The present study was designed to establish a model of repeated brief myocardial ischemia(RBMI)and investigate the effects of RBMI on regional myocardium in conscious rabbits(pure Strain of Japan). The results showed that there is no alteration of ultrastrueture and accumulative ECG injury, but a significant increase in capillary density(P

In order to investigate the pathogenetic role of CGRP in septic shock, the effect of extraneous CGRP on septic shock was observed on late septic shock model produced by cecal ligature and puncture (CLP) in rats. The results showed that plasma CGRP elevated significantly in septic shock rat (14.3?4.0 vs sham 5.5?1.8 pg/ml, P

In oeder to investigate the pathogenetic role of mitochondria in the patho-genesis of intracellular calcium overload in septic rat. The present study observed the cal-cium content and calcium influx into myocardial mitochondria on the early and late sepsisof rat produced by cecal ligature and puncture. The results showed that mitochondrialcalcium contents increased markedly in both early (180%) and late (330%) sepsis. Thecalcium transport capacity of mitochondria in late sepsis decreased dramatically (uptakedecreased 34.6%, uptake velocity lowered 33.3%, p

cDNA of human interleukin-8 was expressed in E. coli bacteria, and recombi-nant human interleukin-8 ( rhIL- 8 ) was produced. The latter was used for treatment of rat intestinal ischemia-reperfusion(I-R) injury, and it was found that rhIL-8 significantly improved the hypotensive state of the animals,and it also inhibited the elevation of plasma endothelin level , decreased the intestinal myeloperoxidase activity, and obviously prolonged the survival timeof the animals. Perfusion of isolated rat superior mesenteric artery with rhIL-8 markedly inhibited endothelin synthesis or (and) release induced by anoxia. The above results suggest that rhIL- 8 may be an effective preventive and therapeutic agent for I-R injury through its inhibition on leukocyte adhesion and endothelin synthesis or (and) release.

AIM:To study alterations of cardiac sarcoplasmic reticulum (SR) function in vitamin D 3-induced calcium overload rats. METHODS: The Ca-overload rat models were prepared by vitamin D 3 plus nicotine. Cardiac SR was seperated by centrifuging. The measurement of SR Ca 2+ uptake and Ca 2+ release activities were preformed by the Millimore filtration technique. Specific SR [ 3H]-ryanodine binding capacity was measured by radioligand method. RESULTS: Compared with control,myocardial calcium content in calcium overload rats increased by 78%( P