Influence of pinacidil on the myocardial mitochondrial structure and the respiratory function in scalded rats / 中华烧伤杂志

<p><b>OBJECTIVE</b>To investigate the influence of pinacidil preconditioning on the protection of the structure and respiratory function of injured myocardial mitochondria in scalded rats.</p><p><b>METHODS</b>Seventy-five healthy Wistar rats, weighed 250 approximately 300 g, were randomly divided into three groups: i.e. control (n = 9, with intraperitoneal injection of 50 microg/kg isotonic saline), scald (n = 33, with 30% TBSA full thickness scald) and pre-conditioning (n = 33, with same extent of scald injury after intraperitoneal injection of 50 microg/kg pinacidil) groups. Mitochondrial ultrastructure was observed by transmission electron microscope. The mitochondrial respiratory function, the MDA content and the superoxide anion level were determined with corresponding methods.</p><p><b>RESULTS</b>The degree of injury to rat myocardial mitochondria in pre-conditioning group was less intensive than that in scald group (P < 0.05 or 0.01). The respiratory control rate in pre-conditioning group was obviously higher than that in scald group (P < 0.05), and the contents of MDA and superoxide anion in pre-conditioning group were markedly lower than those in scald group (P < 0.05 or 0.01), as evidenced by their contents at 3 post scalding hours (0.60 +/- 0.09 micromol/g and 0.127 +/- 0.020) were obviously lower than those in scald group (0.83 +/- 0.07 micromol/g and 0.169 +/- 0.015) (P < 0.01).</p><p><b>CONCLUSION</b>Pinacidil preconditioning was beneficial in the protection of myocardial mitochondria in scalded rats, and it might be related to the pre-opening of potassium channel which was sensitive to mitochondrial ATP.</p>

Change of cardiac myocyte nuclear inositol 1,3,4,5-tetrakisphosphate receptor binding properties in rat with myocardial ischemic reperfusion / 中华心血管病杂志

<p><b>OBJECTIVE</b>To observe the alteration of cardiac myocyte nuclear inositol 1,3,4,5-tetrakisphosphate receptor (IP(4)R) binding properties in rat subjected to myocardial ischemic reperfusion in order to further make it clear whether this change is involved in the molecule mechanism of cell apoptosis of rat with myocardial ischemic reperfusion.</p><p><b>METHODS</b>Extracting of cardiac myocyte nucleus was accomplished by saccharose density gradient centrifugation method, the binding properties of nuclear IP(4)R in different conditions were detected by radioligand binding assay. Apoptosis index of myocardial cell was determined by using TUNEL assay.</p><p><b>RESULTS</b>(1) Myocardial cell apoptosis index in rat heart underwent 30 min regional ischemia and 3 h reperfusion increased distinctly compared with that in control group (P < 0.01). (2) There were two IP(4) binding sites located to the nuclear envelope. (3) In ischemic reperfusion injury (IRI) group, Bmax from high affinity binding site of nuclear IP(4)R significantly increased compared with that in sham-operated group, whereas Bmax from low affinity binding site didn't change. Kd values of both sites were all significantly decreased by 63% and 55%, respectively. (4) Phosphorylation of nuclear IP(4)R by PKC increased markedly its binding ability both in IRI and control group (P < 0.05), which was more apparent in IRI group. (5) In sham-operated group, the binding ability of nuclear IP(4)R increased with increasing free calcium concentrations in cytoplasm, and the binding properties of IP(4)R in IRI group were also increased in the condition of calcium overloading.</p><p><b>CONCLUSION</b>The increasing of binding properties of nuclear IP(4)R from ischemic reperfusion heart may be one of important mechanism involved in myocardial cell apoptosis, furthermore resulting in myocardial IRI.</p>

Changes of ICAM-1 expression of myocardial ischemic reperfusion injury in old rats and cardiac protective effect of Esmolol / 中国康复理论与实践

@#ObjectiveTo investigate the changes of expression of intercellular adhesion molecule 1 (ICAM-1) on myocardial ischemic reperfusion injury(IRI) in old rats and the cardiac protective effect of Esmolol(ES). Methods116 rats were divided into three groups: IR group, IR+ES group and Sham group. The ischemic samples were observed in ischemia and 3,6,12,24 hours after IR. The myocardial levels of expression of ICAM-1 mRNA were evaluated by method of IN Situ Hybridization and the protein were evaluated by immunocytochemistry. The content of infiltration of polymorphonuclear neutrophils(PMNs), malomdialdehyde(MDA), superoxides dismutase(SOD) and the myocardial infarction area were measured too. ResultsAfter IR, myocardial levels of expression of ICAM-1 mRNA, protein,MDA and PMNs were increased significantly; SOD was decreased significantly. Between the levels of expression of ICAM-1 protein and PMNs, infarction area of myocardium, a close correlation were observed(P<0.05). In IR+ES group, all of the indicators were increased after IR, but the levels of increase in IR+ES group were more significantly modification as compared with IR group(P<0.05-0.01).Conclusions The findings indicate that PMNs could induce myocardial IRI after IR, which result from the ICAM-1 mediated PMNs adhesion.ES is able to decrease myocardial IRI by blocking the expression of ICAM-1 partially.