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OBJECTIVE: In this study, the antiarrhythmic and anti-ischemic effects of a 6 µg kg(-1) min(-1) infusion dose of remifentanil are investigated in a central sympathetic hyperactivity model in rabbits. METHODS: In this study, 18 New Zealand rabbits were used. The subjects were randomly divided into three groups (n=6) and received 10 µmol L(-1) glutamate intracerebroventricularly to provide the central sympathetic hyperactivity. In group 1, 10 µmol L(-1) glutamate was used; in group 2, 1 h before L-glutamate injection, 40 mg kg(-1) N (omega)-nitro-L-arginine methyl ester was intravenously (iv) administered; and in group 3, also 1 h before L-glutamate injection, 40 mg kg(-1) N (omega)-nitro-L-arginine methyl ester was iv administered. A 6 µg kg(-1) min(-1) dose of remifentanil infusion was administered 5 min before L-glutamate injection. Heart rate, systolic arterial pressure and mean arterial pressure were measured and recorded. Within 15 min of the intracerebroventricular L-glutamate injection, premature ventricular complexes, bigeminy ventricular arrhythmia, ventricular tachycardia, ST-segment shift and T-wave inversions were recorded. RESULTS: When incidences of heart rate, rate pressure product, premature ventricular complexes and bigeminy ventricular arrhythmia were compared between groups, significant differences were not determined. Mean arterial pressure was more significantly increased in group 2 than in the other groups (p<0.05). Ventricular tachycardia, ST-segment shift and T-wave inversions were significantly lower in group 3 than in groups 1 and 2 (p<0.05). CONCLUSION: Remifentanil (6 µg kg(-1) min(-1) for 5 min of infusion) prevented life-threatening ventricular tachycardia and electrocardiographic signs of myocardial ischemia in a model of arrhythmia resulting from the association of central sympathetic overactivity.

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BACKGROUND: Cardioversion (CV), a painful procedure, requires sedation and analgesia. Although several sedation agents currently are in use for CV, data on age-specific efficacy and side effects of midazolam and propofol have been limited. OBJECTIVES: To compare the efficacy and side effects of midazolam and propofol in patients of two different age groups, younger than 65 years and 65 years and over, who were going through CV. METHODS: Seventy consented patients with CV indications caused by atrial fibrillation were included in this clinical trial. The participants were placed into four groups by using a stratified randomization method: patients aged younger than 65 years who were receiving midazolam (n = 12) or propofol (n = 11) and patients 65 years and over who were receiving midazolam (n = 25) or propofol (n = 22). Medications were administered by slow intermittent bolus injections. During CV, time to reach Ramsay Sedation Scale level 5 (RSS-5; induction time); time to reach RSS-2 (recovery time); and side effects including desaturation, apnea, and changes in hemodynamic parameters were recorded by a person blinded to the patient treatment allocation. RESULTS: Mean induction time was similar in all four groups. Mean recovery time (min +/- SD) was shorter in both propofol groups when compared with both midazolam groups: 18.8 (+/- 4.06) and 40.33 (+/- 20.8) in the group younger than 65 years and 18.2 (+/- 5.12) and 54.2 (+/- 20.85) in the group 65 years or older, respectively (p < 0.001). Older participants in each medication group needed less medication than younger patients. There were no hemodynamic differences between the groups. Desaturation was higher in both midazolam groups as compared with individuals in the age-matched propofol groups (both p < 0.05). Patient reactions were less in propofol groups with similar joules during CV procedures than were those in the midazolam groups. CONCLUSIONS: Propofol appears to be a better choice for CV sedation in elders because of its short recovery time, fewer side effects, and its more comfortable sedative effect.

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The cytokine erythropoietin (EPO) possesses potent neuroprotective activity against a variety of potential brain injuries, including transient ischemia and reperfusion. It is currently unknown whether EPO will also ameliorate spinal cord injury. Immunocytochemistry performed using human spinal cord sections showed abundant EPO receptor immunoreactivity of capillaries, especially in white matter, and motor neurons within the ventral horn. We used a transient global spinal ischemia model in rabbits to test whether exogenous EPO can cross the blood-spinal cord barrier and protect these motor neurons. Spinal cord ischemia was produced in rabbits by occlusion of the abdominal aorta for 20 min, followed by saline or recombinant human (rHu)-EPO (350, 800, or 1,000 units/kg of body weight) administered intravenously immediately after the onset of reperfusion. The functional neurological status of animals was better for rHu-EPO-treated animals 1 h after recovery from anesthesia, and improved dramatically over the next 48 h. In contrast, saline-treated animals exhibited a poorer neurological score at 1 h and did not significantly improve. Histopathological examination of the affected spinal cord revealed widespread motor neuron injury associated with positive terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling in control but not in rHu-EPO-treated animals. These observations suggest both an acute as well as a delayed beneficial action of rHu-EPO in ischemic spinal cord injury. Because rHu-EPO is currently used widely with an excellent safety profile, clinical trials evaluating its potential to prevent motor neuron apoptosis and the neurological deficits that occur as a consequence of ischemic injury are warranted.

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