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Ventricular hypertrophy blocked delayed anesthetic cardioprotection in rats by alteration of iNOS/COX-2 signaling.

Ma L, Kong F, Ge H, Liu J, Gong F, Xu L, Hu B, Sun R - Sci Rep (2014)

Bottom Line: The hemodynamics, infarct size, apoptosis, nitric oxide synthase (NOS), cyclooxygenase-2 (COX-2), Cleaved Caspase-3 and production of NO were determined.We found that the hemodynamic parameters were all markedly improved during the reperfusion period and the myocardial infarct size and apoptosis was significantly reduced by delayed isoflurane preconditioning in sham-operated rats.Our results demonstrated that ventricular hypertrophy abrogated isoflurane-induced delayed cardioprotection by alteration of iNOS/COX-2 pathway.

View Article: PubMed Central - PubMed

Affiliation: 1] Department of Critical Care Medicine, Zhejiang Provincial People's Hospital, Hangzhou, China [2] Department of Anesthesiology, Hangzhou First People's Hospital, Nanjing Medical University, Hangzhou, China [3] Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.

ABSTRACT
The aim of the current study was to determine whether ventricular hypertrophy affects the delayed isoflurane preconditioning against myocardial ischemia-reperfusion (IR) injury. Transverse aortic constriction (TAC) was performed on male Sprague-Dawley rats to induce left ventricular (LV) hypertrophy, then sham-operated or hypertrophied rat hearts were subjected to isoflurane preconditioning (2.1% v/v, 1 h). 24 h after exposure, the hearts were isolated and perfused retrogradely by the Langendorff for 30 min (equilibration) followed by 40 min of ischemia and then 120 min of reperfusion. The hemodynamics, infarct size, apoptosis, nitric oxide synthase (NOS), cyclooxygenase-2 (COX-2), Cleaved Caspase-3 and production of NO were determined. We found that the hemodynamic parameters were all markedly improved during the reperfusion period and the myocardial infarct size and apoptosis was significantly reduced by delayed isoflurane preconditioning in sham-operated rats. However, such cardiac improvement induced by delayed isoflurane preconditioning was not observed in hypertrophied hearts. The expression of iNOS, COX-2 and NO was markedly enhanced, whereas Cleaved Caspase-3 activity was inhibited by delayed isoflurane preconditioning in sham-operated rats, a phenomenon was not found in TAC-control groups pretreated with isoflurane. Our results demonstrated that ventricular hypertrophy abrogated isoflurane-induced delayed cardioprotection by alteration of iNOS/COX-2 pathway.

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Effects of delayed isoflurane preconditioning on the expression of eNOS (A), iNOS(B), COX-2 (C), Cleaved Caspase-3 (D) in rat hearts exposed to ischemia-reperfusion (IR).IR: ischemia reperfusion; Iso: isoflurane; TAC: Transverse aortic constriction. Data are mean ± SD, n = 6 hearts/group. *P < 0.05 vs. Sham + IR.
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f3: Effects of delayed isoflurane preconditioning on the expression of eNOS (A), iNOS(B), COX-2 (C), Cleaved Caspase-3 (D) in rat hearts exposed to ischemia-reperfusion (IR).IR: ischemia reperfusion; Iso: isoflurane; TAC: Transverse aortic constriction. Data are mean ± SD, n = 6 hearts/group. *P < 0.05 vs. Sham + IR.

Mentions: As shown in Fig. 3A and B, total myocardial eNOS expression was not significantly different among all groups. The myocardial iNOS expression was markedly enhanced in Sham + IR + Iso compared with that in Sham + IR (P < 0.05), which was not found in TAC + IR + Iso compared with that in TAC + IR (P > 0.05). There was no significant difference of myocardial iNOS expression between Sham + IR and TAC + IR (Fig. 3A and B).


Ventricular hypertrophy blocked delayed anesthetic cardioprotection in rats by alteration of iNOS/COX-2 signaling.

