Abstract
While catecholamines like epinephrine (E) and norepinephrine (NE) are commonly used in emergency medicine, limited studies have discussed the harm of exogenously induced catecholamine overdose. We investigated the possible toxic effects of excessive catecholamine administration on cardiopulmonary function and structure via continuous 6 h intravenous injection of E and/or NE in rats. Heart rate, echocardiography, and ventricular pressure were measured throughout administration. Cardiopulmonary structure was also assessed by examining heart and lung tissue. Consecutive catecholamine injections induced severe tachycardia. Echocardiography results showed NE caused worse dysfunction than E. Simultaneously, both E and NE led to higher expression of Troponin T and connexin43 in the whole ventricles, which increased further with E+NE administration. The NE and E+NE groups showed severe pulmonary edema while all catecholamine-administering groups demonstrated reduced expression of receptor for advanced glycation end products and increased connexin43 levels in lung tissue. The right ventricle was more vulnerable to catecholamine overdose than the left. Rats injected with NE had a lower survival rate than those injected with E within 6 h. Catecholamine overdose induces acute lung injuries and ventricular cardiomyopathy, and E+NE is associated with a more severe outcome. The similarities of the results between the NE and E+NE groups may indicate a predominant role of NE in determining the overall cardiopulmonary damage. The results provide important clinical insights into the pathogenesis of catecholamine storm.
Highlights
The autonomic nervous system regulates human responses to environmental change
Our results showed that the expression of troponin T and Cx43 was significantly increased in the E and NE groups and the E+NE group showed greater changes in the RV, septum, and LV lateral walls compared to the sham group
One study reported that E leads to LV apical hypokinesis [31]; in our study the different parts of the LV were not analyzed; but the results showed that NE overdose impaired SV, cardiac output (CO), and MV E Vel more significantly than E, which may suggest a greater risk of cardiac systolic and diastolic dysfunction in the NE group (Figure 2)
Summary
The autonomic nervous system regulates human responses to environmental change. When humans are subjected to threatening events, sympathetic neurons release catecholamines like epinephrine (E) and norepinephrine (NE) to engage the fight-or-flight response. Toxics 2020, 8, 69 in stress-induced physiological processes through binding with catecholamines to regulate vascular resistance and heart rate. These neurohormonal mechanisms are mediated from the sympathetic nervous system, such as baroreflex sensitivity for adrenergic signaling [1]. The latest version of the advanced cardiac life support (ACLS) guidelines, focusing on cardiopulmonary resuscitation published by the American Heart Association in 2019, suggests up to 1 mg E to be administered intravenously (IV)
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