Background:Nitrogen may contribute to reperfusion injury. Some studies have shown that helium as a replacement for nitrogen in breathing gas (heliox) reduces cell necrosis after ischemia/reperfusion when used in a preconditioning fashion (intermittent heliox exposure). Our aim was to test whether heliox, breathed continuously throughout the ischemic and reperfusion periods, reduced necrosis and a marker of reperfusion injury, the no-reflow phenomenon.Methods and Results:Anesthetized, open-chest rabbits received 30 min coronary artery occlusion/3 hrs reperfusion. Before CAO rabbits were randomized to heliox (30% oxygen + 70% helium, n=8) or air supplemented with oxygen to achieve blood gas values within physiologic range (n = 8). Rabbits received the appropriate mix during ischemic and reperfusion periods. Infarct size (% risk zone) and no-reflow defect were measured at the end of the reperfusion period. The ischemic risk zone was similar in both groups (28% of left ventricle in heliox and 29% in control). Heliox breathing did not reduce necrosis; infarct size, expressed as a percentage of the risk region was 44±4% in the heliox group and 49±5% in controls, p = 0.68. The extent of the no-reflow defect was not altered by heliox, either expressed as a percent of the risk region (29±4% in heliox and 28±3% in control) or as a percent of the necrotic zone (65±5% in heliox and 59±8% in control).Heliox treatment had no effect on hemodynamic parameters or arterial blood gas values.Conclusion:Continuous heliox breathing does not appear to be cardioprotective in the setting of acute myocardial infarction in the rabbit model. Heliox respiration administered during 30 minutes of ischemia and 180 minutes of reperfusion did not alter infarct size or the extent of no-reflow.
Pilot studies in 31 rats to detect gases in the brain during anesthesia demonstrated the presence of gas microbubbles in electron photomicrographs of brains taken from anesthetized and unanesthetized control animals. Gas microbubbles were numerous in specimens preserved with near-isotonic xatives, but nearly absent in brains xed with a substantially hypertonic xative solution. Hypertonic xation appears to deplete extracellular and intracellular uid to an extent that tissue entrapped bubbles collapse and are ushed away. Using near-isotonic xative solutions, it was shown that gas microbubbles may play important roles in Toxicology (CCl4-induced hepatotoxicity), Physiology (oxygen transport), and Pharmacology (inhalation anesthesia). Excessively hypertonic tissue xative solutions are unsuitable for the histological study of tissue gases.Initially, the purpose of this study was merely to determine whether microbubbles of gas could be found in the brains of rats anesthetized with gas and volatile anesthetics. The premise was that anesthetic gas bubbles might interfere with normal brain function by simple physical mechanisms. A pilot study, conducted on rats anesthetized with methoxy urane, halothane, ethyl ether, or nitrous oxide, con rmed the presence of gas microbubbles in brains xed in 2% glutaraldehyde. Surprised to nd gas bubbles in the brain of an unanesthetized control rat, the author reviewed earlier literature to determine which xatives were optimum for rat brains. In 1969, Sumi found that mitochondria were swollen and vacuolated and the neuroprocesses were swollen in 24-h-old ether-anesthetized rats perfused with 50 to 100 mL of 1.2% glutaraldehyde buffered to 280 mOsm/kg (isotonic). These ndings were attributed to poor tissue xation, since they disappeared in rats perfused with 50 to 100 mL of 4% glutaraldehyde buffered to 710 mOsm/kg (»2.5 £
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