Beneficial effects of hyperosmotic perfusion in the myocardium after ischemia/reperfusion injury in isolated rat hearts

Abstract

Objective: A simple method to reduce the ischemia/ reperfusion injury that can accompany cardiac surgery would have great clinical value. This study was to investigate the effect of hyperosmotic perfusion on ischemia/reperfusion injury in isolated perfused rat hearts.Method: Forty male Sprague-Dawley rats were randomly divided either to have their isolated hearts perfused with normal osmotic buffer or buffer made hyperosmotic by addition of glucose. Hearts were then subjected to 30 min ischemia followed by 30 min reperfusion. Coronary flow, time to ischemic arrest, reperfusion arrhythmia, and ventricular function were recorded. Creatine phosphokinase leakage into the coronary artery, and myocardial content and activity of superoxide dismutase and catalase were also examined.Results

Hyperosmotic Environment Blunts Effectivity of Ischemic Preconditioning Against Ischemia-Reperfusion Injury and Improves Ischemic Tolerance in Non-Preconditioned Isolated Rat Hearts

“…It confirms that HO conditions exert cardioprotective effects. Beneficial effect of hypertonicity and related prevention of release of molecular substances (creatine phosphokinase) from the myocytes is also supported by experimental study of Cao et al (2013). Similarly, in vivo experiments in pigs confirmed the favorable effects of hyperosmotic environment induced by intracoronary application of mannitol.…”

Potentially Detrimental Effects of Hyperosmolality in Patients Treated for Traumatic Brain Injury

“…Hyperosmolality increases the mRNA of aquaporin-1, mRNA of upregulated aquaporin-7, protein glycosylation, and intracellular translocation, which may modulate water transport in cardiac myocytes [41][42][43]. A rapid increase in plasma osmolality following hypertonic saline administration depresses the sensitivity of the cardiac baroreflex independently of changes in blood pressure, causing an increase in heart rate [44]. Accumulating data have shown that a rapid increase in plasma osmolality activates sympathetic nerve activity, both in humans and animals [45][46][47].…”

Preservation solutions for attenuation of ischemia–reperfusion injury in vascularized composite allotransplantation

“…Consequently, further cell swelling induced by hypoosmotic stress leads to water influx and irreversible damage to the plasma membrane, organelle breakdown, and cell membrane rupture. 42 While the return of oxygenated blood results in a transition from anaerobic back to aerobic respiration pathways, mitochondria damaged during ischemia continue to produce ROS due to aberrant oxidative phosphorylation caused by the altered-ETC (a-ETC). The ROS cannot be eliminated because the non-enzymatic antioxidant defenses are greatly reduced or entirely depleted during ischemic generation of ROS.…”

“…Consequently, further cell swelling induced by hypoosmotic stress leads to water influx and irreversible damage to the plasma membrane, organelle breakdown, and cell membrane rupture. 42…”