Evaluation of antiallergic activity (type I hypersensitivity) of Inula racemosa in rats.

Alcoholic extract of root of Inula racemosa, was studied for its antiallergic effect in experimental models of type I hypersensitivity, viz. egg albumin induced passive cutaneous anaphylaxis (PCA) and mast cell degranulation in albino rats. The alcoholic extract was prepared by the process of continuous heat extraction. LD50 of this extract was found to be 2100 +/- 60 mg/kg, i.p. Assessment of protection against egg albumin induced passive cutaneous anaphylaxix by different doses of Inula racemosa was done by giving drug intraperitoneally or orally for seven days or once only. Mast cell degranulation studies were done by using compound 48/80 as degranulation agent with same dosage schedule. Inula racemosa (i.p. as well as p.o.) showed significant protection against egg albumin induced PCA. Protection against compound 48/80 induced mast cell degranulation by alcoholic extract of Inula racemosa (single dose) was similar to that of disodium cromoglycate. The seven days drug treatment schedule showed greater protection than disodium cromoglycate intraperitoneally. The results suggest that Inula racemosa possesses potent antiallergic properties in rats.

Role of dopaminergic system in opioid-induced cardiovascular responses in dogs.

A study was carried out to determine the involvement of dopaminergic system in opioid-induced cardiovascular responses in the dogs. The study population consisted of 32 mongrel dogs of either sexes. The results show that morphine given in small dose (2 mg/kg I.V.) causes significant fall in blood pressure. The results also show that there is involvement of dopaminergic system in opioid-induced vasomotor responses in dogs. Partial blockade of the parenterally induced hypotensive response of morphine by haloperidol given centrally induced hypotensive responses of morphine by haloperidol given centrally in doses, which are too low to be effective by the peripheral route, strongly favours the involvement of central dopaminergic system in the morphine-induced hypotensive responses. The results also show that the hypotensive response of morphine was almost completely blocked after naloxone pretreatment by central route.

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.

Central histaminoceptor-adrenoceptor interrelations in the release of adrenocorticotrophic hormone.

Intracerebroventricular administration of adrenaline, noradrenaline phenylephrine, clonidine and histamine produced a significant rise in plasma cortisol concentration whereas isoprenaline had no effect. alpha-Adrenoceptor blockers (yohimbine or piperoxon) per se did not alter the plasma cortisol level. Central pretreatment with yohimbine or piperoxin, blocked the rise in plasma cortisol level induced by icv noradrenaline, phenylephrine and clonidine. In another set of experiments, both H1 and H2 receptor antagonists (mepyramine, and metiamide) per se had not significant effect on plasma cortisol concentration. Central histamine induced rise in plasma cortisol concentration was significantly blocked by icv pretreatment with both H1 and H2 receptor blockers. Furthermore, yohimbine also significantly prevented the rise of plasma cortisol level induced by icv histamine.