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Biomedical subjects

Y K Gupta

Publications and source records attributed to Y K Gupta.

At least 73 records · Page 4Linked to original sources
PubMed1998

Development of neurogenic pulmonary edema at different grades of intracranial pressure in cats.

Development of neurogenic pulmonary edema (NPE) subsequent to increased intracranial pressure (ICP) was evaluated in an experimental model in cats. Experiments were conducted in chloralose anaesthetised animals, either on spontaneous respiration or on intermittent positive pressure ventilation. Hemodynamic parameters i.e., mean arterial pressure (MAP) and heart rate (HR) were continuously monitored. Pulmonary artery/right ventricular systolic pressure was recorded in cats on spontaneous respiration. Increase in ICP for 180 minutes caused an increase in extravascular lung water (EVLW) content in both spontaneously breathing and artificially ventilated animals. In spontaneously breathing animals EVLW to blood free dry weight ratio (EVLW/BFDW) was 3.95 +/- 0.16 and 4.96 +/- 0.16 at ICP 40 and 80 mm Hg respectively while in animals on artificial ventilation, at 40, 60, 80 and 100 mm Hg ICP, it was 3.88 +/- 0.11, 4.09 +/- 0.10, 4.50 +/- 0.13 and 5.03 +/- 0.17 respectively. These values were significantly greater (P < 0.05) as compared to that in sham operated animals (3.43 +/- 0.10). This was accompanied by rise in MAP, HR and pulmonary artery pressure. The study establishes the graded development of NPE, the severity of which is proportional to the levels of ICP.

Animals↗
PubMed1997

Antiemetic efficacy of ginger (Zingiber officinale) against cisplatin-induced emesis in dogs.

Effect of ginger (Zingiber officinale Roscoe, Zingiberaceae) extracts (acetone, 50% ethanolic and aqueous) were investigated for antiemetic activity against emesis induced by 3 mg/kg cisplatin (the 100% emetic dose i.v.) in-healthy mongrel dogs. The acetone and 50% ethanolic extract at the doses of 25, 50, 100 and 200 mg/kg p.o. exhibited significant protection while aqueous extract at these doses was ineffective against cisplatin emesis. The acetone extract was more effective than ethanolic extract. However, both were less effective when compared to 5-HT3 receptors antagonist-granisetron. Neither of the ginger extract was effective against apomorphine-induced emesis. The findings suggest that ginger could be an effective and cheap antiemetic adjunct to cancer chemotherapy.

Animals↗
PubMed1997

Effect of adenosine receptor modulation on pentylenetetrazole-induced seizures in rats.

1. The effects of adenosine, the adenosine analogue, 2-chloroadenosine (2-CADO), the specific adenosine A1 receptor agonist, N6-cyclopentyladenosine (CPA) and A2 receptor agonist 5'-(N-cyclopropyl) carboxamidoadenosine (CPCA), were examined against seizures induced by acute administration of pentylenetetrazole (PTZ), 60 mg kg-1, and PTZ kindled seizures, in rats. 2. Adenosine 1000 mg kg-1, i.p., 5 min pretreatment and CPA 10 mg kg-1 i.p., 60 min pretreatment, showed significant protection against acute PTZ-induced seizures while, CPCA up to 10 mg kg-1 was ineffective. The adenosine analogue 2-CADO in a dose of 5 mg kg-1 was only partially protective and on increasing the dose to 10 mg kg-1, this protection was lost. 3. Theophylline, a non specific adenosine receptor antagonist at 50 mg kg-1 and the specific adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), at 1 mg kg-1, if administered before the maximally protective doses of adenosine and CPA, completely reversed the protection afforded by them against PTZ seizures. While, pretreatment with the adenosine A2 receptor antagonist, 3,7-dimethyl-1-propargylxanthine (DMPX), failed to reverse the protection. 4. Adenosine and the adenosine A1 receptor agonist in doses that protected against seizures after acute PTZ administration, offered only incomplete protection when tested against PTZ kindled seizures. 5. The effects of adenosine and adenosine receptor agonists on mean arterial pressure, heart rate and rectal temperature were studied, to rule out the possibility of their systemic effects mediating the protection of PTZ seizures. All these agents produced a fall in mean arterial pressure, heart rate and hypothermia in the doses exhibiting an anticonvulsant response. While the effect on blood pressure and heart rate was immediate i.e. seen within 5 min and, maintained throughout the observation period, the development of hypothermia lagged behind the onset of hypotension and bradycardia. However, there was no correlation between haemodynamic and hypothermic response and the anticonvulsant effect. 6. The results indicate that the adenosine mediated anticonvulsant effect is via stimulation of A1 receptors. Hypotension and hypothermia do not appear to contribute to the protection observed with adenosine and the adenosine A1 receptor agonists.

