Effects of methane in cardiovascular system
Information on the cardiovascular effects of methane is sparse. In a historical paper, Deinega et al. observed an increased survival time in hemorrhaged rats after treatment with a methane-air mixture.
Polymorphonuclear leukocytes (PMNs) have been observed to generate ROS during myocardial ischemia/ reperfusion (I/R). Activation of the PMN membrane–associated NADPH oxidase system initiates a respiratory burst characterized by a marked increase in cellular oxygen consumption and generation of superoxide anions. Oxidants from activated PMNs can also cause depression of calcium transport in isolated cardiac myocyte sarcoplasmic reticulum and PMN-derived hydrogen peroxide may promote the release of proinflammatory arachidonic acid metabolites (ie, prostacyclin) from cultured endothelial cells. It is documented that oxygen-derived free radicals can induce vascular contraction in isolated arteries, and in isolated perfused hearts, they aggravate postischemic coronary endothelial dysfunction and decrease left ventricular mechanical performance. Most stimuli that induce superoxide generation by PMNs also cause the release of myeloperoxidase (MPO) from the azurophil granules. MPO is a promising biomarker for the risk of cardiovascular diseases prediction. Zhang et al. showed a strong association between MPO levels and risk of coronary artery disease (CAD) and found that MPO activity were higher in patients with CAD and this increased activity was significantly associated with the presence of CAD. It is well known that biomarkers are important tools for an understanding of pathophysiological processes or the evaluation of pharmacologic responses to therapy. MPO catalyzes the conversion of chloride and hydrogen peroxide to hypochlorite and is secreted during inflammatory conditions as it has been implicated in the oxidation of lipids contained within LDL cholesterol. In addition, MPO consumes endothelial-derived NO, thereby reducing NO bioavailability, impairing its vasodilating and anti-inflammatory properties. The cardioprotective potential of PMN inhibition in intact animals subjected to myocardial ischemia and reperfusion has been widely used to indirectly assess the role of PMNs. The antioxidants have favorable effects on myocardial reperfusion injury, along with its documented cardioprotective effects. Beside the antioxidants, administration of NO donors or L-arginine was shown to reduce tissue damage and PMN accumulation after I/R. However, to date the consequences of methane administration in association with inflammatory processes on cardiovascular system is not clarified.
In the gastrointestinal tract, a potent anti-inflammatory profile of exogenous methane is verified. This anti-inflammatory effect in close correlation with a modulation of I/R- induced ROS generation and PMN leukocyte activation. The results showed that normoxic ventilation with 2.5 % methane supplementation protects the tissues by mitigating effects of an ischemia-reperfusion insult. The addition of 2.5 % methane limited the extent of I/R damage in the small intestine in association with a reduced level of PMN leukocyte activation and reduction in the formation of oxygen-nitrogen-centered radicals. Methane supplementation significantly decreased the MPO activity in both intestine and plasma. Tissue-specific ROS generation were reduced, the mesenteric vascular resistance changes were only moderate and a pCO2 gap (a marker of the microcirculation) tended to normalize after reperfusion.