Sildenafil Postconditioning in a Rat Model of Ventricular Fibrillation/ Resuscitation
- *Corresponding Author:
- Ward Y Vanagt
Department of Physiology, Cardiovascular Research Institute Maastricht CARIM
Maastricht University, Maastricht, The Netherlands
E-mail: [email protected]
Received date: May 13, 2017; Accepted date: June 26, 2017; Published date: June 30, 2017
Citation: Vanagt WY, Amin H, Brouwers A, Pöttgens CCH, Wolfs TGAM, et al. (2017) Sildenafil Postconditioning in a Rat Model of Ventricular Fibrillation/Resuscitation. J Clin Exp Cardiolog 8:530. doi: 10.4172/2155-9880.1000530
Copyright: © 2017 Vanagt WY, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Objective: To evaluate the multi-organ postconditioning potential of sildenafil during resuscitation. Circulatory arrest/resuscitation induces ischemia/reperfusion (I/R) injury in all organs. I/R injury can be reduced using postconditioning during reperfusion. Sildenafil has proven strong single-organ postconditioning properties.
Methods: Ventricular fibrillation (VF) was induced and left untreated for 6 min in anesthetized adult male Wistar rats. During resuscitation, placebo (n=10) or intravenous sildenafil 0.2 mg/kg (n=10) was administered. Troponin-i release, lactate release, blood gases and hemodynamic parameters were assessed. After 3 h of reperfusion, rats were euthanized; brain and heart were removed for infarct staining with triphenyltetrazolium chloride. Urinary kidney injury molecule (KIM-1) was assessed. Data expressed as median (interquartile range), p<0.05 significant.
Results: Resuscitation/defibrillation resulted in return of spontaneous circulation in all rats. Compared with the sildenafil group, the control group showed higher overall troponin release (Control 50 (32-60) versus Sildenafil 16 (12-42) h·microg/L, p=0.032) and higher left ventricular infarct percentage (Control 19 (16-24) versus Sildenafil 16 (12-18)%, p=0.039). There was no significant difference between the groups with respect to mortality, hemodynamic recovery, cerebral cortex infarct percentage, lactate release, blood gas values and urinary KIM-1 release. Three rats in the sildenafil group developed pulmonary edema versus none in the control group.
Conclusions: Sildenafil postconditioning during resuscitation significantly reduces cardiac injury but does not affect mortality, cerebral and renal injury after resuscitation.