Usha Nayar

The formalin test: A tonic pain model in the primate

&NA; The formalin test has been used in monkeys for assessing pain. After formalin injection in the palmar surface of the hand just proximal to the base of the fingers, the monkeys responses are rated for 1 h according to objective behavioral criteria. The present ‘tonic’ pain model has a fair degree of objectivity, validity, reproducibility and quantifiability. The analgesic effects of morphine and pethidine have been evaluated.

Modulation of glycemic response by protein, fat and dietary fibre

Abstract Five healthy young male volunteers were given isocaloric meals composed of glucose alone or in combination with protein, fat, or dietary fiber. Glycemic response was blunted in case of all mixed meals, the glucose level at 2.0 h and the area under the 2-h glucose curve being significantly lower (p

Interaction of ouabain and propranolol in the central nervous system. Neurally-mediated effects on the cardiovascular system.

The effect of intracerebroventricular (i.c.v.) ouabain alone and after pretreatment with i.c.v. (+/-)-propranolol, (+)-propranolol, UM-272 (a quaternary analogue of propranolol) and lignocaine, on arterial blood pressure (BP), heart rate (HR) and cardiac rhythm was investigated in chloralose anesthetized, vagotomized cats. Ouabain elicited an increase in BP and HR followed by cardiac arrhythmias of ventricular origin. Pretreatment with (+/-)-propranolol, (+)-propranolol or UM-272 attenuated/prevented the cardiovascular effects of ouabain whereas lignocaine did not modify the response appreciably. Since UM-272, which lacks local anesthetic activity and beta-blocking activity also shared the antagonism with (+/-)-and (+)-propranolol, it is deduced that neither beta-blocking nor local anesthetic activity of propranolol could be responsible for this antagonism. This is supported by the fact that lignocaine which has a comparable local anesthetic effect of propranolol failed to modify significantly the cardiovascular response to ouabain. The antagonism appears to be a direct neural depressant effect independent of local anesthetic action. The neural depressant effect may be due to an interference in depolarization process and/or a neurone-blocking effect.

Effect of Fenfluramine on the single neuron activities of the hypothalamic feeding centers

Electrical activity of single neurons of the hypothalamic satiety and feeding centers and other adjacent areas was recorded by means of stereotaxically guided steel microelectrodes, before and after Fenfluramine infusion in doses of 1.5 mg/kg body wt. In addition arterial and venous blood glucose estimations were carried out to assess the levels of glucose utilization. The spike frequency of satiety center units increased while that of feeding center units decreased, in response to Fenfluramine while other hypothalamic units did not show any changes. The A-V glucose differences also increased showing increased level of glucose utilization. The significance of these findings in explaining the effects of Fenfluramine in depressing appetite have been discussed.

Antiarrhythmic effects of prostaglandins E2 and I2 on ouabain-induced cardiac arrhythmias in cats: Effect of vagotomy and adrenergic neuron blockade

The effects of i.v. prostaglandins (PGs) E2 and I2 on ouabain-induced cardiac arrhythmias were investigated in chloralose-anaesthetized cats. Bilateral vagotomy and guanethidine-pretreatment interventions were employed to elucidate the involvement of vagal and sympathetic neural influences in these effects. PGE2 (1 micrograms/kg/min i.v. infusion for 5 min) and PGI2 (4-16 microgram/kg i.v. bolus injections) effectively suppressed the ouabain-induced arrhythmias in a control group of cats. The bilateral vagotomy or guanethidine-pretreatment interventions did not significantly alter the antiarrhythmic effects of PGE2 and PGI2. It is concluded that the presence of functionally intact sympathetic and vagal nerve supply to the heart is not a prerequisite for the antiarrhythmic effects of i.v. administered PGE2 and PGI2. The possible role of direct action of these PGs on the myocardium is discussed.

Ontogeny of Hypothalamic Glucostatic Feeding Mechanisms in Developing Rats

Development of glucose sensitivity of hypothalamic feeding centers (LH and VMN) has been studied by recording the change in their electrical activity in response to a glucose challenge in rats of different age groups. Glucoresponse of LH in 13-15 day rats was significantly increased (unlike adults) in high-voltage (H) activity; in 20-23 day rats the response was significantly decreased (like adults). In 13-15 day rats there was some increase in H activity, which further increased in 20-23 day rats. The effects lasted for about an hour. It is concluded that the immature LH responds differently than the mature LH, and that the glucostatic mechanism matures around the weaning period.

