Direct effect of mild hypothermia on the coronary vasodilation induced by an ATP-sensitive K channel opener, a nitric oxide donor and isoflurane in isolated rat hearts

Tosaka, Reiko; Tosaka, Shinya; Cho, Sungsam; Maekawa, Takuji; Hara, Tetsuya; Sumikawa, Koji

doi:10.1007/s00540-010-0941-2

Cited by 3 publications

(1 citation statement)

References 21 publications

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“…Hypothermic mechanisms providing myocardial protection have not been completely elucidated but include improved energy production during ischemia [38], inhibition of apoptosis [27], increased calcium sensitivity of myocytes [39], regulation of mitochondrial oxidative phosphorylation [38], attenuation of reactive oxygen species generation after ischemia-reperfusion [40], and preserved myocardial vascular autoregulation [41]. All these mechanisms translate into increased myocardial contractility [39,42], which should potentially be enhanced by IATH.…”

Section: Discussionmentioning

confidence: 99%

Intra-arrest hypothermia during cardiac arrest: a systematic review

et al. 2012

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IntroductionTherapeutic hypothermia is largely used to protect the brain following return of spontaneous circulation (ROSC) after cardiac arrest (CA), but it is unclear whether we should start therapeutic hypothermia earlier, that is, before ROSC.MethodsWe performed a systematic search of PubMed, EMBASE, CINAHL, the Cochrane Library and Ovid/Medline databases using "arrest" OR "cardiac arrest" OR "heart arrest" AND "hypothermia" OR "therapeutic hypothermia" OR "cooling" as keywords. Only studies using intra-arrest therapeutic hypothermia (IATH) were selected for this review. Three authors independently assessed the validity of included studies and extracted data regarding characteristics of the studied cohort (animal or human) and the main outcomes related to the use of IATH: Mortality, neurological status and cardiac function (particularly, rate of ROSC).ResultsA total of 23 animal studies (level of evidence (LOE) 5) and five human studies, including one randomized controlled trial (LOE 1), one retrospective and one prospective controlled study (LOE 3), and two prospective studies without a control group (LOE 4), were identified. IATH improved survival and neurological outcomes when compared to normothermia and/or hypothermia after ROSC. IATH was also associated with improved ROSC rates and with improved cardiac function, including better left ventricular function, and reduced myocardial infarct size, when compared to normothermia.ConclusionsIATH improves survival and neurological outcome when compared to normothermia and/or conventional hypothermia in experimental models of CA. Clinical data on the efficacy of IATH remain limited.

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Section: Discussionmentioning

confidence: 99%

Intra-arrest hypothermia during cardiac arrest: a systematic review

et al. 2012

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Cardiovascular and microvascular responses to mild hypothermia in an ovine model

Taccone

et al. 2012

Resuscitation

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Age-Related Changes and Effects of Mild Hypothermia on Carotid Artery Reactivity in Newborn Rats

Cavallaro

Bijker

Strackx³

et al. 2015

CNSNDDT

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Therapeutic hypothermia has become a standard neuroprotective treatment in term newborn infants following perinatal asphyxia. Hypothermia-induced changes in the reactivity of the vessels supplying the brain might play a role in its therapeutic or side effects. We investigated the putative age-related changes and the effect of clinically relevant cooling (33°C) on the reactivity of the newborn rat carotid artery. Carotid artery rings from 2-3 days old and 9-10 days old rats were mounted in myographs and studied at 33°C and 37°C. Hypothermia did not significantly affect the contractions induced by KCl and U46619, nor the relaxations induced by acetylcholine (ACh), the nitric oxide (NO) donor sodium nitroprusside (SNP), the NO-independent stimulator of soluble guanylate cyclase (sGC) BAY 41-2272, the β -adrenoceptor agonist isoproterenol, the adenylate cyclase activator forskolin, and acute hypoxia (PO2 3 kPa). The relaxations induced by ACh, isoproterenol, the β 2-adrenoceptor agonist salbutamol, the β 3-adrenoceptor agonist CL-316243 and acute hypoxia increased with postnatal age and were impaired by endothelium removal or by inhibition of NO synthase (L-NAME) or sGC (ODQ). In contrast, the relaxations induced by SNP, BAY 41-2272 and forskolin were endothelium-independent and did not change with age. In conclusion, mild hypothermia (33°C) does not affect the reactivity of neonatal rat carotid arteries. Our data suggest a reduced NO bioavailability in the carotid artery during the first days of life. This transient reduction in endothelium-dependent relaxation might play a role in the adaptation of the circulatory system to birth and in the neonatal vascular response to insults such as hypoxia.

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Direct effect of mild hypothermia on the coronary vasodilation induced by an ATP-sensitive K channel opener, a nitric oxide donor and isoflurane in isolated rat hearts

Cited by 3 publications

References 21 publications

Intra-arrest hypothermia during cardiac arrest: a systematic review

Intra-arrest hypothermia during cardiac arrest: a systematic review

Cardiovascular and microvascular responses to mild hypothermia in an ovine model

Age-Related Changes and Effects of Mild Hypothermia on Carotid Artery Reactivity in Newborn Rats

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