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Xenon produces minimal haemodynamic effects in rabbits with chronically compromised left ventricular function
Authors:Preckel B  Schlack W  Heibel T  Rütten H
Affiliation:1Klinik für Anaesthesiologie, Universitätsklinikum Düsseldorf, Postfach 10 10 07, D-40001 Dusseldorf and 2Aventis Pharma Deutschland GmbH, Frankfurt, Germany*Corresponding author
Abstract:Background. Xenon has only minimal haemodynamic side-effectson normal myocardium and might be a preferable anaesthetic agentfor patients with heart failure. We studied the haemodynamicchanges caused by 70% xenon in rabbits with chronically compromisedleft ventricular (LV) function. Methods. Anaesthetized rabbits were thoracotomized and a majorcoronary artery was ligated to induce ischaemic heart disease.Nine weeks later, rabbits were again anaesthetized (ketamine/propofol),and haemodynamics were measured during inhalation of 70% xenonusing echocardiography [LV end-diastolic dimension (LVedD),fractional shortening (FS), velocity of circumferential fibreshortening (VcF), ejection fraction (EF)] in closed-chest animals.Subsequently, rabbits were thoracotomized and instrumented formeasurement of LV pressure (tip manometer), LV dP/dtmax andcardiac output (ultrasonic flow probe). Haemodynamics were recordedagain during inhalation of 70% xenon. Results. All rabbits had compromised LV function 9 weeks aftercoronary artery ligation. Mean LVedD increased from 12.9 (SD0.9) mm to 17.1 (0.4) mm; EF decreased from 73 (9) to 64 (8)%;FS decreased from 36 (7) to 29 (5)%; VcF decreased from 28.9(6.8) to 17.6 (4.7) mm s–1; all P<0.05. Inhalationof 70% xenon had no effect on haemodynamics in closed-chestrabbits, as measured by echocardiography. After invasive instrumentation,small decreases in LV pressure from 78 (20) to 72 (19) mm Hg,LV dP/dtmax from 3081 (592) to 2633 (503) mm Hg s–1 andcardiac output from 239 (69) to 225 (71) ml min–1 wereobserved during xenon inhalation (all P<0.05). Conclusion. These data show that xenon has only minimal negativeinotropic effects in rabbits with LV dysfunction after coronaryartery ligation. Br J Anaesth 2002; 88: 264–9
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