• Journal of Chest Surgery
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• v.37 no.3
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• pp.245-251
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• 2004

Hemostatic function is regarded to be preserved after an off-pump coronary artery bypass grafting (CABG), compared to conventional CABG, and the preserved hemostatic function may increase thrombotic occlusion of the graft. We studied the changes of hemostatic variables in patients undergoing off-pump CABG, and compared to those of on-pump CABG. We studied the changes of coagulation function in 11 patients who underwent off-pump CABG (group I), and compared them with those of 11 patients who underwent on-pump CABG and Dor procedure (group II). Coagulation status was evaluated by thromboelastography and blood coagulation test preoperatively, postoperative 1$^{st}$ day, 2$^{nd}$ day, 3$^{rd}$ day, and 5$^{th}$ day, respectively. Among the variables measured by thromboelastography (such as r time, k time, $\alpha$ angle, and MA value) and blood coagulation test (such as factor Ⅶ, protein S, protein C, antithrombin III, activated protein C resistance test, plasminogen, D-dimer, prothrombin time, activated partial thromboplastin time, platelet count, hemoglobin, and fibrinogen), there were significant differences in the MA value, $\alpha$ angle, and platelet counts between the two groups. MA values were 140$\pm$72% and 153$\pm$98% in group I, and 87$\pm$27% and 78$\pm$28% in group II, at postoperative 3$^{rd}$ and 5$^{th}$ days, respectively (p<0.05). $\alpha$ angle was 122$\pm$92% in group I and 69$\pm$23% in group II at postoperative 3$^{rd}$ day (p=0.09). Platelet count was 63$\pm$55% in group I and 33$\pm$13% in group II at postoperative 3$^{rd}$ day (p<0.05). Patients who underwent off-pump CABG showed increased coagulability during postoperative periods, compared to those who underwent on-pump CABG. Our data suggest that aggressive perioperative anticoagulation therapy is warranted in patients undergoing off-pump CABG. CABG.

• Biomolecules & Therapeutics
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• v.9 no.3
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• pp.167-175
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• 2001

Recent studies have shown that cytokines are capable of modulating cardiovascular function and that some drugs used in the treatment of heart failure variably modulate the production of cytokines. Hige- namine, a positive inotropic isoquinoline alkaloid, has been used traditionally as cardiac stimulant, and reported to reduce nitric oxide (NO) and inducible nitric oxide synthase (iNOS) expression in LPS- and/or cytokine-activated cells in vitro and in vivo. Therefore, we investigated whether higenamine modulates the production of proinflammatory cytokines in myocardial infarction. In addition, effects of higenamine on antioxidant action and antioxidant enzyme expression (MnSOD) were studied. Myocardial infarction (MI) was confirmed by measuring left ventricular (LV) pressure after occlusion of the left anterior descending coronary artery (LAD) for 5 weeks in rats. Treatment of higenamine (10 mg/kg/day) reduced infarct size about 35 %, which accompanied by reduction of production TNF-$\alpha$, IL-6, but not IFN-${\gamma}$ and IL-1$\beta$ in the myocardium. The expression of TNF-$\alpha$ mRNA in infracted myocardium was significantly reduced by higenamine. Although iNOS mRNA was not detected, nitrotyrosine staining was significantly increased in myocardium of Ml compared to higenamine-treated one, Indicating that peroxynitrite-induced damage is evident in MI. Cytochrome c oxidation by peroxynitrite was concentration-dependently reduced by higenamine, an effect which was almost compatible to glutathion. Higenamine treatment did not affect the expression of MnSOD mRNA in myocardial tissues in MI. Taken together, higenamine may be beneficial in oxidative stress conditions such as ischemic-reperfusion injury and MI due to antioxidant action as well as modulation of cytokines.

• Journal of Chest Surgery
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• v.42 no.5
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• pp.576-587
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• 2009

Background: The up-regulation of the nitric oxide (NO)-cGMP pathway might be involved in the change of vascular reactivity in rats 3 days after they suffer acute myocardial infarction. However, the underlying mechanism for this has not been clarified. Material and Method: Acute myocardial infarction (AMI) was induced by occluding the left anterior descending coronary artery (LAD) for 30 min (Group AMI), whereas the sham-operated control rats were treated similarly without LAD occlusion (Group SHAM), The concentration-response relationships for phenylephrine (PE), KCl, acetylcholine (Ach) and sodium nitroprusside (SNP) were determined in the endothelium intact E(+) and endothelium denuded E(-) thoracic aortic rings from the rats 3 days after AMI or a SHAM operation. The concentration-response relationships of PE in the E(+) rings from the AMI rats were compared with those relationships in the rings pretreated with nitric oxide synthase (NOS) inhibitor $N{\omega}$-nitro-L-arginine methyl ester (L-NAME) or the cyclooxygenase inhibitor indomethacin. The plasma nitrite/nitrate concentrations were checked via a Griess reaction. The cyclic GMP content in the thoracic aortic rings was measured by radioimmunoassay and the endothelial nitric oxide synthase (eNOS) mRNA expression was assessed by real time PCR. Result: The mean infarct size (%) in the rats with AMI was $21.3{\pm}0.62%$. The heart rate and the systolic and diastolic blood pressure were not significantly changed in the AMI rats. The sensitivity of the contractile response to PE and KCl was significantly decreased in both the E(+) and E(-) aortic rings of the AMI group (p<0.05). L-NAME completely reversed these contractile responses whereas indomethacin did not (p<0.05). Moreover, the sensitivity of the relaxation response to Ach was also significantly decreased in the AMI group (p<0.05). The plasma nitrite and nitrate content (p<0.05), the basal cGMP content (p<0.05) and the eNOS mRNA expression (p=0.056) in the AMI rats were increased as compared with the SHAM group. Conclusion: Our findings indicate that the increased eNOS activity and the up-regulation of the NO-cGMP pathway can be attributed to the decreased contractile or relaxation response in the rat thoracic aorta 3 days after AMI.