Early and delayed protection by capsaicin against reperfusion injury in rat hearts.
Abstract
AIM:
To study early or delayed cardioprotection afforded by pretreatment with capsaicin.
METHODS:
The isolated rat heart was perfused in a Langendorff model. Heart rate, coronary flow, left ventricular pressure, and its first derivative (+/- dp/dtmax) were recorded, and the calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) and the release of creatine kinase (CK) were measured.
RESULTS:
Capsaicin (50 mg.kg-1, s.c.) improved the recovery of cardiac function and decreased the release of CK. CK was (2.12 +/- 0.40) and (0.26 +/- 0.04) u.min-1.g-1(wet wt) for ischemia-reperfusion (I/R) and capsaicin + I/R, respectively (P < 0.05). Capsaicin treatment caused an increase in the concentration of CGRP-LI in plasma. CGRP-LI was (135 +/- 12) and (304 +/- 45) ng.L-1 for vehicle + I/R and capsaicin + I/R, respectively (P < 0.05). After pretreatment with capsaicin to deplete the sensory nerve transmitter content, the cardioprotection and the increased level of CGRP by capsaicin were abolished. A delayed protection was shown in the hearts obtained from the rats pretreated with capsaicin 24 h or 48 h before the experiments.
CONCLUSION:
Pretreatment with capsaicin induces the early and delayed cardioprotection, which may be related to stimulation of CGRP release in the rat.
Keywords:
To study early or delayed cardioprotection afforded by pretreatment with capsaicin.
METHODS:
The isolated rat heart was perfused in a Langendorff model. Heart rate, coronary flow, left ventricular pressure, and its first derivative (+/- dp/dtmax) were recorded, and the calcitonin gene-related peptide-like immunoreactivity (CGRP-LI) and the release of creatine kinase (CK) were measured.
RESULTS:
Capsaicin (50 mg.kg-1, s.c.) improved the recovery of cardiac function and decreased the release of CK. CK was (2.12 +/- 0.40) and (0.26 +/- 0.04) u.min-1.g-1(wet wt) for ischemia-reperfusion (I/R) and capsaicin + I/R, respectively (P < 0.05). Capsaicin treatment caused an increase in the concentration of CGRP-LI in plasma. CGRP-LI was (135 +/- 12) and (304 +/- 45) ng.L-1 for vehicle + I/R and capsaicin + I/R, respectively (P < 0.05). After pretreatment with capsaicin to deplete the sensory nerve transmitter content, the cardioprotection and the increased level of CGRP by capsaicin were abolished. A delayed protection was shown in the hearts obtained from the rats pretreated with capsaicin 24 h or 48 h before the experiments.
CONCLUSION:
Pretreatment with capsaicin induces the early and delayed cardioprotection, which may be related to stimulation of CGRP release in the rat.