Protective effect of dexmedetomidine against myocardial ischemia-reperfusion injury in rabbits

Abstract Purpose: To investigate the influence of dexmedetomidine on myocardial ischemia-reperfusion injury (IRI) in rabbits. Methods: Twenty-four New Zealand white rabbits were randomly divided into two equal-sized groups: IRI group (group IR) and dexmedetomidine group (group D). Systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), left ventricular diastolic pressure (LVDP), +dp/dtmax, -dp/dtmax, and t-dp/dtmax were recorded and calculated at the following time points: before (T0) and after (T1) dexmedetomidine infusion, after 30-min ischemia (T2), and after 120-min reperfusion (T3). The levels of plasma endothelin 1 (ET-1), thromboxane A2 (TXA2), and platelet activating factor (PAF); area of myocardial infarction (MI); and no-reflow area were evaluated. Results: SBP, DBP, LVSP, LVEDP, LVDP, and +dp/dtmax at T3 were higher in group D than in group IR (P<0.05). The average no-reflow area in group IR was significantly smaller than that in group D (14±3% vs. 38±5%, P=0.0116). The ET-1, TXA2, and PAF levels at T2 and T3 were higher than those at T0 in both groups (P<0.05). Conclusion: Dexmedetomidine could reduce the magnitude of ischemic myocardial no-reflow area and protect the myocardium with ischemia-reperfusion injury.

High admission levels of γ-glutamyltransferase predict poor myocardial perfusion after primary percutaneous intervention

OBJECTIVE: This retrospective study aimed to investigate the relationship between admission levels of serum y-glutamyltransferase and poor myocardial perfusion after primary percutaneous coronary intervention in patients with acute myocardial infarction. INTRODUCTION: Reperfusion injury caused by free radical release and increased oxidative stress is responsible for the pathophysiology of the no-reflow phenomenon in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention. Serum ϒ-glutamyltransferase is an established marker of increased oxidative stress. METHODS: The study population consisted of 80 patients (64 men and 16 women, mean age = 67.5 + 6.6 years) with thrombolysis in myocardial infarction 0/1 flow pre-procedurally. The patients were divided into two groups according to thrombolysis in myocardial perfusion grades that were assessed immediately following primary percutaneous coronary intervention. The two groups (group 1 and group 2) each consisted of 40 patients with thrombolysis in myocardial perfusion grades 0-1 and thrombolysis in myocardial perfusion grades 2-3, respectively. RESULTS: Admission pain to balloon time, ϒ-glutamyltransferase and creatine kinase-MB isoenzyme levels of group 1 patients were significantly higher than those of group 2 patients. Pain to balloon time, ϒ-glutamyltransferase, peak creatine kinase-MB isoenzyme, low left ventricular ejection fraction and poor pre-procedural thrombolysis in myocardial infarction grade were significantly associated with poor myocardial perfusion by univariate analysis. However, only pain to balloon time and ϒ-glutamyltransferase levels showed a significant independent association with poor myocardial perfusion by backward logistic regression analysis. Adjusted odds ratios were calculated as 4.92 for pain to balloon time and 1.13 for ϒ-glutamyltransferase. CONCLUSION: High admission ϒ-glutamyltransferase levels are associated with poor myocardial perfusion in patients with acute myocardial infarction undergoing primary percutaneous coronary intervention, particularly in patients with prolonged pain to balloon time.