Adenosine↗
PubMed1997

Effect of theophylline on diazepam and sodium valproate protection in pentylenetetrazole - kindled seizures in rats.

Theophylline is well known for its convulsant and proconvulsant action. Some experimental studies also suggest that theophylline and other methylxanthines may impair the protection of antiepileptic drugs. The interaction of theophylline and the antiepileptic drugs diazepam and sodium valproate was studied in pentylenetetrazole (PTZ) - kindled seizures in rats. Pretreatment with both diazepam 4 mg/kg and sodium valproate 300 mg/kg, i.p., showed protection against PTZ kindled seizures. Theophylline, 50 mg/kg, i.p., when given before the antiepileptic drugs, failed to reverse their protection. Since theophylline has an adenosine receptor antagonist activity which may be responsible for its convulsant potential, the results indicate non-involvement of adenosinergic mechanisms in the mechanisms of actions of these antiepileptic drugs.

Animals↗
PubMed1997

Adenosinergic system as an endogenous anticonvulsant mechanism.

The treatment of epilepsies remains far from adequate primarily due to inadequate understanding of the pathophysiology of seizures. The conventional approach for research into epilepsy has been study of factors responsible for initiation of seizures. However, now attention is being drawn to the spontaneous and abrupt arrest of seizures which suggests a distinct possibility of activation of an endogenous anticonvulsant mechanism(s), which may be targeted in future for controlling seizures. Of the various endogenous anticonvulsant mechanisms, the concept of an endogenous anticonvulsant substance has gained much experimental support and, many potential candidates have been postulated. Of these adenosinergic system appears to be the most promising. This review discusses the possible role of adenosinergic system in seizures, in relation to the available antiepileptic drugs and its therapeutic implications.

Adenosine↗
PubMed1996

An experimental model to study intracranial hypertension-induced vomiting in conscious dogs.

An experimental model to study vomiting due to acute increases in intracranial pressure (ICP) was standardized in dogs. Chronic lateral cerebral ventricle cannulated animals were partially restrained in an observation chamber. The cannula was connected to a buffered saline pressure head which could be adjusted to the required height with the help of a pulley system to attain the desired intracranial pressure. In separate sets of experiments the ICP was raised and maintained at 20, 40, 60 and 80 mmHg for 30 min. The incidence of vomiting and/or retching was observed and the vomiting/retching score (V/R score) was calculated to quantify the severity. The V/R score increased with the level of ICP, maximum being at ICP 80 mmHg. At this level, the effect of pretreatment with propranolol, prazosin and ondansetron was studied. Prazosin and propranolol treatment reduced the vomiting/retching score, while ondansetron failed to do so. This model can be used for evaluating therapeutic interventions for elevated ICP-induced vomiting.

Adrenergic alpha-Antagonists↗
PubMed1993

Recovery from reperfusion injury in intact canine heart by nifedipine.

Effect of nifedipine post-treatment (100 micrograms/kg slow bolus followed by 3 micrograms/kg/min infusion) on the functional and metabolic changes of the heart after a brief regional ischemia (I) (20 min.) followed by 1 hr of reperfusion (R) was studied in pentobarbitone-anaesthetized open-chest coronary ligated dogs. In the control group, 1 hr of reperfusion failed to cause any significant recovery of the depressed LVdP/dtmax and that of the elevated LVEDP (LVdP/dtmax, pre-ischemic: 2720 +/- 90 mm Hg/sec., 20 min. of I: 2410 +/- 120 mm Hg/sec and 60 min. of R: 2210 +/- 130 mm Hg/sec. LVEDP, pre-ischemic: 5.25 +/- 0.2 mm Hg, 20 min. of I: 10.5 +/- 0.9 mm Hg and 60 min. of R: 7.5 +/- 0.5 mm Hg). However, 1 hr of reperfusion caused a significant recovery of ischemia-induced depletion of myocardial creatine phosphate (CP) content only, but not that of ATP. On post-treatment with nifedipine (i.e., infusion started just before reperfusion), there was a significant recovery in LVEDP (8.25 +/- 0.6 mm Hg after 20 min. of ischemia to 5.0 +/- 0.4 mm Hg after 1 hr of reperfusion) and there was no further deterioration in LVdP/dtmax, as observed in untreated dogs. More significantly, nifedipine caused a near normal recovery of both ATP and CP contents of the affected myocardium. Therefore, the present study shows that post-ischemic administration of nifedipine prevented reperfusion injury of the ischemic myocardium, as evidenced by both functional and metabolic recovery.

Adenosine Triphosphate↗
PubMed1993

Effect of verapamil post-treatment in myocardial reperfusion injury.

