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Objective: Cardioprotection with postconditioning has been well demonstrated after a short period of reperfusion. This study was designed to investigate whether hypoxia inducible factor-1α (HIF-1α), the major transcription factor and key regulator of adoptive responses to hypoxia, was expressed during myocardial ischemia postconditioning (MIP). Methodes: Male adult rats undergoing 45 min left anterior descending artery occlusion were divided into MI/R (myocardial ischemia and reperfusion) group with 3 h of full reperfusion and MIP group with three l0 s cycles of reperfusion and re-occlusion applied at the onset of 3 h of reperfusion. The expression of HIF-1α was examined by immunohistochemistry and western blot. Myocardial infarct size was identified by Evans blue and TTC staining. Cardiomyocyte apoptosis was qualitatively analyzed by terminal dUTP nick end-labeling (TUNEL) assay. Result: Compared with MI/R group, treatment with MIP reduced myocardial infarct size (16.3±1.7% vs. 27.1±2.3%, P<0.05), decreased cardiomyocyte apoptosis (10.2±2.0% vs.18.2±3.7%, P<0.05). The expression of HIF-1α was significant increased with 1.4-fold in MIP groups versus MI/R groups. Conclusion: MIP has a protective effect on ischemic reperfused myocardium and the effect is intimately related to upregulation of HIF-1α. [ABSTRACT FROM AUTHOR]

Objective: To determine whether the cardiac function of aged rats is more susceptible to ischemia/reperfusion injury than that of adult heart and, if so, to clarify the mechanisms. Methods: SD rats were randomly divided into 4 groups: normal adult group (5-6 months), normal old group (22-24 months), adult-myocardial ischemia/reperfusion (MI/R, the rats were subjected to 30 minutes of myocardial ischemia via ligating the left anterior descending coronary artery followed by 3 hours of reperfusion) group and old-MI/R group. The cardiac function of left ventricle was continuously measured. The content of total nitric oxide (NOx) and nitrotyrosine, and the expression of iNOS in myocardium were detected. Results: A significantly exacerbated cardiac reperfusion injury was found in old-MI/R group as evidenced by aggravated cardiac function compared with adult -MI/R group, especially the diastolic function. Aged hearts had a markedly increased basal NOx compared to young adult hearts (1.3 folds, P<0.05). Marked higher myocardial NOx contents, nitrotyrosine contents and iNOS expression was found in old-MI/R group than that in adult -MI/R group. Conclusion: Our results demonstrated that in aged hearts high levels of NO might form iNOS attributed to the increased susceptibility of ischemic-reperfusion injury in cardiac function. [ABSTRACT FROM AUTHOR]

Objective: To observe the effect of autoantibody against α1-adrenoceptor (α1-AR) on vasoconstriction. Methods: The synthetic peptide corresponding to the sequence of the second extracellular loop of the rat α1-AR was used as the antigen to screen the anti-α1-AR antibodies from the sera of immunized group and vehicle group by SA-ELISA. The IgGs from the positive sera were purified by affinity chromagraphy. The effects of antibody against α1-AR on the vasoconstriction of rats in vitro or blood pressure of rats in vivo were observed by tension of isolated thoracic aortic rings or tail-cuff method respectively. Results: In immunized group, the antibodies emerged at 3 weeks after initial immunization with the synthetic peptide, and reached the peak (1:5109±2.4) at 5 weeks, then persisted within 2 months; 3.5 months after immunization, the systolic blood pressure of the rats in immunized group was higher than that of vehicle group. The antibodies against α1-AR (10-6mol/L) increased the tension of isolated thoracic aortic ring from 1.06±0.08g to 1.88±0.06g (P<0.05, vs. control group),which is similar to the α1-AR agonist, phenylephrine (10-6mol/L), increased the tention from 1.04±0.07g to 2.26±0.03g. Conclusions: Our results demonstrated that the anti-α1-AR antibody exhibited remarkable effects of vascular contraction in vitro, and also can induce blood pressure increasing in vivo. Thus, autoantibody against α1-AR may play a role in both the initiation and maintenance of the hypertension. [ABSTRACT FROM AUTHOR]