General pharmacology最新文献

1. The present study investigated whether stimulation of the GABA-ergic system affects spatial navigation (water-maze, WM) deficit induced by nicotinic blockade (mecamylamine). 2. The effects of various doses of gamma-vinyl-GABA (GVG: 50, 150 and 300 mg/kg) and mecamylamine (2.5 and 10 mg/kg) were examined alone and in combination. 3. GVG at the dose 150 mg/kg alone did not impair the performance of rats in the WM task. 4. Mecamylamine at the dose 2.5 and 10 mg/kg clearly impaired the performance of rats in WM task. 5. When the two drugs were co-administered, no interaction between mecamylamine and GVG was observed. 6. Combined nicotinic and muscarinic blockade did not interact as well with GVG administration. 7. Our results do not provide support for any interaction between cholinergic and GABA-ergic mechanisms.

1. Thermoregulatory effector processes were investigated in rabbits after treatment with 1 and 2 micrograms/kg of lipopolysaccharide Escherichia coli (LPS). Both doses produced a fever reaction resulting from stimulation of the metabolic rate and heat conservation responses. 2. BE 2254 administered in feverish rabbits reduced the metabolic as well as pyretic activity produced by both doses of pyrogen. 3. It is suggested that stimulation of the thermoregulatory heat production which contributes to a febrile rise in body temperature is dependent on alpha 1-adrenoceptor mechanisms.

1. NS-398 (N-[2-cyclohexyloxy-4-nitrophenyl] methanesulfonamide) is a new non-steroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic effects. 2. The anti-inflammatory potency of NS-398 in rat carrageenin-induced edema was as potent as that of indomethacin and 8 times more potent than diclofenac. In rat adjuvant arthritis, NS-398 showed a therapeutic effect comparable to that seen with loxoprofen but less than that seen with indomethacin and diclofenac. 3. The analgesic potency of NS-398 in rat adjuvant arthritic pain was much the same as that of indomethacin, and was about 3-5 times higher than that of diclofenac and loxoprofen. In the Randall-Selitto method in rats, NS-398 was 2-7 times as potent as loxoprofen, diclofenac and indomethacin. In acetic acid-induced writhing in mice, NS-398 was equipotent to indomethacin and diclofenac. 4. In LPS-induced fever in rats, NS-398 was 1.5-4.5 times as potent as loxoprofen and indomethacin, but less potent than diclofenac. 5. NS-398 produced little gastric ulceration in doses of up to 1000 mg/kg, while reference drugs produced distinct stomach lesions in doses of 10-30 mg/kg. 6. NS-398 inhibited prostaglandin (PG) endoperoxide synthase from sheep seminal vesicle microsomes less potent than that of ibuprofen.

1. The mean levels of lipid peroxidation products, namely conjugated diene and malonaldehyde, were increased in the soleus muscles of hyperthyroid cats, while the mean glutathione peroxidase activity was decreased. No corresponding similar changes were noted in the fast extensor digitorum longus muscles and serum. 2. Propranolol administration prevented the increase in conjugated diene level in the soleus muscles of hyperthyroid cat but not the malonaldehyde level. It also prevented the reduction in glutathione peroxidase activity in the slow oxidative soleus muscles of hyperthyroid cats. 3. Maximal twitch tension, subtetanic tension and maximum tetanic tension of soleus and EDL muscles were reduced in hyperthyroid cats. Propranolol administration for 5 weeks to hyperthyroid cats did not prevent the reduction in tension of contractions of these muscles. 4. It is suggested that lipid peroxidation might not be responsible for the myopathy in hyperthyroidism and propranolol administration does not improve skeletal muscle function in hyperthyroid animals.

1. Clinical and experimental evidence suggest that changes in the autonomic tone play a role in the pathogenesis of atrial fibrillation. 2. We have studied the distribution of molecular forms of acetylcholinesterase (AChE) in atrial biopsies obtained from individuals without arrhythmias and in patients with atrial fibrillation. 3. Analysis of the distribution of globular and asymmetric AChE forms, showed a decrease in the amount of the globular forms of biopsies taken from atria during fibrillation. 4. This study is the first attempt to characterize the molecular forms of AChE in the human heart of patients with sinus rhythm and chronic atrial fibrillation.

1. [3H]N-[1-(2-Benzo(b)thiophenyl)cyclohexyl]piperidine ([3H]BTCP) labels in vivo the dopamine uptake complex in the mouse striatum. 2. In mice treated with gamma-butyrolactone (GBL, 400 mg/kg), [3H]BTCP specific binding was increased and ID50 values of BTCP and cocaine for the prevention of [3H]BTCP binding were significantly lowered. 3. In GBL-treated mice, cocaine (5 mg/kg, s.c.) had no effect on the BTCP ID50 value, whereas GBR 12783 (2 mg/kg, s.c.) increased it significantly. 4. Thus in vivo, endogenous dopamine and cocaine are competitive and non-competitive inhibitors, respectively, of the binding of [3H]BTCP.