Treating myocardial stunning randomly, with either propofol or isoflurane following transient coronary occlusion and reperfusion in pigs

Abstract

Propofol and isoflurane may be used during fast track anesthesia for off-pump bypass, where transient ischemia is common. The purpose of this study was to compare the effects of propofol vs isoflurane in a porcine model of acute coronary occlusion. Twenty five pigs were randomized to receive general anesthesia with either isoflurane, 1 MAC (n = 13), or propofol, 3 mg/kg bolus followed by 200 microg/ kg/min infusion (n = 12). Pressure-tipped catheters were placed in the left ventricle (LV) and carotid artery; cardiac output was measured by ultrasound; two pairs of ultrasonic dimension catheters were placed in the subendocardium of LV. The slope of LV end-systolic pressure-volume relationship (Emax) was calculated. Reversible ischemia for 15 mins was accomplished with an occluder around the left anterior descending artery followed by reperfusion period. Measurements were done at baseline, end ischemia, early (5 min) and late (30 min) reperfusion. The data collected included systemic hemodynamics, LV end-diastolic pressure (LVEDP), dP/dt, Emax, and the presence of ventricular arrhythmias. The number of animals studied to completion was 19 (n = 11 in the isoflurane group; n = 8 in propofol group). There was a significant difference in Emax between isoflurane and propofol during early and late reperfusion [3.4 (0.5) and 4.0 (0.3) vs 2.6 (0.4) and 3.2 (0.5) mmHg/sec, respectively; P < 0.05]. Postreperfusion ventricular fibrillation occurred in 54% animals in the propofol group vs none in the isoflurane group ( P 0.05). Isoflurane administration was found to be cardioprotective against ventricular depression and arrhythmias compared to propofol.

Coronary Microcirculation Changes during Myocardial Stunning in Dogs

“…Although the pathological and biochemical mechanisms underlying myocardial stunning have not been elucidated, impaired calcium homeostasis and excitation-contraction coupling in cardiac myocytes, generation of free radicals and oxidative stress, inflammation and endothelial injuries have been implicated [1,6]. The use of calcium antagonists, free radical scavengers and neutrophil depletion has been found to improve stunning in experimental models [7,8]. A better understanding of the molecular mechanism underlying myocardial stunning and its clinical significance will provide a rationale for developing novel therapeutic strategies for the prevention of postischemic dysfunction in patients.…”

Fraud in anaesthetic research and publication

“…The paper “Urdaneta F, Willert JL, Beaver T, Naik B, Kirby DS, Lobato EB. Effects of a new phosphodiesterase enzyme Type V inhibitor (UK 343-664) versus milrinone in a porcine model of acute pulmonary hypertension”[8] was voluntarily retracted by the authors after hearing the publicity of fraud (retraction announced in Ann Thorac Surg 2011;91:338).…”

Medical research: Is everything all right?

“…In his editorial describing the fabricated research, Dr Steven L. Shafer[4] of Columbia University, Editor-in-Chief of Anesthesia & Analgesia , writes, “My commitment to ‘unimpeachable integrity’ means that credible allegations of misconduct are not ignored or swept under the rug, but are pursued, relentlessly, and sometimes at considerable personal cost.” With retraction notices posted everywhere, Urdaneta et al . voluntarily retracted their paper published in Annals of Cardiac Anaesthesia,[5] after Annals of Thoracic Surgery retracted their paper published in 2004. [6] Needless to say, these papers have seriously dented the true value of evidences and have raised a question mark on the veracity of the scientific literature.…”