Hyperglycemia-Induced Oxidative Stress Abrogates Remifentanil Preconditioning-Mediated Cardioprotection in Diabetic Rats by Impairing Caveolin-3-Modulated PI3K/Akt and JAK2/STAT3 Signaling

Table 2

Hemodynamics at baseline and after 2 h of reperfusion.

	HR (bpm)	LVSP (mmHg)	+dp/dt (mmHg/s)	-dp/dt (mmHg/s)
Baseline (10 min before ischemia)
C
C+RPC
D	^#	^#	^#	^#
D+RPC	^#	^#	^#	^#
D+NAC	^#		^$	^$
D+NAC+RPC	^#		^$	^$
After 2 h of reperfusion
C
C+RPC	^#	^#	^#	^#
D	^,#	^,#	^,#	^,#
D+RPC	^,#	^,#	^,#	^,#
D+NAC	^,$	^,$	^,$	^,$
D+NAC+RPC	^$,&	^$,&	^$,&	^$&

Control (C), diabetic (D), and N-acetylcysteine-treated diabetic rats (D+NAC, 1.5 g/kg/day) were subjected to myocardial ischemia/reperfusion or remifentanil preconditioning (RPC). The heart rate (HR), left ventricular systolic pressure (LVSP), maximum rate of increase of left ventricular developed pressure (+dp/dt), and maximum rate of decrease of left ventricular developed pressure (-dp/dt) were recorded at 10 min before ischemia (baseline) and 2 h after reperfusion. All the results are expressed as , . Differences in hemodynamics at baseline and after 2 h of reperfusion were analyzed by two-way repeated-measures ANOVA followed by Bonferroni’s post hoc test. vs. their corresponding baseline; vs. their corresponding C group; vs. their corresponding D group; and vs. their corresponding D+NAC group.