| IntroductionCurrent investigations support the notion that postresuscitation myocardial dysfunction is one of the main causes which lead to deaths after initially successful cardiopulmonary resuscitation ( CPR). As the preferred vasopressor agent, adrenaline has been confirmed to improve coronary and cerebral perfusion and enhance the restoration of spontaneous circulation ( ROSC ) during CPR widely in many clinical settings. However, some evidences showed that adrenaline increased the severity of postresuscitation myocardial dysfunction in consequence of its PJ - adrenergic actions during CPR. The present study was designed to evaluate the effect of esmolol, a short -acting (3, - adrenergic blocking agent, on postresuscitation myocardial injury when it was administered combining with adrenaline during CPR by way of observing the ultrastructure changes of myocardium and ATPase activity of mitochondria, as well as the superoxide dismutase(SOD) activity and malondialdehyde ( MDA) content of myocardial tissue in a rat model of asphyxia! cardiac arrest.Material and methodsSixty - six male Wistar rats( 180 -250g) were fasted overnightexcept for free access to water. The animals were allocated to three groups randomly. All animals were anesthetized with isoflurane and intubated after tracheotomy. Both femoral artery were cannulated. EGG, MAP ,HR and temperature were measured continuously. Cardiac arrest was induced by asphyxiation. After lOminutes asphyxia , resuscitation was achieved remotely by a slow, intra - aortic infusion of oxygenated blood (withdrawn from the same rat before asphyxia) along with a resuscitation cocktail containing heparin, sodium bicarbonate, and adrenaline ( AD group ) /or adrenaline with esmolol ( AD + Es group) through the resuscitation channel. The animals in sham group were not subjected to blood withdrawn, asphyxia and cardiac arrest. The animals were killed on the point SOminutes, 120minutes, 1 SOminutes after ROSC in AD group and AD + Es group and the corresponding data from sham group was assigned to fifteen minutes after surgical preparation.Myocardial mitochondria were detached by differential centrifuga-tion and broken by freezing and melting. ATPase was determined by phosphorus assay while SOD and MDA in myocardium tissue were determined by xanthinoxidase technique and thiobarbituric acid technique respectively. Protein was determined by Coomassie light blue technique.The specimen fixed in 2. 5% glutaral were dehydrated, fixed, embed, and stained in a routine way . Ultrastructure changes in myocardium were examined under electron microscopy.Statistical analysis was performed with the use of the SPSS program. Analysis of variance ( ANOVA) was used to compare between -group means and within - group means, Student - Newan - Keuls (SNK) multiple comparisons were made to determine differences be-tween time points within groups or between groups at a given time point. All data are reported as mean ?SD. A value of p <0. 05 was considered statistically significant.ResultsBaseline hemodynamic measurements did not differ significantly among three groups. There were no difference in MAP between AD group and AD + Es group after successful resuscitation ( P > 0. 05). Heart rates were magnified after adrenaline. The duration of circulatory arrest and the interval from beginning of resuscitation to ROSC were no difference between AD group and AD + Es group( P > 0.05).Myocardial mitochondria Na+ - K+ ATPase and Ca * ATPase activity were decreased significantly both in AD and AD + Es group compared with that of sham group ( P < 0. 01) , but ATPase activity were higher in AD + Es group than that in AD group ( P < 0. 05 ) . Meanwhile SOD activity in myocardium were decreased and MDA contents increased significantly after resuscitation compared with sham group ( P <0. 01) , SOD and MDA in AD + Es group were higher or lower than that in AD group respectively ( P <0. 01). The ultrastructure in sham group was nearly normal. But it revealed different degree pathologic...
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