Prevention of oculocardiac reflex (O.C.R) during extraocular muscle surgery.

In the present study the effectiveness of intravenous atropine sulphate which blocks the peripheral muscarinic receptors at the heart and retrobulbar xylocaine hydrochloride which blocks the conduction at ciliary ganglion on the afferent limb of OCR was studied during strabismus surgery. The study was conducted on fifty three patients of either sex having squint of more than ten years duration. The patients were randomly allocated into four groups. No preanaesthetic medication with atropine or retrobulbar block with xylocaine was given in control group of patients. In the second group, only preanaesthetic medication with atropine was given; while in the third group only retrobulbar injection of xylocaine was given five minutes before operation. In the last group both atropine as preanaesthetic medication and xylocaine as retrobulbar block were given. The electrocardiographic recordings were taken before and throughout the operative procedure. It was interesting to note that in the group where atropine and xylocaine were used none of the patients exhibited activation of OCR. Results have been discussed.

Effect of metoclopramide on gastric ulceration and secretion in albino rats.

The antiulcer and antisecretory effects of metoclopramide were studied in aspirin-induced and pylorus-ligated gastric ulcers. The effects were compared with ranitidine (10 mg/kg, orally). The effect of propantheline alone and in combination with metoclopramide was studied against aspirin-induced gastric ulcers only. Metoclopramide (20 mg and 50 mg/kg) produced an ulcer protective effect both in aspirin-induced and pylorus-ligated experimental models. Its ulcer protective effect against aspirin-induced and pylorus-ligated gastric ulcers was comparable to ranitidine. Metoclopramide reduced the volume of gastric secretion but did not alter the total acidity; however, significant reduction in free acidity was noted. The ulcer protective effect of metoclopramide appeared to have multiple mechanisms like reduction in gastric secretion and free acidity, increased gastric emptying and cytoprotective action.

Evidence for the presence of osmoreceptors in medulla of the dog.

Hypertonic solutions of different substances were injected into the vertebral artery of dogs anesthetized with chloralose, preventing their access to the hypothalamic osmoreceptors by ligating the basilar artery and both the external carotid arteries. The hypertonic solution of sodium chloride produced graded inhibition of water diuresis and a concomitant rise in plasma antidiuretic hormone (ADH) level; hypertonic solution of glucose produced lesser effect. Hypertonic urea solution, on the other hand, did not alter the course of water diuresis. It was concluded that osmoreceptors are also present in the medulla which sense the changes in blood osmolarity and accordingly modify the ADH release.

Effect of garlic pretreatment on isoprenaline-induced myocardial necrosis in albino rats.

Albino rats were pretreated orally for seven days with different doses of the essential oil and juice of garlic. These animals were challenged with isoprenaline (85 mg/kg, s.c.) on day six and seven to induce myocardial necrosis. The same rats were also subjected to swimming test before and after forty eight hr of first injection of isoprenaline. Pretreatment with essential oil (2.0 and 4.0 mg/kg) and juice (2.0 and 4.0 ml/kg) significantly protected the myocardium from isoprenaline-induced necrosis. These animals also exhibited better swimming performance. In separate group of animals, pretreatment with garlic juice (4.0 ml/kg) or essential oil (4.0 mg/kg) improved the chances of survival in isoprenaline-challenged animals.

A simple gravimetric method for estimation of plasma fibrinogen.

The study was undertaken to evaluate a new method of estimating plasma fibrinogen levels, gravimetrically using calcium chloride in albino rats. The results were compared with the standard method in which thrombin was used as clotting agent and were found to be statistically not significant. Advantages of using calcium chloride instead of thrombin have been discussed.

Some clinical pharmacological studies with terfenadine, a new antihistamine drug.

1 A double-blind cross-over trial between placebo, chlorpheniramine, and terfenadine, a new antihistamine drug, was performed in healthy male volunteers to determine and compare their CNS and autonomic effects. 2 Terfenadine and chlorpheniramine were administered orally in therapeutic doses. 3 In objective tests of critical flicker frequency, pursuit rotor, reaction time, salivary volume and pupillary diameter, no statistically significant difference was observed between the treatments. 4 On analogue rating scales, chlorpheniramine produced a statistically significant (P less than 0.05) degree of sedation and impaired concentration as compared to placebo and terfenadine. 5 The results obtained in analogue rating scales were not normally distributed and, therefore, use of non-parametric statistical methods for analysis of such data is strongly advocated.

Central mechanism of vasopressin-induced changes in antidiuretic hormone release.

1. Intracerebroventricularly (i.c.v.) administered vasopressin (0.001-1.0 u) in dogs anaesthetized with chloralose produced adose-dependent increase in urine flow with a concomitant decrease in the levels of antidiuretic hormone (ADH) in jugular vein blood. 2. Higher doses of vasopressin (1.5-2.0 u, i.c.v) on the other hand had an antidiuretic effect and produced an increase in blood ADH level. 3. Pretreatment (i.c.v.) with a beta-adrenoceptor antagonist completely blocked the diuretic response of low doses of vasopressin (i.c.v.) but did not influence the antidiuretic response obtained with high doses. 4. Repeated administration of vasopressin (1.0 u, i.c.v.) induced tachyphylaxis; central catecholamine depletion with tetrabenazine significantly inhibited the vasopressin-induced diuretic response. 5. It is concluded that intracerebroventricular vasopressin-induced changes in ADH secretion are mediated through the release of catecholamines in the central nervous system.

Mechanism of histamine-induced antidiuretic response.

1. In dogs anaesthetized with alpha-chloralose, intracerebroventricular (i.c.v.) injection of histamine induced antidiuresis and increase in jugular vein blood antidiuretic hormone (ADH) level but no change in urinary electrolytes. The mechanism of the histamine-induced antidiuretic response was analysed by the use of pharmacological agents.2. Histamine (i.c.v.) in 1-20 mug doses produced a variable effect on urine outflow as well as on the blood ADH concentration; however, higher doses (25-500 mug) of histamine elicited a dose-dependent antidiuretic response with concomitant rise in blood ADH titre.3. Repeated administration of high doses of i.c.v. histamine (400 mug) elicited a diminishing antidiuretic response which was not observable after the fourth dose, thus exhibiting tachyphylaxis. The antidiuretic response to histamine could be restored by central administration of noradrenaline (500 mug).4. Central pretreatment with mepyramine (5 mg) prevented the histamine-induced antidiuresis. Atropine (2 mg i.c.v.) was ineffective in blocking the antidiuretic effect of histamine. A diuretic response to histamine (400 mug i.c.v.) was obtained in phenoxybenzamine (i.c.v.) pretreated animals; this response could be blocked by i.c.v. injection of propranolol. Tetrabenazine pretreatment prevented the antidiuretic response to histamine.5. The results of the study lead us to conclude that histamine releases central catecholamines which activate the central adrenergic mechanism for the release of antidiuretic hormone.