Inhaled matters of the Heart

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.

Myocardial SERCA2 Protects Against Cardiac Damage and Dysfunction Caused by Inhaled Bromine

“…Since more than 70% of cytosolic calcium is removed by SERCA2 activity, it is a major regulator of cardiac relaxation and normal cardiac function. Our studies have shown that highly reactive species produced in the pulmonary bed upon halogen inhalation reach the heart and modify and inactivate cardiac SERCA2 and cause biventricular cardiac dysfunction ( Ahmad et al, 2014 , 2015 , 2019 ; Zakyet al, 2015a , b ; Juncos et al, 2020 ; Masjoan Juncos et al, 2021 ). To further understand the role of SERCA2 in inhaled bromine-induced cardiotoxicity, we used inducible cardiomyocyte-specific excision of SERCA2 ( Supplemental Fig.…”