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Biomedical subjects

C L Kaul

Publications and source records attributed to C L Kaul.

At least 55 records · Page 3Linked to original sources
PubMed1993

Comparative pharmacokinetics and amoebicidal activity of metronidazole and satranidazole in the golden hamster, Mesocricetus auratus.

The pharmacokinetic properties of metronidazole and satranidazole were studied in the golden hamster (Mesocricetus auratus), at a dose of 80 mg/kg po. Blood and liver samples were collected at frequent time intervals and assayed for metronidazole and satranidazole by HPLC. Satranidazole exhibited significantly higher plasma concentrations than metronidazole at 1 and 2 h post-dose, but the comparative Cmax values were not significantly different. The satranidazole plasma elimination half-life of 1.01 h was significantly shorter than the corresponding metronidazole half-life of 3.62 h. The comparative liver pharmacokinetic parameters Cmax, Tmax and T1/2 did not differ significantly. Satranidazole however exhibited significantly higher liver concentrations at 1 h post-dose and Cmax and AUC0-infinity values were approximately 35% higher. The in-vivo amoebicidal activity of both compounds was evaluated in the acute hamster hepatic model of amoebiasis. Both metronidazole and satranidazole were administered as single graded doses po, and their dose-response profiles were characterized. Satranidazole demonstrated significantly greater amoebicidal activity than metronidazole with an ED50 value of 19.5 mg/kg, compared to an ED50 value of 45 mg/kg for metronidazole. These data suggest that higher plasma and liver concentrations of satranidazole and greater intrinsic potency probably contribute to superior amoebicidal activity in the hamster model of hepatic infection.

Administration, Oral↗
PubMed1985

Pharmacological profile of 1-methylsulphonyl-3-(1-methyl-5-nitro-2-imidazolyl)-2-imidazolidinone (Go-10213), a new antiprotozoal agent, in comparison with metronidazole.

A new antiprotozoal agent, 1-methylsulphonyl-3-(1-methyl-5-nitro-2-imidazolyl)-2-imidazolidinone (Go-10213) has a distinct advantage over metronidazole when their respective neuropharmacological effects on central and peripheral nervous functions are compared in different animal species. The results show that at equivalent dosage schedules with repeated high dosages, Go-10213 is devoid of adverse central and peripheral neural effects in monkeys; cats and dogs, whereas unequivocal evidence of metronidazole neurotoxicity was obtained in all the three species. Go-10213 compares favourably with metronidazole in animal tests for cardiovascular tolerability.

Animals↗
PubMed1981

On the mechanism of action of an adrenergic blocking guanidine (CG8345-Go).

CG 8345 depletes noradrenaline stores in the rat, cat and dog tissues at a dose range of 1--50 mg/kg p.o. Unlike guanethidine there is no marked difference in the depleting effect of CG 8345 when given orally or intraperitoneally. The effect on the noradrenaline stores is longer lasting in cats and dogs as compared to rat. Like guanethidine CG 8345 releases H3-NA from the rat heart mainly in the form of bases. The compound gets accumulated into the sympathetically innervated organs by a specific uptake process which is similar to noradrenaline "pump" mechanism from where it can be released by reserpine. CG 8345 is stored in the same storage sites as noradrenaline in the rat heart.

Amphetamine↗
PubMed1980

Participation of adrenal medulla in 6-amino-nicotinamide-induced hyperglycaemia in the rat.

In fasted rats 6-aminonicotinamide (6-AN) produced delayed hyperglycaemia, the peak effect being seen by 7 h. Fasting plasma insulin concentrations were not significantly altered but liver glycogen concentrations were decreased following treatment with 6-AN. Adrenalectomy, demedullation and pretreatment with reserpine, phentolamine, nicotinamide and nicotinic acid completely blocked the hyperglycaemic response whereas guanethidine and propranolol or oxprenolol were ineffective. Catecholamine concentrations in the adrenal venous plasma were markedly increased by treatment with 6-AN, the peak effect being seen by 5 h. It is concluded that adrenal medullary release, which is slow in onset, is mainly responsible for the development of sustained hyperglycaemia in the rat.

6-Aminonicotinamide↗
PubMed1980

Increased urinary excretion of catecholamines and their metabolites in streptozotocin diabetic rat.