The vagal involvement in the antiarrhythmic and arrhythmogenic effects of prostaglandin F2α on ouabain-induced cardiac arrhythmias in cats

The effects of prostaglandin F2 alpha (PGF2 alpha) on ouabain-induced cardiac arrhythmias were investigated in chloralose-anaesthetized cats. Bilateral vagotomy and atropine intervention were employed to elucidate the involvement of vagal neural influences. PGF2 alpha (2-16 micrograms/kg i.v. bolus) predominantly suppressed the ouabain-induced ventricular and supraventricular arrhythmias and less commonly aggravated them in vagi-intact cats. The antiarrhythmic effect of PGF2 alpha was considerably, but not statistically significantly, decreased while its arrhythmogenic effect was significantly (p less than 0.05) increased in atropine-pretreated group. In vagotomised group PGF2 alpha failed to abolish the arrhythmias but it aggravated them to a degree comparable to that observed in vagi-intact group. It is concluded that the PGF2 alpha exhibits both antiarrhythmic and arrhythmogenic properties and these are largely due to elicitation of two opposing neural reflexes - one being protective and another being deleterious to ouabain-induced arrhythmias.

Neurally induced digitalis arrhythmias and the adrenoceptors

Abstract Intracerebroventricular (i.c.v.) administration of ouabain to chloralose-anesthetized, vagotomized cats elicited a dose-related increase in blood pressure and heart rate followed by ventricular arrhythmias; these effects were attributable to a sympathoadrenal discharge triggered fromthe centeral nerouv system. In presence of an effective vascular α-blockade with an i.v. α-blocker, the vasopressor response to i.c.v. ouabain was reverse toa vasodepressor one; this is reminiscent of the ‘vasomotor reversal phenomenon of Dale’. On the other hand, in the presence of an effective β-blockade with an i.v. β-blocker the vasopressor response was augmented. The vascular response to i.lc.v. oubain is thus the net effect mediated by both α- and β-2-receptors and the blockade of one unmasks the other. The pre-existing α-blockade prevented the appearance of arrhythmias after i.c.v. auabain. This may have been due to the ability of the α-blocker to prevent the rise in BP, however, a direct antiarrhythmic effect on the heart may also have been involved. The pre-existing β-blockade failed to significantly affect the tachycardia and the incidence of arrhythmias. This suggests that adrenergic neurogenic arrhythmias differ from the arrhythmias induced by exogenously administered catecholamines, since the latter are completely antagonized by β-blockers wehreas the former and less readily antagonized. Further, the ability of a β-blocker to inhibit the isoprenaline-induced tachycardia (as a test of β-blockade) may not accurately reflect the ability to antagonized the cardiac effects evoked by a strong and diffused sympathetic stimulation. Futhermore, it appears that the blockade of cardiac β-receptors is not equivalent to surgical sympathetic denervation of the heart and that the arrhythmogenic stimuli originating in the central nervous system may travel to the heart through pathways resistant to conventionally employed antagonists such as β-blockers.

The lack of involvement of central nervous system in the antiarrhythmic effects of prostaglandins E2, F2α, and I2 in cat

The role of the central nervous system (CNS) in the antiarrhythmic effects of prostaglandins (PGs) E2, F2 alpha, and I2 was studied by administering each agent into the left lateral cerebral ventricle (i.c.v. administration) of chloralose-anaesthetized cats. The cardiac arrhythmias were produced by intravenous (i.v.) infusion of ouabain (1 microgram/kg/min). The PGs E2, F2 alpha and I2 on i.c.v. administration in the dose range of 1 ng to 10 micrograms failed to inhibit ouabain-induced cardiac arrhythmias. However, when infused i.v., PGE2 (1 microgram/kg/min), PGF2 alpha (5 micrograms/kg/min), and PGI2 (2 micrograms/kg/min) effectively suppressed these arrhythmias. The standard antiarrhythmic drug propranolol (0.5-8.0 mg) on i.c.v. administration also significantly reduced the ouabain-induced cardiac arrhythmias. It is suggested that the CNS is not the site of action of PGs E2, F2 alpha, and I2 in antagonising the ouabain-induced cardiotoxicity in cats.

Behavioral scoring using programmable calculators: A technique usable in the field

A simple method of recording the time spent in various behavioral categories during behavioral scoring is described. Use is made of a programmable calculator which is made to function as a multiple timer, keeping track of each of the categories. Any number of mutually exclusive categories can be scored using a single key press, by assigning a pre-set code to each. A print-out of the analysed frequency or duration data can be obtained either concurrently or at any time after the experiment, as required. The least count of the technique is about 1-2 seconds and this precludes its use for extremely rapidly changing behaviors. Apart from this, it is convenient, time-saving and especially suitable for field use.