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Biomedical subjects

L Finch

Publications and source records attributed to L Finch.

At least 73 records · Page 4Linked to original sources
PubMed1973

A comparison of the effects of chemical sympathectomy by 6-hydroxydopamine in newborn and adult rats.

1. The effects of chemical sympathectomy with 6-hydroxydopamine (6-OHDA) on the cardiovascular system of the rat were compared in, (a) 10-week-old rats treated during the first 14 days after birth with 150 mug/g subcutaneously, and (b) adult rats injected intravenously with 2 x 50 mg/kg on day 1 and 2 x 100 mg/kg on day 7 and the experiments performed on day 8.2. Intravenous administration of 6-OHDA to adult rats almost completely abolished the pressor responses to stimulation of the entire sympathetic outflow in the pithed rat, the contractions of the lower eyelid to stimulation of the cervical sympathetic trunk and the vasconstrictor responses produced by periarterial nerve stimulation of the isolated renal artery preparation. Pressor responses to physostigmine and to tyramine were markedly reduced or abolished in anaesthetized and pithed rat preparations, respectively.3. In corresponding experiments, 10-week-old rats treated as newborns with 6-OHDA showed a marked reduction in the stimulation-induced pressor responses and contractions of the lower eyelid, but completely normal vasoconstrictor responses to periarterial nerve stimulation of the isolated perfused renal artery were obtained. The pressor responses to physostigmine were slightly reduced but the tyramine responses were unchanged.4. Treatment with 6-OHDA at birth caused an almost complete and long-lasting noradrenaline depletion in the heart, spleen, salivary glands and ileum but only a partial depletion in the mesentery from 10-week-old rats. These low noradrenaline levels showed no recovery in rats up to an age of 4 months. The tyrosine hydroxylase activity in both the cervical and stellate ganglia from 10-week-old rats was markedly reduced by treatment with 6-OHDA after birth.5. Injections of 6-OHDA after birth produce an almost complete and permanent sympathectomy of various adrenergically innervated organs in the rat. The vascular system represents a major exception, exhibiting a surprisingly high resistance to this type of chemical adrenergic denervation.

Age Factors↗
PubMed1971

Cardiovascular reactivity in the experimental hypertensive rat.

1. In pithed preparations, deoxycorticosterone (DOCA)/NaCl-induced hypertensive rats showed increased cardiovascular reactivity to injected noradrenaline, DMPP, tyramine, angiotensin and to sympathetic nerve stimulation.2. Pithed, chronic renal hypertensive rats showed similar hyperreactivity to noradrenaline, DMPP and tyramine but responses to sympathetic nerve stimulation were within normal limits.3. In the isolated, Krebs perfused mesentery preparation, vessels obtained from both DOCA/NaCl and renal hypertensive rats showed hyperreactivity to injected noradrenaline. Responses to periarterial nerve stimulation were also markedly increased in preparations from DOCA/NaCl hypertensive rats, while preparations from renal hypertensive rats showed this effect only at higher rates of stimulation (12 and 25 Hz).

Angiotensin II↗
PubMed1970

The contribution of the sympathetic nervous system to the development and maintenance of experimental hypertension in the rat.

1. Experimental hypertension in the rat, induced either by renal artery stenosis or by treatment with deoxycorticosterone acetate (DCA) developed maximally over a period of 8 weeks. In both types of hypertension the rate of development was unaffected by immunosympathectomy or by chemical sympathectomy following the administration of 6-hydroxydopamine.2. The effect of 6-hydroxydopamine on chronic renal hypertensive rats was to produce a hypotensive action of longer duration than when similarly administered to DCA-induced hypertensive or normotensive rats. Reserpine (5-10 mg/kg intraperitoneally) produced a more marked hypotensive effect on both types of hypertensive rats although it was of much shorter duration.3. It is concluded that experimental hypertension of renal origin or induced by DCA treatment can develop even though most of the sympathetic nervous system has been destroyed. The maintenance of chronic hypertension in these conditions may depend on the adrenal glands or a hormonal system as yet undetected.

Animals↗
PubMed1969

The role of the sympathetic nervous system in the cardiovascular responses to angiotensin in the pithed rat.

1. Angiotensin (200-500 ng, intravenously) produced a biphasic pressor response accompanied by reflex bradycardia in rats anaesthetized with sodium pentobarbitone. In pithed rats and in anaesthetized animals treated with a ganglion blocking agent there was a similar pressor response but an increase in the heart rate which was coincident with the second phase of the pressor response. In pithed preparations an increase in cardiac contractile force accompanied the heart rate changes.2. Acute or chronic adrenalectomy did not alter the pressor responses and chronotropic effect of angiotensin in the pithed rat. Propranolol abolished the chronotropic and inotropic action of angiotensin, but left the biphasic pressor response unaltered. Bethanidine, or pretreatment with reserpine, altered the pressor response to a simple rise, and also abolished the chronotropic action of angiotensin. Phentolamine also abolished the second pressor component. Desmethylimipramine produced a marked potentiation of the cardiovascular effects of angiotensin at all dose levels tested (10-500 ng).3. It is concluded that in the rat only large doses of angiotensin are capable of indirectly stimulating the sympathetic nerves either at the site of their ganglionic cells or their post-ganglionic nerve ending.

Adrenalectomy↗
PubMedDate not supplied

A centrally acting antihypertensive agent (R28935) not mediated via central alpha-adrenoreceptors.

Intraventricular administration (i.c.v.) of R28935 (25 mug) produced a marked fall in blood pressure without any bradycardia in conscious renal hypertensive cats. This hypotensive effect was not antagonised by central administration of tolazoline (200 mug i.c.v.) or phentolamine (200 mug). However, these doses of alpha-adrenoreceptor blocking agents did antagonise the centrally mediated hypotensive actions of clonidine (20 mug i.c.v.) or alpha-methyl-dopa (1 mg i.c.v.). Infusions of R28935 in the perfused artery preparation did not modify the basal perfusion pressures or modify the vasoconstrictor actions of noradrenaline or 5-hydroxytryptamine. The results suggest that R28935, an analogue of pimozide, exerts a central hypotensive effect not mediated via central alpha-adrenoreceptors, and does not have any peripheral sympathomimetic action.

Animals↗
PubMedDate not supplied

The cardiovascular effects of intraventricular 5,6-dihydroxytryptamine in conscious hypertensive rats.

1. Conscious experimental hypertensive rats injected intraventricularly with 5,6-dihydroxytryptamine (50 microgram) responded with a rapid and long-lasting (4 days) fall in blood pressure and this was accompanied by a bradycardia of similar duration. 2. The acute actions of 5,6-dihydroxytryptamine on the cardiovascular system were not modified by pretreatment with bromolysergide (0.5 mg/kg, i.p.), methysergide (2.5 mg/kg, i.p.) or intraventricular phentolamine (200 microgram). 3. The results suggest that central serotonergic neurones play an important role in the regulation of blood pressure. However, the site of action remains to be investigated.

5,6-Dihydroxytryptamine↗