Xenon and nitrous oxide do not depress cardiac function in an isolated rat heart model

Nakayama, Harumi; Takahashi, Hiroshi; Okubo, Naomitsu; Miyabe, Masayuki; Toyooka, Hidenori

doi:10.1007/bf03017325

Cited by 16 publications

(9 citation statements)

References 30 publications

(33 reference statements)

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“…The minimal cardiovascular effects of xenon we observed are consistent with previous findings in experimental models such as isolated perfused hearts [7,8], dogs with overpacing-induced cardiomyopathy [5], and rabbits with coronary artery ligation-induced left ventricular dysfunction [6]. It has been suggested that the underlying mechanism is the slight or nonexistent electrophysiological action of xenon on the important cation channels, including sodium, L-type calcium, and inward-rectifier and outward voltage-gated potassium channels [7,14].…”

Section: Discussionsupporting

confidence: 89%

Cardiovascular effects of xenon and nitrous oxide in patients during fentanyl‐midazolam anaesthesia*

et al. 2004

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SummaryXenon anaesthesia appears to have minimal haemodynamic effects. The purpose of this randomised prospective study was to compare the cardiovascular effects of xenon and nitrous oxide in patients with known ischaemic heart disease. In 20 patients who were due to undergo coronary artery bypass graft surgery, 30 min following induction of anaesthesia with fentanyl 30 lg.kg )1 and midazolam 0.1 mg.kg )1 but prior to the start of surgery, xenon or nitrous oxide 60% was administered for 15 min. The results showed that xenon caused a minimal decrease in the mean arterial pressure (from 81 (7) to 75 (8) mmHg, mean (SD)), but did not affect the systolic function of the left ventricle, as demonstrated by unchanged left ventricular stroke work index (LVSWI) and the fractional area change of the left ventricle (FAC) derived from transoesophageal echocardiography (TOE). However, in contrast, nitrous oxide was found to decrease the mean arterial pressure (from 81 (8) to 69 (7) mmHg), the LVSWI, and the FAC. The cardiac index, central venous and pulmonary artery occlusion pressures, systemic and pulmonary vascular resistances, and the TOE-derived E ⁄ A ratio through the mitral valve were unchanged by xenon or nitrous oxide. We conclude that xenon provides improved haemodynamic stability compared with nitrous oxide, conserving the left ventricular systolic function.

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Section: Discussionsupporting

confidence: 89%

Cardiovascular effects of xenon and nitrous oxide in patients during fentanyl‐midazolam anaesthesia*

et al. 2004

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“…50 Most available data suggest that less suppression of cardiovascular feedback loops together with absence of vasodilating properties probably provides a reasonable hypothesis for the often quoted cardiovascular stability. This would fit with observations of preserved cardiac myocyte, 51 muscle bundle 52 and global left ventricular function with xenon, which is reported from laboratory 53,54 as well as clinical studies. 39,55 From a functional point of view, xenon obviously can induce some vasoconstriction leading to a limited decrease of cardiac output, together with a small reduction in heart rate.…”

Section: Dovepresssupporting

confidence: 87%

Xenon-based anesthesia: theory and practice

Baumert¹

2009

OAS

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Xenon has been in use as an anesthetic for more than 50 years. Although it exhibits some of the properties of an ideal anesthetic, the technical complexity of xenon equipment and the high cost of the gas have prevented widespread use of xenon anesthesia. The main beneficial features of xenon anesthesia are fast induction and emergence because of low solubility in blood and tissues, along with remarkably stable hemodynamics even in patients with impaired cardiac function. Xenon has proven to be a safe and well-tolerated anesthetic in clinical trials. The primary mechanism by which xenon produces anesthesia-antagonism at the neuronal N-methyl-D-aspartate receptor-and the absence of vasodilating effects distinguish xenon from most other inhaled and intravenous anesthetics. In addition, xenon can protect cells from ischemia-reperfusion damage. This effect was demonstrated in myocardium and neuronal cells as well. Myocardial and cerebral infarction sizes after ischemia can be reduced substantially by xenon, even when administered after the initial insult. Because of its high cost, routine xenon anesthesia may be justified only if it is associated with fewer perioperative complications, shorter duration of hospital stay or significant reduction of perioperative risk. Clinical studies to identify a specific group of patients in which these requirements are met are still lacking.

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“…27 There is also no effect of xenon on contractility of the isolated, perfused rat heart. 28 These findings were recently confirmed in vivo in rabbits with ischaemic cardiomyopathy. 29 A rise in total oxygen consumption reported with xenon 30 may partly be caused by an increase in myocardial oxygen demand but there are currently no published data.…”

Section: Groupmentioning

confidence: 75%