Cardiovascular Function in Hypothermic Anesthetized Man

Rose, John C.; McDermott, Thomas F.; Lilienfield, Lawrence S.; Porfido, Frank A.; Kelley, Robert T.

doi:10.1161/01.cir.15.4.512

Cited by 27 publications

(3 citation statements)

References 16 publications

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“…Rose et al [32] studied cardiovascular function in 10 anaesthetized humans, comparing cardiovascular parameters in the patients at normothermia, at 32.5 mC and at 30 mC. They found consistent changes in heart rate, with significant bradycardia, but inconsistent changes in measured cardiac output.…”

Section: Discussionmentioning

confidence: 99%

Threshold for adrenomedullary activation and increased cardiac work during mild core hypothermia

et al. 2001

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Postoperative hypothermia increases the incidence of ischaemic cardiac events in patients at risk, but the underlying mechanism is unclear. One possibility is increased cardiac work related to the sympathoneural or adrenomedullary hormonal responses. In awake human volunteers, the present study assessed the effects of mild core hypothermia on these responses, and on the associated changes in indices of cardiac work. A total of 11 healthy men were studied on two separate days. On one day, core temperature (T(c)) was decreased by the intravenous infusion of cold normal saline (4 degrees C; 60 ml/kg over 30 min) through a central venous catheter. On the other day (normothermic control), warm normal saline (37 degrees C; 60 ml/kg over 30 min) was given intravenously. Transthoracic echocardiograms, the sympathoneural response (noradrenaline) and the adrenomedullary response (adrenaline) were evaluated before, during and after the intravenous infusions. Echocardiography was used to measure left ventricular function and cardiac output. Compared with the normothermic control treatment, core cooling of 0.7 degrees C was associated with increased plasma noradrenaline (220% increase; P=0.001), whereas adrenaline, cardiac output, heart rate and the rate-pressure product were unchanged. After core cooling of 1.0 degrees C, increases in noradrenaline (by 230%; P=0.001), adrenaline (by 68%; P=0.05), cardiac output (by 23%; P=0.04), heart rate (by 16%; P=0.04) and rate-pressure product (by 25%; P=0.007) were all significant compared with the normothermic control treatment. In conclusion, there is a T(c) threshold, below which an adrenomedullary (adrenaline) response is triggered in addition to the sympathoneural (noradrenaline) response. This T(c) threshold (approximately 1 degrees C below the normothermic baseline) is also associated with an increase in haemodynamic indices of cardiac work. Mild core hypothermia therefore constitutes a catecholamine-mediated cardiovascular "stress test".

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Section: Discussionmentioning

confidence: 99%

Threshold for adrenomedullary activation and increased cardiac work during mild core hypothermia

et al. 2001

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“…This reduction in heart rate might in turn give rise to a reduction in cardiac output, although this is not sufficiently severe enough to lead to hemodynamic compromise (10,88). At this stage, the hypothermia-induced vasoconstriction of peripheral arteries and arterioles might increase the systemic vascular resistance and lead to a slight increase in the arterial pressure (88,99,100). However, cardiac arrest patients who have been cooled also develop a hypotensive response as a consequence of the "post-cardiac arrest syndrome," which is characterized by myocardial dysfunction, a systemic ischemia-reperfusion response, as well as a systemic inflammatory response (66).…”

Section: Complications Of Ht and Its Managementmentioning

confidence: 99%

Hypothermia Therapy

Delhaye

Mahmoudi

Waksman

2012

Journal of the American College of Cardiology

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Due to its protective effect on the brain and the myocardium, hypothermia therapy (HT) has been extensively studied in cardiac arrest patients with coma as well as in patients presenting with acute myocardial infarction (MI). In the setting of cardiac arrest, randomized studies have shown that HT decreases mortality and improves neurological outcomes. Subsequent guidelines have therefore recommended cooling (32°C to 34°C) for 12 to 24 h in unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest due to ventricular fibrillation. Observational studies have also confirmed the feasibility of this therapy in clinical practice and support its early application in patients with nonventricular fibrillation cardiac arrest and in post-resuscitation circulatory shock. In patients with acute MI, available clinical evidence does not yet support HT as the standard of care, because no study to date has shown a clear net benefit in such a cohort. After a brief review of the mechanisms of action for HT, we provide a review of the clinical evidence, cooling techniques, and potential adverse effects associated with HT in the setting of post-cardiac arrest patient and acute MI.

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“…In the analysis of differentially expressed miRNAs, the P value and FDR had the following criteria: (1) fold change>1.5 or <0.667 and (2) FDR<0.05. 19 The data are shown with a volcano plot. The intersection of hypothermia compared with normothermia under hypoxia causing differentially expressed miRNAs was calculated and described with a Venn diagram.…”

Section: Methodsmentioning

confidence: 99%

Therapeutic Hypothermia Inhibits Hypoxia‐Induced Cardiomyocyte Apoptosis Via the MiR‐483‐3p/Cdk9 Axis

Xue

Zhang

Guo

et al. 2023

JAHA

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Background Therapeutic hypothermia has a beneficial effect on cardiac function after acute myocardial infarction, but the exact mechanism is still unclear. Recent research has suggested that microRNAs participate in acute myocardial infarction to regulate cardiomyocyte survival. This study aimed to explore the ability of hypothermia‐regulated microRNA‐483‐3p (miR‐483‐3p) to inhibit hypoxia‐induced myocardial infarction. Methods and Results Primary cardiomyocytes were cultured under hypoxia at 32 °C to mimic therapeutic hypothermia, and the differentially expressed microRNAs were determined by RNA sequencing. Therapeutic hypothermia recovered hypoxia‐induced increases in apoptosis, decreases in ATP levels, and decreases in miR‐483‐3p expression. Overexpression of miR‐483‐3p exhibited effects similar to those of therapeutic hypothermia on hypoxia in the treatment of cardiomyocytes to associate with maintaining the mitochondrial membrane potential, and cyclin‐dependent kinase 9 (Cdk9) was identified as a target gene with downregulated expression by miR‐483‐3p. Knockdown of Cdk9 also promoted cardiac survival, ATP production, and mitochondrial membrane potential stability under hypoxia. In vivo, the expression of miR‐483‐3p and Cdk9 was tested in the cardiac tissue of the mice with acute myocardial infarction, and the expression of miR‐483‐3p decreased and Cdk9 increased in the region of myocardial infarction. However, miR‐483‐3p was overexpressed with lentivirus, which suppressed apoptosis, infarct size (miR‐483‐3p, 22.00±4.04% versus negative control, 28.57±5.44%, P <0.05), and Cdk9 expression to improve cardiac contractility. Conclusions MiR‐483‐3p antagonizes hypoxia, leading to cardiomyocyte injury by targeting Cdk9, which is a new mechanism of therapeutic hypothermia.

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Cardiovascular Function in Hypothermic Anesthetized Man

Cited by 27 publications

References 16 publications

Threshold for adrenomedullary activation and increased cardiac work during mild core hypothermia

Threshold for adrenomedullary activation and increased cardiac work during mild core hypothermia

Hypothermia Therapy

Therapeutic Hypothermia Inhibits Hypoxia‐Induced Cardiomyocyte Apoptosis Via the MiR‐483‐3p/Cdk9 Axis

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