ED50 and ED95 of intrathecal isobaric levobupivacaine coadministered with fentanyl for transurethral resections: randomized, double-blind trial.

BACKGROUND: Levobupivacaine use is progressively increased for intrathecal anesthesia in transurethral resections. The aim was to determine ED(50) and ED(95) of intrathecal isobaric levobupivacaine by addition of 25 mcg fentanyl for patients undergoing transurethral resections. METHODS: A total of 100 patients undergoing transurethral resections with ASA I-III, were randomized to groups receiving intrathecal 0.5% isobaric levobupivacaine in doses of 6, 8, 10, 12 or 14 mg in equal volumes with 25 mcg intrathecal fentanyl addition. Sensorial block level was determined by pinprick and motor block by Bromage scale. RESULTS: Mean onset time of sensorial block in 6 mg group was significantly longer than that of sensorial block in 10 mg, 12 mg and 14 mg groups (p<0.01), 8 mg was longer than 12 mg and 14 mg (p<0.01), and 10 mg onset time of sensorial block was significantly longer than 12 mg and 14 mg (p<0.01). Mean onset time of T10 sensory level in 6 mg group was significantly longer than mean onset time of T10 sensory level in 10 mg, 12 mg and 14 mg (p<0.01), the mean onset time of T10 sensory level in 8 mg group was also significantly longer than that of 12 mg, 14 mg groups (p<0.01). ED(50) and ED(95) of levobupivacaine coadministered with 25 mcg fentanyl were 7.32 mg and 10.88 mg, respectively. CONCLUSION: Levobupivacaine with opioid co-administration can be used in doses considerably lower than doses proposed for routine use as it is a safe drug depending on its hemodynamic effects, side effects.

The role of NO in the posterior hypothalamus in amygdala-generated pressor responses in conscious rats.

The nitrergic system modulates cardiovascular functions of the central nucleus of amygdala (CeA) and the posterior hypothalamus (PH) which are involved in the central regulation of the cardiovascular system. The aim of this study was to investigate the contribution of nitric oxide (NO) in the PH in eliciting cardiovascular responses produced through electrical stimulation (ES) of the CeA. Rats were implanted with a stimulation electrode and a parenchymal cannula system into the CeA and a parenchymal cannula or a microdialysis probe into the PH. The next day, the femoral artery was cannulated for haemodynamic measurement. The CeA was electrically stimulated to produce cardiovascular response. The nitric oxide synthetase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 400 nmol/100 nl) or artificial cerebrospinal fluid were injected into the PH or the CeA before the ES of the CeA. The dialysates were collected from the PH to determine the L-citrulline and the L-glutamic acid levels. L-NAME injection into the CeA but not to the PH suppressed the increases in the mean arterial pressure produced by the ES of the CeA significantly; however, heart rate was not affected by L-NAME injection into either the PH or the CeA. L-citrulline and L-glutamic acid levels in the PH were shown to be increased by the ES of the CeA. NO is involved between the PH and the CeA which has a considerable role in the central regulation of the cardiovascular system.