Chen T Y, Chang C L, Lan A K, Tseng C C, Tsai Y C, Cheng J T
Department of Anesthesiology, College of Medicine & Hospital, National Cheng Kung University, Taiwan, R.O.C.
Acta Anaesthesiol Sin. 1997 Sep;35(3):155-9.
Recently, some studies suggested that nitric oxide (NO) plays a role as a mediator in the central nociceptive pathways and is possibly involved the mechanisms of anesthesia and wakefulness. Inhibition of the L-arginine-NO pathway in the central nervous system may result in an anesthetic, analgesic, or sedative effect. The aim of the present study was to evaluate the effects of the nitric oxide synthase inhibitor (NOSI), nitroG-L-arginine methyl ester (L-NAME), on the threshold for isoflurane anesthesia in rabbits.
Sixteen New Zealand rabbits were randomly divided into two groups, with eight rabbits in each group. In the study group, a dose of L-NAME 30 mg/kg was injected i.v. daily as pretreatment on three consecutive days, and the fourth dose of L-NAME was given 30 min before the study began. Normal saline was given to the control group. Data of minimal alveolar concentration (MAC), blood pressure (BP), and heart rate (HR) were collected from both groups. Vital signs, such as EtCO2, O2 saturation, and temperature, were maintained within the normal range. All data were described as mean +/- SEM. Statistical analysis was performed using Student's t-test, where p < 0.05 was considered significant.
MAC of isoflurane in the control group was 1.90 +/- 0.12%. MAC of the L-NAME group was 1.70 +/- 0.22%, significantly lower than the control group (p < 0.05).
Our preliminary result shows that the MAC of isoflurane in animals treated with L-NAME was lower than that in the control group. It is suggested that inhibition of the nitric oxide pathway may enhance the effect of isoflurane.
