[Expression of bone morphogenetic protein receptor IA in rats after contusive spinal cord injury].

OBJECTIVE: To observe the expression pattern of bone morphogenetic protein receptor IA (BMPR IA) in rats after contusive spinal cord injury. METHODS: The expressions of BMPR IA, IB, and II were detected by immunochemistry in the spinal cord of normal adult rats, and the expression of BMPR IA was detected in the infinite horizons impactor model at 1, 3, 7, 14, 30, and 60 days after spinal cord injury. RESULTS: In the spinal cord of normal adult rats, BMPR IA and II were expressed predominantly in the oligodentrocytes and neurons in the grey matter, and also in some astrocytes and numerous microglia cells. Only a low level of BMPR IB expression was detected in the neurons of the grey matter. After spinal cord injury, the expression of BMP IA markedly increased with sustained strong expression in the astrocytes till one month after the injury; its expression was also increased obviously in the microglia cells activated by the injury. CONCLUSION: The expression of BMPR IA increases significantly in the astrocytes and activated microglia cells in rats after contusive spinal cord injury, suggesting the involvement of BMP signaling pathway in the physiological and pathological role of glia cells.

[Effect of isoflurane delayed preconditioning on myocardial ischemia reperfusion injury in rabbits].

OBJECTIVE: To investigate the protective effect of isoflurane delayed preconditioning on myocardial ischemia reperfusion injury and the potential mechanism in rabbits. METHODS: Thirty New Zealand male white rabbits were randomly assigned to 3 groups: Control group; I/R group; and 2.0% isoflurane group. Isoflurane group was exposed to 2.0% isoflurane-100% oxygen for 2 hours. Control group and I/R group were exposed to 100% oxygen for 2 hours and served as untreated controls. Twenty-four hours later I/R group and isoflurane group underwent 40 minutes of coronary occlusion followed by 2 hours of reperfusion. Blood samples were taken from the arterial line at 20 minutes before the occlusion(T1), 20 minutes after the occlusion(T2), 40 minutes after the occlusion(T3), 1 hours after the reperfusion(T4), and 2 hours after the reperfusion(T5) to determine the plasma level of TNF-alpha. At the end of the reperfusion, infarct size and area at risk were defined by Evans and TTC staining. The heart was harvested and levels of the p38MAPK activity were determined by Western blot, and ultrastructures were observed under the electron microscope. RESULTS: The p38MAPK activity of isoflurane group was significantly lower than that of I/R group (P<0.05). Isoflurane significantly (P<0.05) reduced the infarct size(19.7%+/-2.8% in isoflurane group) of the left ventricular area at risk as compared with the controls (37.8%+/-1.7% in I/R group).The injury of I/R group was worse than that of isoflurane group under the light microscope. Isoflurane group had a lower level of TNF-alpha than I/R group. CONCLUSION: Isoflurane can inhibit p38MAPK activity during myocardial ischemia reperfusion and modulate the cytokine expression, which may be one of the molecular mechanisms of isoflurane delayed preconditioning on cardioprotection.

[Protective effect of heat-shock protein 27 on myocardium with isoflurane preconditioning in myocardial ischemia/reperfusion injury of myocardium in rabbit].

OBJECTIVE: To investigate the mechanism and the protective effect of heart-shock protein 27 (HSP27) on rabbit myocardium with isoflurane preconditioning in myocardial ischemia/reperfusion (I/R) injury. METHODS: Thirty New Zealand white rabbits were randomly assigned to three groups (each n = 10):(1)Sham operation group (C group); (2)I/R group; (3)Two percent in volume is of isoflurane group (S group). S group was exposed to 2.0% isoflurane-pure oxygen for 2 hours. C group and I/R group were exposed 2 hours to pure oxygen to serve as untreated controls. Twenty-four hours later the rats in I/R group and S group underwent 40 minutes of coronary occlusion followed by 120 minutes of reperfusion. At the end of the reperfusion, infarct size (IS) was defined by Evan's blue and triphenyltetrazolium chloride (TTC) staining. Blood samples were taken from arterial line for determination of malondialdehyde (MDA) levels. Western Blotting was used to determine the expression of HSP27 and nuclear factor-KappaB (NF-KappaB) in myocardium. RESULTS: Isoflurane preconditioning could decrease I/R induced myocardial infarct size [(19.7 +/- 2.8)% vs.(37.8 +/- 1.7)%]. This was accompanied by an increase in the expression in HSP27 [(84.5 +/- 4.3) gray scale value vs. (53.1 +/- 3.8) gray scale value] and a decrease in NF-KappaB [(58.6 +/- 4.2) gray scale value vs. (119.3+/-5.6) gray scale value] and MDA [(5.24 +/- 0.45)kU/L vs. (9.42 +/- 0.83)kU/L]. CONCLUSION: The expression of HSP27 induced by isoflurane preconditioning plays an important role in protecting myocardium against ischemia/reperfusion injury.

[Effects of ulinastatin on cerebral inflammatory response during cardiopulmonary bypass].

OBJECTIVE: To investigate the effects of ulinastatin (UTI) on cerebral inflammatory response during cardiopulmonary bypass (CPB). METHODS: Twenty-four NYHA II-III patients (13 males and 11 females) aged 23-45 years, undergoing elective cardiac valve replacement under hypothermic CPB were randomly divided into 2 groups: ulinastatin group (Group U, n=12) and control group (Group C, n=12). In group U, UTI (1.2 x 10(4) U/kg) was given intravenously after the induction of anesthesia, 0.6 x 10(4) U/kg UTI was added to the priming solution, and 0.6 x 10(4) U/kg UTI was given about 5 min before the aortic decamping. In Group C, normal saline was given instead of UTI. Internal jugular vein was cannulated and the catheter was advanced retrogradely till jugular bulb. Blood samples were taken simultaneously from artery and jugular bulb after induction of anesthesia (T1), 60 min (T2) and 6 h (T3) after discontinuation of CPB for determination of TNFalpha, IL-6, IL-8 and IL-10. The juguloarterial gradients of these cytokines (deltaTNFalpha, deltaIL-6, deltaIL-8, and deltaIL-10) were calculated. RESULTS: In Group C, arterial levels of TNFalpha, IL-6, IL-8, IL-10 at T2 and T3, deltaTNFalpha, deltaIL-8 and deltaIL-10 at T2, deltaTNFalpha, deltaIL-6 and deltaIL-10 at T3 significantly increased (P < 0.01). deltaIL-8 increased at T3 (P < 0.05). In Group U, arterial levels of IL-6, IL-8, IL-10 at T2, arterial levels of IL-6, IL-8,IL-L-10 and deltaTNFalpha, deltaIL-8 at T3 significantly increased (P < 0.01). Arterial levels of TNFalpha at T2 and T3, deltaTNFalpha, deltaIL-10 at T2, deltaIL-6 at T3 increased (P < 0.05). Arterial levels of TNFalpha, IL-6 and deltaTNFalpha, deltaIL-8 at T2, arterial levels of TNFalpha and deltaIL-6 at T3 in Group U were lower than those in Group C (P < 0.05). Arterial levels of IL-6 at T3, IL-8 at T2 and T3 in Group U were significantly lower than those in Group C (P < 0.01). Arterial levels of IL-10 and deltaIL-10 at T3 in Group U were higher than those in Group C (P < 0.05). CONCLUSION: Systemic and cerebral activation of inflammatory response during CPB can be alleviated by ulinastatin.