An attempt has been made to measure changes in the endogenous noradrenaline contents of hearts and brains in rats made diabetic by intravenous administration of streptozotocin. There was no significant change in the endogenous noadrenaline content in the hearts and brains of these diabetic rats. However, all the diabetic animals showed increased excretion of adrenaline, noradrenaline and 3-methoxy-4-hydroxy mandelic acid. This increased excretion was seen as early as 3 days after streptozotocin injections. The rate of disappearance of (3H)-noradrenaline from the heart was significantly higher in these diabetic rats when compared to age-matched controls. It is concluded that there is an increased sympathetic activity in these diabetic animals which is reflected by increased disappearance of (3H)-noradrenaline and increased urinary catecholamine excretion.

Animals↗
PubMed1979

Potentiation of the diabetogenic effect of streptozocin by phentolamine in the rat.

The effect of alpha- and beta-adrenoceptor blocking agents and a beta2-agonist, salbutamol, on the diabetogenic effects of streptozocin (threshold doses) was investigated in the rat. Phentolamine and salbutamol potentiated the diabetogenic effect of streptozocin but phenoxybenzamine, tolazoline, oxprenolol and propranolol were without effect. The potentiating effect of phentolamine was blocked by oxprenolol. Potentiation of the diabetogenic effect by phentolamine is not related to alpha-adrenoceptor block, vasodilatation or insulin release. But it may be related to its ability to stimulate beta-adrenoceptors.

Animals↗
PubMed1978

Hyperglycemic, antihypertensive and antidiuretic properties of Go. 8288 and its comparison with diazoxide.

Hyperglycemic, antihypertensive and antidiuretic activities of Go.8288 and diazoxide were evaluated in the rat. Go.8288 and diazoxide induced hyperglycemia which was blocked by adrenalectomy and demedullation. Pretreatmnet with hydrocortisone completely restored the hyperglycemic effect of diazoxide but only partially that of Go.8288. The hyperglycemic effect of Go.8288 and diazoxide was antagonized by glibenclamide, whereas tolbutamide antagonized only diazoxide-induced hyperglycemia. Pretreatment with oxprenolol antagonized diazoxide-induced hyperglycemia but not that of Go.8288. Guanethidine antagonized the hyperglycemic effect of Go.8288 but not that of diazoxide. Go.8288 and diazoxide markedly inhibited insulin secretion in vivo. Unlike Go.8288, diazoxide further accentuated the hyperglycemic effect in the streptozotocin diabetic rat. Diazoxide significantly increased plasma FFA and plasma renin activity but Go.8288 had no effect. In the normotensive cats and dogs and renal hypertensive rats both compounds lowered arterial blood pressure. Unlike diazoxide, Go.8288 was active orally in normotensive dogs. Similar to diazoxide Go.8288 showed an antidiuretic effect in the rat. It is therefore concluded that despite some similarities, Go.8288 shows important differences in its biological profile from that of diazoxide.

Amidines↗
PubMed1978

Effects of glucose and some oral hypoglycemic agents upon the plasma glucose and immuno-reactive insulin (IRI) in normal and streptozotocin induced diabetic rat.

An investigation has been made to see the effect of oral hypoglycemic agants on the blood sugar (BS) and plasma Immuno-Reactive Insulin (IRI) in normal and streptozotocin diabetic rats. Plasma IRI was significantly reduced in a streptozotocin treated diabetic rat 8 weeks after streptozotocin injection. In normal rats oral administration of Sodium tolbutamide (TOL) and Glybenclamide (GLI) produced a significant fall in BS and a concurrent increase in plasma IRI, but phenformin (PHE) was without any effect on both these parameters. Unlike normal rats streptozotocin treated diabetic rats did not show lowering of BS and increase in plasma IRI following TOL and GLI. PHE, however, did produce a significant fall in BS. Oral glucose load did show a typical glucose tolerance curve and insulin release in normal rats. However, in the diabetic rats there was no significant increase in plasma IRI following glucose load. It is therefore concluded that streptozotocin treated diabetic rats differ from the maturity onset diabetic as regards the responses of TOL and GLI are concerned and this animal model can therefore be useful in differentiating the two types of oral hypoglycemic agents.

Animals↗
PubMed1977

Synthesis and antitussive activity of 3-azabicyclo[3.2.2]nonane derivatives.

Mannich bases derived from a number of substituted acetophenones and propiophenones and 3-azabicyclo[3.2.2]nonane have been evaluated for antitussive activity. One of these compounds was as potent as codeine and dextromethorphan in its antitussive activity. The most potent compound of the series, 3-(3-azabicyclo[2.2.2]nonan-3-yl)-4'-benzyloxy-2-methyl propiophenone, also exhibited antimorphine activity. There was no direct correlation between the antitussive effect and antimorphine activity.

Animals↗