ABSTRACT
<p><b>OBJECTIVE</b>To observe the polyamines metabolism changes in rat cardiomyocytes underwent ischemia-reperfusion (I/R) injury.</p><p><b>METHODS</b>A branch of the descending left coronary artery was occluded to induce rat myocardial I/R injury (30 min ischemia followed by 2 h, 6 h, 12 h, and 24 h reperfusion). RT-PCR and Western blot were performed to detect the expression of spermidine/spermine N1-acetyltransferase (SSAT) and ornithine decarboxylase (ODC), the concentrations of polyamines were measured with high performance liquid chromatography in hearts with or without I/R.</p><p><b>RESULTS</b>The myocardial transcription and expression of SSAT and ODC were significantly upregulated. Compared with the sham group, ODC mRNA and SSAT mRNA respectively increased 3.1 fold and 3.8 fold and their proteins respectively increased 3.1 fold and 2.9 fold at 24 h of reperfusion (P < 0.01); the concentrations of spermidine, spermine and the total polyamine pool respectively decreased by 33.6%, 35.3% and 32.9% while putrescine concentration increased by 58.9% at 24 h of reperfusion (P < 0.01).</p><p><b>CONCLUSION</b>Our results suggest that ischemia-reperfusion in the heart may affect polyamine metabolism and the disturbance of polyamine metabolism might thus play a critical role in myocardial I/R injury in this model.</p>
Subject(s)
Animals , Female , Male , Rats , Disease Models, Animal , Myocardial Reperfusion Injury , Metabolism , Myocardium , Metabolism , Polyamines , Metabolism , Rats, Wistar , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
<p><b>OBJECTIVE</b>To investigate the role of exogenous carbon monoxide (CO) in protection of rat hearts from ischemia/reperfusion injury and its underlying mechanisms.</p><p><b>METHODS</b>Cardiac contractility, lactate dehydrogenase(LDH), creatine kinase(CK) and infarct area were analyzed by the Langendorff isolated rat hearts. All isolated hearts were subjected to 30 min of ischemia followed by 120 min of reperfusion.</p><p><b>RESULTS</b>Perfusion with 25 micromol/L of CORM-2 (an exogenous CO releaser) during the first 10 min of reperfusion prevented the increase in LVEDP and decrease in LVDP, +dp/dt(max) in isolated ischemia/reperfusion hearts. CORM-2(25 micromol/L) had no effect on the changes of coronary flow, but it really inhibited the release of LDH and CK, and also reduced the infarct size. Perfusion with 10 micromol/L of CORM-2 decreased the LDH, CK and infarct size, but it did not improve the contractility of ischemia/reperfusion hearts. However, perfusion with 100 micromol/L of CORM-2 exacerbated the injury induced by ischemia/reperfusion. Pretreatment of a NOS inhibitor L-NAME and a HO-1 inhibitor ZnPP partly abolished the protection effect of CORM-2(25 micromol/L) on LVEDP, and L-NAME and a GC inhibitor methylene blue could also cancel the enhance of LVDP and +dp/dt(max) incuced by CORM-2. All of the inhibitor (methylene blue, L-NAME, a mitoK(ATP )channel blocker 5-HD and ZnPP) could partly enlarge infarct area compared with CORM-2 treatment.</p><p><b>CONCLUSIONS</b>Exogenous CO could protect heart from ischemia/reperfusion injury. The cardiac protection of CO might be through NOS-cGMP and HO-1 pathway, and the activation of mitoK(ATP)channel might be also involved in.</p>