BACKGROUND: Xenon has only minimal haemodynamic side-effects on normal myocardium and might be a preferable anaesthetic agent for patients with heart failure. We studied the haemodynamic changes caused by 70% xenon in rabbits with chronically compromised left ventricular (LV) function. METHODS: Anaesthetized rabbits were thoracotomized and a major coronary 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% xenon using echocardiography [LV end-diastolic dimension (LVedD), fractional shortening (FS), velocity of circumferential fibre shortening (VcF), ejection fraction (EF)] in closed-chest animals. Subsequently, rabbits were thoracotomized and instrumented for measurement of LV pressure (tip manometer), LV dP/dtmax and cardiac output (ultrasonic flow probe). Haemodynamics were recorded again during inhalation of 70% xenon. RESULTS: All rabbits had compromised LV function 9 weeks after coronary artery ligation. Mean LVedD increased from 12.9 (SD 0.9) 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. Inhalation of 70% xenon had no effect on haemodynamics in closed-chest rabbits, 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) and cardiac output from 239 (69) to 225 (71) ml min(-1) were observed during xenon inhalation (all P<0.05). CONCLUSION: These data show that xenon has only minimal negative inotropic effects in rabbits with LV dysfunction after coronary artery ligation.
BACKGROUND:Xenon has only minimal haemodynamic side-effects on normal myocardium and might be a preferable anaesthetic agent for patients with heart failure. We studied the haemodynamic changes caused by 70% xenon in rabbits with chronically compromised left ventricular (LV) function. METHODS: Anaesthetized rabbits were thoracotomized and a major coronary 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% xenon using echocardiography [LV end-diastolic dimension (LVedD), fractional shortening (FS), velocity of circumferential fibre shortening (VcF), ejection fraction (EF)] in closed-chest animals. Subsequently, rabbits were thoracotomized and instrumented for measurement of LV pressure (tip manometer), LV dP/dtmax and cardiac output (ultrasonic flow probe). Haemodynamics were recorded again during inhalation of 70% xenon. RESULTS: All rabbits had compromised LV function 9 weeks after coronary artery ligation. Mean LVedD increased from 12.9 (SD 0.9) 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. Inhalation of 70% xenon had no effect on haemodynamics in closed-chest rabbits, 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) and cardiac output from 239 (69) to 225 (71) ml min(-1) were observed during xenon inhalation (all P<0.05). CONCLUSION: These data show that xenon has only minimal negative inotropic effects in rabbits with LV dysfunction after coronary artery ligation.
Authors: Mallory K Tate; William S Lawrence; Randy L Gourley; Diana L Zavala; Lori E Weaver; Scott T Moen; Johnny W Peterson Journal: BMC Res Notes Date: 2011-09-05
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