Search

Objective: To study the protective effect of carbon monoxide (CO) inhalation on the serious limb ischemia/reperfusion (I/R) injury, and which effects caused to shock in rats., Methods: 36 SD rats were randomly divided into I/R, I/R + CO (RC), sham operation (S) groups. I/R injury models were made by the occlusion of the femoral artery for 8 h and the reperfusion for 12 h, 10 d. Before reperfusion of 2 h, RC group started to breathe medical air containing CO (the volume fraction of CO: 0.075%) continuously, until after reperfusion for 4 h, a total of inhalation 6 h. S, I/R groups exposed to air, breathe freely. Caudal artery pressures (CAP), ten days survival rate, serum lactate dehydrogenase (LDH) and creatine kinase (CK) activity, limb wet - to - dry weight ratio (W/D) and the pathologic changes of limb were observed., Results: Once the reperfusion started, the CAP decreased rapidly in I/R group, and the mean reduced to(5.3259 +/- 0.3832) kPa when reperfusion for 8 h. Compared to I/R group, the CAP decreased slower and smaller in RC group, moreover, its mean reduced to (8.3300 +/- 0.4224) kPa when reperfusion for 8 h. The 10 d survival rate in I/R group was that 8 rats died all between reperfusion for 13 - 20 h. Only 1 rat died in RC group and the other 7 rats were still alive when reperfusion for 10 d. Compared to I/R group, the pathological features of the ischemic limb were significant ly improved, and the figures of W/D, serum LDH and CK value were remarkable lower in RC group (P < 0.05)., Conclusion: Inhaling exogenous low-dose CO has a reverse regulation in the blood pressure decline caused by serious limb I/R injury in rats. And at the same time, it can effectively prevent the occurrence of shock, reduce physical damage, significantly increase the survival rate of animals.

Objective: To study the protective effect of carbon monoxide(CO) inhalation in the limb ischemia/reperfusion (I/R) injury of rats., Methods: Forty-four Sprague-Dawley rats were randomly divided into three groups: S, I/R and RC groups. I/R injury model was made by the occlusion of the femoral artery for four hours and the reperfusion for forty-eight hours. RC group was exposed to medical air mixed CO (the volume fraction of CO: 0.05%) during limb reperfusion in rats. The other two groups were exposed to the routine air. Gross morphology of the ischemic limb, wet-to-dry weight ratio (W/D), and skeletal muscle histopathology were observed. The apoptosis index and expression levels of Bax and Bcl-2 in the muscle were assessed with Flow Cytometry. The activities of serum lactate dehydrogenase (LDH) and creatine kinase (CK) were tested by Automatic Biochemical Analyzer., Results: Compared to I/R group, W/D, serum LDH and CK activities, the apoptosis index and Bax expression level in the muscle were all significantly decreased, the Bcl-2 expression level was significantly increased, gross morphology of the ischemic limb and muscle histopathology were obviously improved in RC group., Conclusion: Inhaling exogenous CO can attenuate limb I/R injury.

Aim: To investigate the protective effect of exogenous carbon monoxide (CO) on the liver injury induced by ischemia/reperfusion (I/R) of hind limbs in rats., Methods: 100 SD rats were divided randomly into sham operated group (S), S+ CO group (SC), I/R group (I/R), I/ R+ CO group (RC). A rat model of ischemia in hind limbs and the reperfusion liver injury was established with the occlusion of the femoral arteries for 4 h and re-opening for 6 - 72 h, 10 d. The rats in SC and RC groups were exposed to air containing CO (the volume traction of CO: 0.05%) for 2 h before and after reperfusion or the corresponding control time point, while the other two groups were exposed to the routine air. The pathologic changes of liver tissue were morphologically observed by HE stain. Serum GPT activity was tested by Automatic Biochemical Analyzer. The percentage of apoptosis, expression levels of bax and bcl-2 protein in liver tissue were detected by Flow Cytometry., Results: There was no difference between S and SC groups. Compared with SC group: (1) Pathological changes in liver tissue were significant in I/R and RC groups. (2) The serum GPT activity of I/R and RC groups was obviously increased. (3) In IR and RC groups, the percentage of apoptosis in liver tissue was all significantly increased. (4) The bax expression level was significantly increased. Compared RC group with I/R group: (1) Pathological change was slight. (2) The serum GPT activity was depressed. (3) The percentage of apoptosis and expression level of bax protein in liver tissue were depressed. (4) The expression level of bcl-2 protein in liver tissue was increased., Conclusion: Exogenous CO could attenuate liver tissue injury induced by limbs I/R in rats.

Aim: To detect the changes of inducible heme oxygenase (HO-1) expression in liver following ischemia/reperfusion (I/R) of hindlimbs and to elucidate their significance., Methods: I/R was established using the occlusion of the femoral arteries for 4h and reopening for 2-24 h in rats. The expression of HO-1 mRNA and HO-1 protein in liver tissue were detected with reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical technique, respectively. The observation of pathologic changes of liver was made following the inhibition of HO-1 by zinc protoporphyrin (ZnPP)., Results: Compared with control groups, the relative expression level of HO-1 mRNA significantly increased in I/R group. There were more HO-1 positive hepatocytes in I/R group than control groups. The pathologic changes of liver tissue became more severe in I/R + ZnPP group., Conclusion: The expressions of HO-1 mRNA and protein in liver tissue are significantly upregulated, induction of HO-1 is involved in protection for hepatocytes during the I/R of hindlimbs.

Aim: To detect the changes of inducible nitric oxide synthase (iNOS) expression in liver following ischemia/reperfusion (I/R) of hindlimbs and to elucidate their significance., Methods: I/R was established using the occlusion of the femoral arteries for 4 h and reopening for 2-24 h in rats. The expression of iNOS mRNA, and iNOS protein and the nitrotyrosine (NT), a marker of peroxynitrite (ONOO-), in liver tissue were detected with reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical technique, respectively. The liver superoxide dismutase (SOD) activity and malondialdehyde (MDA) contents were spectrophotometrically measured. The observation of pathologic changes of liver was made following the inhibition of iNOS by aminoguanidine (AG)., Results: Compared with control groups, the relative expression level of iNOS mRNA significantly increased in I/R group. There were more iNOS positive hepatocytes and more NT positive hepatocytes in I/R group than control groups. The contents of MDA markedly increased, while the activity of SOD significantly decreased in I/R group, compared with those in the control groups. The pathologic changes of rat liver became milder in I/R group following the inhibition of iNOS by AG., Conclusion: The expressions of iNOS mRNA and protein in liver are significantly upregulated, excess induction of iNOS-NO is contributed to the liver injury during the I/R of hindlimbs.