Ma L, Kong F, Ge H, Liu J, Gong F, Xu L, Hu B, Sun R - Sci Rep (2014)

Effects of delayed isoflurane preconditioning on the expression of eNOS (A), iNOS(B), COX-2 (C), Cleaved Caspase-3 (D) in rat hearts exposed to ischemia-reperfusion (IR).IR: ischemia reperfusion; Iso: isoflurane; TAC: Transverse aortic constriction. Data are mean ± SD, n = 6 hearts/group. *P < 0.05 vs. Sham + IR.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4233333&req=5

f3: Effects of delayed isoflurane preconditioning on the expression of eNOS (A), iNOS(B), COX-2 (C), Cleaved Caspase-3 (D) in rat hearts exposed to ischemia-reperfusion (IR).IR: ischemia reperfusion; Iso: isoflurane; TAC: Transverse aortic constriction. Data are mean ± SD, n = 6 hearts/group. *P < 0.05 vs. Sham + IR.
Mentions: As shown in Fig. 3A and B, total myocardial eNOS expression was not significantly different among all groups. The myocardial iNOS expression was markedly enhanced in Sham + IR + Iso compared with that in Sham + IR (P < 0.05), which was not found in TAC + IR + Iso compared with that in TAC + IR (P > 0.05). There was no significant difference of myocardial iNOS expression between Sham + IR and TAC + IR (Fig. 3A and B).

Bottom Line: The hemodynamics, infarct size, apoptosis, nitric oxide synthase (NOS), cyclooxygenase-2 (COX-2), Cleaved Caspase-3 and production of NO were determined.We found that the hemodynamic parameters were all markedly improved during the reperfusion period and the myocardial infarct size and apoptosis was significantly reduced by delayed isoflurane preconditioning in sham-operated rats.Our results demonstrated that ventricular hypertrophy abrogated isoflurane-induced delayed cardioprotection by alteration of iNOS/COX-2 pathway.

View Article: PubMed Central - PubMed

Affiliation: 1] Department of Critical Care Medicine, Zhejiang Provincial People's Hospital, Hangzhou, China [2] Department of Anesthesiology, Hangzhou First People's Hospital, Nanjing Medical University, Hangzhou, China [3] Shanghai Institute of Cardiovascular Diseases, Zhongshan Hospital, Fudan University, Shanghai, China.

ABSTRACT
The aim of the current study was to determine whether ventricular hypertrophy affects the delayed isoflurane preconditioning against myocardial ischemia-reperfusion (IR) injury. Transverse aortic constriction (TAC) was performed on male Sprague-Dawley rats to induce left ventricular (LV) hypertrophy, then sham-operated or hypertrophied rat hearts were subjected to isoflurane preconditioning (2.1% v/v, 1 h). 24 h after exposure, the hearts were isolated and perfused retrogradely by the Langendorff for 30 min (equilibration) followed by 40 min of ischemia and then 120 min of reperfusion. The hemodynamics, infarct size, apoptosis, nitric oxide synthase (NOS), cyclooxygenase-2 (COX-2), Cleaved Caspase-3 and production of NO were determined. We found that the hemodynamic parameters were all markedly improved during the reperfusion period and the myocardial infarct size and apoptosis was significantly reduced by delayed isoflurane preconditioning in sham-operated rats. However, such cardiac improvement induced by delayed isoflurane preconditioning was not observed in hypertrophied hearts. The expression of iNOS, COX-2 and NO was markedly enhanced, whereas Cleaved Caspase-3 activity was inhibited by delayed isoflurane preconditioning in sham-operated rats, a phenomenon was not found in TAC-control groups pretreated with isoflurane. Our results demonstrated that ventricular hypertrophy abrogated isoflurane-induced delayed cardioprotection by alteration of iNOS/COX-2 pathway.

Show MeSH
Related in: MedlinePlus