THE EXPERIMENTAL RESEARCH ON CARDIOPLEGIC SOLU-TION CONTAINING SELENIUM AND MAGNESIUM AGAINST MYOCARDIAL ISCHEMIA REPERFUSION DAMAGE

The model of this test was set up according to Langendoff isolated heart reperfusion mechanics. The experimental research was designed to observe the protective effects on ischemic andreperfuslon myocardial tissue by using ST. Thomas cardioplegic solution containing selenium andmagnesium. We conclude that using cold crystallold cardioplegic solution containing Se'+, Mg' 4 canobviously reduce ischemic and reperfusion myocardlal injury and bas an advantage of recovering myocardial runctlon after operation by observing the content or lactic dehydrogenase (LDH); creatineI,kasphoklnase CK in the coronary vessel's sinus reflux solutlonl glutatblone peroxldase (GPX); suI,eroxlde dismutase (SOD); maloydladehyde (MDA ) I Se4+ .Mg'+ .Ca'+ and cia-nging or myocardialultrastructure.

ACIDIC FIBROBLAST GROWTH FACTOR REDUCES RAT SKELETAL MUSCLE DAMAGE CAUSED BY ISCHEMIA AND REPERFUSION

Acute interruption of arterial blood flow to the extremities is often associated with significant morbidity and mortality. Broad spectrum mitogenic and non mitogenic activities of FGFs inspired us to study its protecting effects on tissue injuries in ischemia reperfusion condition. We found that systemic administration of aFGF after reperfusion onset prevented severe skeletal muscle injuries. In rats treated with aKGF, the tissue edema was reduced significantly, the tissue viability was increased, and the muscle fibers contained more succinate dehydrogenase (SDH) and adenosine triphosphatasc (ATPase). The pathological results supported the concept of improved prevention with aFGF treatment. The possible tissue protection by aFGF may come from its ability to regulate the concentration of evtra- and intracellular calcium ion. Besides, it may moderate other Ca2+ dependent enzyme conversion processes. Also, it may take part in the vascular tone regulation under ischemia and reperfusion conditions. These results suggest further study of tissue ischemia prevention with FGF and its possible mechanisms in the future.

Factors involved in the neuronal death during postischemic reperfusion:experimental study in rabbits

Objective To explore the main pathogenic factors in the development of neuronal death during normothermic reperfusion in rabbits.Methods Ninety six New Zealand rabbits were randomly allocated into two groups: group Ⅰ served as non ischemic controls; group Ⅱ served as postischemic normothermic reperfusion models. Complete cerebral ischemia was induced by the four vessel model for 30 minutes. After ischemia, rabbits in group Ⅱ were further divided into three subgroups according to the duration of reperfusion: subgroup A, 30 minutes; subgroup B, 180 minutes and subgroup C, 360 minutes. Twenty eight biochemical parameters in the brain were measured, and neuronal changes were observed by histomorphological assessment. Neurons of 12 regions were differentiated into four types: type A (normal), type B (mildly damaged), type C (severely damaged) and type D (necrotic). Bivariate correlate analysis between the levels of biochemical parameters and the percentages of each type of neurons was carried out.Results The main parameters involved in the progressive decrement of type A neurons were VIP, β EP, PGI 2, T 3, T 4 and N + a,K + ATPase; in the increment of type B were β EP and TXB 2; in the increment of type C were GLU and TXB 2/PGI 2 respectively; in the stepwise increment of percentages of type D neurons were T 4, N + a,K + ATPase, GLU, T 3 and VIP (P<0.05).Conclusion The main factors involved in the development of neuronal death during postischemic normothermic reperfusion in rabbits include hypermetabolism, deactivation of N + a,K + ATPase, release of excitatory amino acids and disorder of neuropeptides.