In the dog, pancuronium 0.2 mg/kg increased left ventricular systolic pressure and systemic arterial pressure, but did not change central venous pressure. Repeated doses produced diminishing responses and eventually no change in arterial pressure. After tachyphylaxis was established, a pressor response to pancuronium could be induced by an i.v. infusion of noradrenaline. Desipramine, a noradrenaline blocking agent, prevented the restoration of the pressor effect of noradrenaline. Guanethidine and reserpine abollished the restoration of the pressor response to pancuronium by noradrenaline. These findings are consistent with the hypothesis that pancuronium acts on the postganglionic nerve endings and causes release of noradrenaline.

Cymbopogon citratus is one of the most common herbs used in folk medicine due to its anti-inflammatory and antioxidant properties. Taking into account these properties showed on in vitro assays, the aim of this study was to evaluate the anti-inflammatory and analgesic activities of C. citratus leaves infusion (CcE) and its flavonoid-rich (CcF) and tannin-rich (CcT) fractions. The evaluation of the anti-inflammatory activity was performed in the carrageenan-induced rat paw oedema model. Both central and peripheral analgesic activities were evaluated in mice through the hot plate test and the acetic acid-induced writhing test, respectively. In the acute inflammation model, the statistically significant results obtained in percentage of oedema inhibition were 70.80 and 82.30% for CcE (34.12 and 68.24 mg kgG , respectively), 59.00% for CcF 1 (7.42 mg kgG), 61.00% for CcT (5.96 mg kgG) and 84.00% for positive control group 1 1 (10 mg kgG). For the peripheral pain evaluation, statistically significant results showed a pain 1 reduction of 57.00% for CcE (136.48 mg kgG), 54.60% for CcF (14.8 mg kgG), 52.20% for CcT 1 1 (11.92 mg kgG) and 83.00% for positive control group. This study demonstrates that C. citratus 1 infusion compounds are able to reduce inflammation and peripheral pain in vivo, with polyphenols showing a significant contribution for these activities.

The effect of sodium valproate on the binding of thiopentone to serum protein was studied in vitro. In the absence of valproate the unbound fraction of thiopentone was 15.2 +/- 0.64%, but with concentrations of valproic acid in excess of the therapeutic range, it increased to 22.42 +/- 1.65%. Scatchard plots for thiopentone in the absence and presence of valproate were investigated also. The barbiturate was bound by one group of binding sites with the association constant, Ka = 2.81 X 10(3) litre mol-1 and the number of binding sites (n) = 2.3. There was a marked decrease in this association constant in the presence of valproic acid (Ka = 1.82 X 10(3) litre mol-1), but without significant change in the number of binding sites (n = 2.13). Additionally, the effect of administration of sodium valproate i.v. on thiopentone anaesthesia was examined in rabbits. The recovery time from thiopentone was markedly longer in the presence of the anticonvulsant drug (17.0 min v. 37.1 min).