Abstract
Natriuretic peptides (NPs) regulate blood pressure and fluid homeostasis and exert various effects on the cardiovascular system. Recently, the relationship between NPs and the energy metabolism has been reported, and using a cell culture experiment system, we previously showed that NP activated brown cells in a low temperature environment while also suppressing a decrease in the cell temperature. However, few reports have described the secretion of NPs in cold environments, and there have been almost no studies of B-type natriuretic peptide (BNP) in humans. We investigated how NPs respond to cold environments in 21 patients who underwent therapeutic hypothermia (TH) after cardiac arrest. The plasma BNP levels were significantly increased (more than fivefold) during TH (logarithmically from 1.98 ± 0.79 to 2.63 ± 0.59, P < 0.01). During TH, diastolic pulmonary artery pressure (PAP) significantly decreased, and there were no significant changes in the stroke volume index (SVI). This increase of BNP was not associated with any hemodynamic changes. In contrast to our findings for BNP, the change in A-type NP (ANP) was quite small. We detected a significant increase in the plasma BNP levels during TH, unrelated to hemodynamics. This elevation of BNP levels seems to be potential influenced by hypothermia.
Highlights
Natriuretic peptides (NPs) regulate blood pressure and fluid homeostasis and exert various effects on the cardiovascular system
We demonstrated the thermogenic actions of NP in rat brown adipocytes through the p38 mitogen-activated protein kinase (MAPK)-uncoupling protein 1 (UCP1) pathway by increasing the intracellular temperature[13]
These findings suggested that NPs have a novel self-protective function when the core body temperature or the local tissue temperature decreases to a level that results in severe hemodynamic conditions, such as serious heart failure
Summary
Natriuretic peptides (NPs) regulate blood pressure and fluid homeostasis and exert various effects on the cardiovascular system. Few reports have described the secretion of NPs in cold environments, and there have been almost no studies of B-type natriuretic peptide (BNP) in humans. During TH, diastolic pulmonary artery pressure (PAP) significantly decreased, and there were no significant changes in the stroke volume index (SVI) This increase of BNP was not associated with any hemodynamic changes. We demonstrated the thermogenic actions of NP in rat brown adipocytes through the p38 mitogen-activated protein kinase (MAPK)-uncoupling protein 1 (UCP1) pathway by increasing the intracellular temperature[13] These findings suggested that NPs have a novel self-protective function when the core body temperature or the local tissue (including the heart itself) temperature decreases to a level that results in severe hemodynamic conditions, such as serious heart failure. The cause of cardiac arrest Acute MI Acute MI Acute MI CSA ALCAPA Ischemic cardiomyopathy Acute MI Acute MI Acute MI ACS Unknown Acute MI CSA Suspicion of cardiac sarcoidosis Unknown Acute MI Suspicion of DCM Pulmonary thromboembolism Suspicion of Brugada syndrome
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