Inactivation of TOPK Caused by Hyperglycemia Blocks Diabetic Heart Sensitivity to Sevoflurane Postconditioning by Impairing the PTEN/PI3K/Akt Signaling

Table 2

Hemodynamic measurements at baseline, at 15 min of ischemia, and at 2 h of reperfusion in nondiabetic and diabetic rats with or without treatments.

Parameters	Sham	IR	IR+SPostC	IR+SPostC+LY	IR+SPostC+HI	DM+IR	DM+IR+SPostC
Heart rate (beats/min)
Baseline
Ischemia 15 min
Reperfusion 2 h
Mean arterial blood pressure (mmHg)
Baseline
Ischemia 15 min
Reperfusion 2 h

Nondiabetic and diabetic mice (DM) were subjected to myocardial ischemia/reperfusion (IR) with or without sevoflurane postconditioning (SPostC) in the presence or absence of the PI3K inhibitor LY294002 (LY) or the TOPK kinase inhibitor HI-TOPK-032 (HI). All values are expressed as the . per group. Heart rate and mean arterial pressure were measured at baseline and during myocardial IR. vs. their corresponding baseline; ^# and ^## vs. their corresponding IR groups.