol.L(-1) for 10 min were increased by 14%, 17%, 17%, 22%, 15%, 32%, -200%, and -11%, respectively. These parameters were reduced when Sub was increased to 50 mumol.L(-1). Reperfusion aggravated the myocardial damages induced by ischemia. Sub 10 mumol.L(-1) used before and during low-flow ischemia completely restored all above parameters except heart rate to the level of preischemia. When Sub was increased to 50 mumol.L(-1), only an attenuation of myocardial damage was observed.
CONCLUSION: Sub obviously improved the ischemic-reperfused injury in isolated working hearts.
Keywords:
METHODS: The isolated guinea pig working hearts were perfused with edetic acid (0.2 mumol.L(-1))-Krebs-Henseleit solution by left pulmonary vein at 37 +/- 0.5 degrees C. The perfusing pressure of left atrium and the afterload of left ventricle were maintained at 1.0 and 7.2 kPa, respectively. During 50-min low-flow global ischemia, coronary flow was maintained at 4.7 +/- 0.2% of normal working hearts via retrograding perfusion. Reperfusion lasted 35 min following ischemia.
RESULTS: Before ischemia, the aortic pressure, left ventricular systolic pressure, the maximal rate of left ventricular pressure change (+ dp/dtmax and -dp/dtmax), cardiac output, stroke volume, left ventricular end-diastolic pressure, and heart rate of working hearts treated with Sub 10 mumol.L(-1) for 10 min were increased by 14%, 17%, 17%, 22%, 15%, 32%, -200%, and -11%, respectively. These parameters were reduced when Sub was increased to 50 mumol.L(-1). Reperfusion aggravated the myocardial damages induced by ischemia. Sub 10 mumol.L(-1) used before and during low-flow ischemia completely restored all above parameters except heart rate to the level of preischemia. When Sub was increased to 50 mumol.L(-1), only an attenuation of myocardial damage was observed.
CONCLUSION: Sub obviously improved the ischemic-reperfused injury in isolated working hearts.