Effect of verapamil post-treatment (0.2 mg/kg bolus, followed by 0.01 mg/kg/min infusion) on the functional and metabolic changes of the heart after a brief regional ischemia (20 min) followed by 1 hr of reperfusion was studied in open-chest pentobarbitone anaesthetized dogs. In control dogs 1 hr of reperfusion failed to cause any improvement of depressed myocardial contractility (LVdP/dtmax and LVEDP) caused by 20 min of ischemia, which confirmed the earlier reported phenomenon of 'Stunned Myocardium'. Myocardial ischemia caused a significant loss of high-energy phosphate (HEP) content of the affected myocardium (ATP decreased by 60% and CP decreased by 75% of non-ischemic level). Following 1 hr of reperfusion, myocardial ATP was not replenished, though creatine phosphate became near normal. When verapamil was administered just before reperfusion, it showed a profound beneficial effect on the incidence of fatal reperfusion arrhythmias. At the end of 1 hr of reperfusion in this group, the recovery of the myocardial contractility was incomplete, but a significant replenishment of the myocardial HEP content was observed. Thus verapamil post-treatment can prevent reperfusion-induced myocardial injury but functional recovery may be delayed due to the drug's inherent direct myocardial depressant effect.

Adenosine Triphosphate↗
PubMed1991

Modulation of morphine induced antinociception by intracerebroventricularly administered captopril.

Captopril when administered intracerebroventricularly (icv) in doses of 100, 300, 500 and 1000 micrograms induced a dose dependent antinociceptive effect in rats. Naloxone pretreatment (10 mg/kg, ip) completely antagonised antinociceptive effect of captopril, suggesting thereby the involvement of brain enkephalinergic system. Captopril 300 micrograms, icv potentiated the antinociceptive effect of morphine in intact animals. The bilateral adrenalectomy did not have any effect on this potentiation as against the reported blockade of potentiation in adrenalectomized animals when captopril was administered by systemic route. Thus potentiation of morphine induced antinociception by icv captopril is unlikely to be exerted through an effect on adrenal function and is most likely due to increased brain enkephalin levels.

Analgesics↗
PubMed1989

Opposing effect of apomorphine on antinociceptive activity of morphine: a dose-dependent phenomenon.

Apomorphine, when administered intracerebroventricularly (0.05 mg/kg) to rats, increased tail-flick latency (a spinal nociceptive response). However, intraperitoneal administration at doses of 1, 3 and 10 mg/kg had no effect, probably because of a tonic supraspinal inhibitory influence on spinal dopaminergic neurones involved in segmental nociceptive processes. Depending on the doses administered, intraperitoneal administration of apomorphine exhibited opposite effects on antinociceptive activity of morphine. Pretreatment with a low dose of apomorphine (1 mg/kg) attenuated, whereas, a high dose (10 mg/kg) potentiated morphine-induced antinociception. Dopamine antagonists, in doses that preferentially block autoreceptors, i.e., haloperidol (0.1 mg/kg, i.p.) and (-)-sulpiride (5 mg/kg, i.p.), antagonised the attenuation of morphine antinociception by a low dose of apomorphine, while treatment with a high dose of haloperidol (1 mg/kg, i.p.) and pimozide (1.25 mg/kg, i.p.) completely antagonised the potentiating effect of a high dose of apomorphine on the antinociceptive activity of morphine. The attenuation of morphine antinociception thus appears to be due to decreased dopaminergic activity as a result of preferential dopamine autoreceptor stimulation by a low dose of apomorphine, whereas potentiation with a high dose of apomorphine is caused by enhanced dopaminergic activity via postsynaptic receptor stimulation.

Animals↗
PubMed1989

Effect of intracerebroventricular administration of angiotensin II on emetic reflex in dogs.

Area postrema is rich in angiotensin II receptors and intravenous (iv) administration of angiotensin II has been reported to elicit emesis. However, in the present study intracerebroventricular (icv) administration of angiotensin II up to a dose of 10 micrograms failed to elicit emesis. It is suggested that presence of a cerebrospinal fluid-brain barrier in area postrema most probably prevents access of icv angiotensin II to its receptors which are otherwise accessible on iv administration.

Angiotensin II↗
PubMed1989

Role of endogenous opioids and histamine in morphine induced emesis.

The role of opioid and histaminergic system in morphine induced emesis was investigated in dogs. Morphine (25 micrograms, icv) consistently evoked emesis with an average latency of 195 +/- 29 sec which was fully accounted for by an action on the chemoreceptor trigger zone (CTZ) as its ablation rendered animals refractory to vomiting. Intraventricular pretreatment with opioid antagonist naloxone, histamine H1 antagonist mepyramine and H2 antagonists metiamide and cimetidine afforded protection to icv morphine emesis. The CSF histamine concentration was significantly raised 5 min after icv morphine administration. The results suggest that both endogenous opioid and histamine are involved in morphine emesis. Naloxone in high doses (1600 micrograms, icv) elicited emesis which was not blocked by CTZ ablation confirming our earlier report.

Animals↗