Abstract

Inhalations of atmospheric pollutants, especially particulate matters, are known to cause severe cardiac effects and to exacerbate preexisting heart disease. Heart failure is an important sequellae of gaseous inhalation such as that of carbon monoxide. Similarly, other gases such as sulphur dioxide are known to cause detrimental cardiovascular events. However, mechanisms of these cardiac toxicities are so far unknown. Increased susceptibility of the heart to oxidative stress may play a role. Low levels of antioxidants in the heart as compared to other organs and high levels of reactive oxygen species produced due to the high energetic demand and metabolic rate in cardiac muscle are important in rendering this susceptibility. Acute inhalation of high concentrations of halogen gases is often fatal. Severe respiratory injury and distress occurs upon inhalation of halogens gases, such as chlorine and bromine; however, studies on their cardiac effects are scant. We have demonstrated that inhalation of high concentrations of halogen gases cause significant cardiac injury, dysfunction, and failure that can be critical in causing mortalities following exposures. Our studies also demonstrated that cardiac dysfunction occurs as a result of a direct insult independent of coexisting hypoxia, since it is not fully reversed by oxygen supplementation. Therefore, studies on offsite organ effects of inhaled toxic gases can impact development of treatment strategies upon accidental or deliberate exposures to these agents. Here we summarize the knowledge of cardiovascular effects of common inhaled toxic gases with the intent to highlight the importance of consideration of cardiac symptoms while treating the victims.

Highlights

  • Many studies have been performed to investigate the cellular mechanisms of inhaled gasinduced injury to pulmonary tissues, very few have investigated the effect on cardiac tissue

  • Circulating halogen reactants contribute to the additional burden on the heart by damaging important intracellular calcium (Ca2+) regulators such as sarcoendoplasmic reticulum ATPase (SERCA) and causing cytosolic Ca2+ overload [1]

  • Understanding the mechanisms of cardiac tissue injury by inhaled toxic gases is crucial for developing effective therapeutic countermeasures

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Summary

Inhaled matters of the heart

Ahmed Zaky1,2, Aftab Ahmad1, Louis J Dell’Italia2, Leila Jahromi1, Lee Ann Reisenberg1, Sadis Matalon1, and Shama Ahmad1 1Department of Anesthesiology and Perioperative Medicine, University of Alabama at Birmingham, Alabama 2Department of Medicine, Birmingham Veteran Affairs Medical Center, Birmingham, Alabama and Division of Cardiovascular Disease, University of Alabama Medical Center, Birmingham, Alabama

Introduction
Sulfur dioxide
Carbon Monoxide
Mechanism of toxicity
Acute coronary syndrome
Findings
Toxin Model Type
Full Text
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