Objective: To study the changes of oxygen free radical, expression of apoptotic gene, ultrastructure of myocardial cell and second injury of the heart following the intestinal ischemia and reperfusion. Methods: Making...Objective: To study the changes of oxygen free radical, expression of apoptotic gene, ultrastructure of myocardial cell and second injury of the heart following the intestinal ischemia and reperfusion. Methods: Making the models of ischemia and reperfusion by clamping superior mesenteric artery, the concentration of NO and SOD in the blood was examined before clamping the artery and reperfusion for 0, 30, 60 min, 1, 3, and 7 d. The expression of Bax, Bal-2, and p53 in myocardial cell was studied by means of immunohistochemical SP method and the microstructure damage was observed under electron microscopy. Results: After clamping the superior mesenteric artery and reperfusion the concentration of NO increased continuously and reached a peak for reperfusion 7 d (P<0.01) but that of SOD decreased from 30 min to 7 d. The expression of Bax, p53 and Bcl-2 also increased obviously especially for reperfusion 30 min and 7 d following ischemia and reperfusion. After reperfusion for 30 min the positive cell rate of Bax, p53 and Bcl-2 was 53.6%, 45.9% and 67.9%, for reperfusion 7 d it was 52.4%, 43.4% and 31.9% respectively, but the positive cell rate of Bax and p53 was higher than that of Bcl-2. The result of electron microscopy observation showed mfofiliments breaked, dissolved and chromatin condensed. Conclusion: Intestinal ischemia and reperfusion of rat can induced the changes of oxygen free radical and the expression of apoptotic gene and second injury of myocardial cells.展开更多
Objective:To study the effect of reactive oxygen species of inducing apoptosis on the heptocacinoma tissues following ischemia and reperfusion and perfusion hyperoxia liquid of hepatocarcinoma. Methods: The hepatocarc...Objective:To study the effect of reactive oxygen species of inducing apoptosis on the heptocacinoma tissues following ischemia and reperfusion and perfusion hyperoxia liquid of hepatocarcinoma. Methods: The hepatocarcinoma animal models ware established by implantation of VX2 tumor constitution mass into the left middle lobe of liver of rabbits. The animals were subjected to 60 min clamp-induced ischemia of hepatic artery distributing in the left middle lobe followed by reperfusion at 1 h, 1 d, 3 d and 7 d, respectively, and perfusion hyperoxia liquid (partial pressure of oxygen, PO2>80 kPa) at the same time with reperfusion beginning. The concentration of MDA and NO ware tested. Apoptotic changes in the hepatocarcinoma and normal hepatic tissues were observed by means of HE staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL). Results:The concentration of MDA in normal hepatic tissues and hepatocarcinoma tissue increased followed ischemia and reperfusion especially for reperfusion 1 h (4.61±0.40, 3.10±0.23) and restored to normal level at reperfusion 7 d in normal hepatic tissues but still kept high concentration in the hepatocarcinoma tissue. Even though concentration of MDA in normal hepatic tissues is higher than that of before ischemia and reperfusion, no difference have been found after perfusion of hyperoxia liquid, and in the hepatocarcinoma tissue, the increasing of concentration of MDA was obvious after simply ischemia and reperfusion at reperfusion 1 d (4.25±0.45). The concentration of NO in normal hepatic tissues increased for reperfusion 3 d and 7 d(18.17±0.13, 17.45±0.23),while that of hepatocarcinoma tissue decreased at reperfusion 3 d(15.95±043). After perfusion of hyperoxia liquid, the concentration of NO in normal hepatic tissues kept increasing and that decreased in the hepatocarcinoma tissues in all time point and reached the lowest level at reperfusion 1 d(14.62±0.45).The result demonstrated the changes of concentration of NO and MDA in the hepatocarcinoma tissues ware more obvious than that of normal hepatic tissues(P<0.01). Conclusion:Perfusion of hyperoxia liquid from hepatic portal vein can intensify ischemia and reperfusion injury but less so for normal hepatic tissues.展开更多
文摘Objective: To study the changes of oxygen free radical, expression of apoptotic gene, ultrastructure of myocardial cell and second injury of the heart following the intestinal ischemia and reperfusion. Methods: Making the models of ischemia and reperfusion by clamping superior mesenteric artery, the concentration of NO and SOD in the blood was examined before clamping the artery and reperfusion for 0, 30, 60 min, 1, 3, and 7 d. The expression of Bax, Bal-2, and p53 in myocardial cell was studied by means of immunohistochemical SP method and the microstructure damage was observed under electron microscopy. Results: After clamping the superior mesenteric artery and reperfusion the concentration of NO increased continuously and reached a peak for reperfusion 7 d (P<0.01) but that of SOD decreased from 30 min to 7 d. The expression of Bax, p53 and Bcl-2 also increased obviously especially for reperfusion 30 min and 7 d following ischemia and reperfusion. After reperfusion for 30 min the positive cell rate of Bax, p53 and Bcl-2 was 53.6%, 45.9% and 67.9%, for reperfusion 7 d it was 52.4%, 43.4% and 31.9% respectively, but the positive cell rate of Bax and p53 was higher than that of Bcl-2. The result of electron microscopy observation showed mfofiliments breaked, dissolved and chromatin condensed. Conclusion: Intestinal ischemia and reperfusion of rat can induced the changes of oxygen free radical and the expression of apoptotic gene and second injury of myocardial cells.
文摘Objective:To study the effect of reactive oxygen species of inducing apoptosis on the heptocacinoma tissues following ischemia and reperfusion and perfusion hyperoxia liquid of hepatocarcinoma. Methods: The hepatocarcinoma animal models ware established by implantation of VX2 tumor constitution mass into the left middle lobe of liver of rabbits. The animals were subjected to 60 min clamp-induced ischemia of hepatic artery distributing in the left middle lobe followed by reperfusion at 1 h, 1 d, 3 d and 7 d, respectively, and perfusion hyperoxia liquid (partial pressure of oxygen, PO2>80 kPa) at the same time with reperfusion beginning. The concentration of MDA and NO ware tested. Apoptotic changes in the hepatocarcinoma and normal hepatic tissues were observed by means of HE staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL). Results:The concentration of MDA in normal hepatic tissues and hepatocarcinoma tissue increased followed ischemia and reperfusion especially for reperfusion 1 h (4.61±0.40, 3.10±0.23) and restored to normal level at reperfusion 7 d in normal hepatic tissues but still kept high concentration in the hepatocarcinoma tissue. Even though concentration of MDA in normal hepatic tissues is higher than that of before ischemia and reperfusion, no difference have been found after perfusion of hyperoxia liquid, and in the hepatocarcinoma tissue, the increasing of concentration of MDA was obvious after simply ischemia and reperfusion at reperfusion 1 d (4.25±0.45). The concentration of NO in normal hepatic tissues increased for reperfusion 3 d and 7 d(18.17±0.13, 17.45±0.23),while that of hepatocarcinoma tissue decreased at reperfusion 3 d(15.95±043). After perfusion of hyperoxia liquid, the concentration of NO in normal hepatic tissues kept increasing and that decreased in the hepatocarcinoma tissues in all time point and reached the lowest level at reperfusion 1 d(14.62±0.45).The result demonstrated the changes of concentration of NO and MDA in the hepatocarcinoma tissues ware more obvious than that of normal hepatic tissues(P<0.01). Conclusion:Perfusion of hyperoxia liquid from hepatic portal vein can intensify ischemia and reperfusion injury but less so for normal hepatic tissues.
