Open AccessModerate Hypothermia Modifies Coronary Hemodynamics and Endothelium‐Dependent Vasodilation in a Porcine Model of Temperature Management
Author(s) -
Bobi Joaquim,
Solanes Núria,
Dantas Ana Paula,
Ishida Kohki,
Regueiro Ander,
Castillo Nadia,
Sabaté Manel,
Rigol Montserrat,
Freixa Xavier
Publication year - 2020
Publication title -
journal of the american heart association
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.494
H-Index - 85
ISSN - 2047-9980
DOI - 10.1161/jaha.119.014035
Subject(s) - medicine , hypothermia , hemodynamics , vasodilation , cardiology , anesthesia , endothelium , targeted temperature management , resuscitation , cardiopulmonary resuscitation , return of spontaneous circulation
Background Hypothermia has been associated with therapeutic benefits including reduced mortality and better neurologic outcomes in survivors of cardiac arrest. However, undesirable side effects have been reported in patients undergoing coronary interventions. Using a large animal model of temperature management, we aimed to describe how temperature interferes with the coronary vasculature. Methods and Results Coronary hemodynamics and endothelial function were studied in 12 pigs at various core temperatures. Left circumflex coronary artery was challenged with intracoronary nitroglycerin, bradykinin, and adenosine at normothermia (38°C) and mild hypothermia (34°C), followed by either rewarming (38°C; n=6) or moderate hypothermia (Mo HT ; 32°C, n=6). Invasive coronary hemodynamics by Doppler wire revealed a slower coronary blood velocity at 32°C in the Mo HT protocol (normothermia 20.2±11.2 cm/s versus mild hypothermia 18.7±4.3 cm/s versus Mo HT 11.3±5.3 cm/s, P =0.007). Mo HT time point was also associated with high values of hyperemic microvascular resistance (>3 mm Hg/cm per second) (normothermia 2.0±0.6 mm Hg/cm per second versus mild hypothermia 2.0±0.8 mm Hg/cm per second versus Mo HT 3.4±1.6 mm Hg/cm per second, P =0.273). Assessment of coronary vasodilation by quantitative coronary analysis showed increased endothelium‐dependent (bradykinin) vasodilation at 32°C when compared with normothermia (normothermia 6.96% change versus mild hypothermia 9.01% change versus Mo HT 25.42% change, P =0.044). Results from coronary reactivity in vitro were in agreement with angiography data and established that endothelium‐dependent relaxation in Mo HT completely relies on NO production. Conclusions In this porcine model of temperature management, 34°C hypothermia and rewarming (38°C) did not affect coronary hemodynamics or endothelial function. However, 32°C hypothermia altered coronary vasculature physiology by slowing coronary blood flow, increasing microvascular resistance, and exacerbating endothelium‐dependent vasodilatory response.