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Biomedical subjects

W J Lang

Publications and source records attributed to W J Lang.

At least 37 records · Page 2Linked to original sources
PubMed1976

Cutaneous and muscular rasodilation in the canine hindlimb evoked by central stimulation.

Using stereotaxic procedures, we electrically stimulated specific sites in the hypothalamus and midbrain of anesthetized dogs pretreated with guanethidine and atropine methonitrate. A tract in which stimulation caused noncholinergic dilator responses in the hindlimbs was identified. The course of this trace was different from that subserving cholinergic vasodilation in the hindlimb musculature. In a number of experiments we studied the proportional distribution of blood flow to leg and paw. Responses restricted to the paw were regarded as occurring mainly in cutaneous vessels; those restricted to the leg were regarded as occurring mainly in the skeletal muscle vessels. Some dilator responses in both beds were abolished by intra-arterial administration of antihistamines: other dilator responses were abolished by intra-arterial injections of dopamine antagonists. Centrally evoked dilation of leg and paw vessels by noncholinergic pathways suggests physiological roles for these fibers in the regulation of cardiovascular function.

Animals↗
PubMed1975

Vascular dopamine receptors in the canine hindlimb.

1 Increases in femoral blood flow were produced by intra-arterial injections of dopamine (5-50 mug) in some but not all anaesthetized dogs studied, following treatment with the alpha-adrenoceptor antagonist, phentolamine. 2 The dilator effect of dopamine was not due to inhibition of adrenergic vasomotor tone as it was not affected by pharmacological procedures which completely abolished the activity of vastomotor nerves. 3 Blockade of vascular beta-adrenoceptors using propanolol reduced the flow increases produced by dopamine much less than it did those produced by isoprenaline. 4 Responses to dopamine were significantly depressed by intra-arterial administration of ergometrine (0.5 mg). This dose of ergometrine did not reduce femoral dilator responses to acetylcholine, histamine, isopienaline, bradykinin, or 5-hydroxytryptamine. 5 It is concluded that the femoral vascular bed in the dog contains specific vasodilator receptors for dopamine. Ergometrine appears to be a selective antagonist of dopamine at these receptors.

Acetylcholine↗
PubMed1975

The role of the central nervous system in the cardiovascular responses to yohimbine.

Yohimbine injected intravenously or intracerebroventricularly in conscious dogs produced behavioural excitation accompanied by a rise in blood pressure and heart rate. The cardiovascular effects were reduced or abolished by hexamethonium, phenoxybenzamine and reserpine. In conscious cats intravenously administered yohimbine was depressor but intracerebroventricular administration in these animals caused a rise in blood pressure accompanied by behavioural depression. In anaesthetized or decerebrate cats yohimbine was always depressor. Yohimbine injected intracerebroventricularly produced a rise in blood pressure and heart rate in both conscious and anaesthetized rats. When administered intravenously to these animals there was a fall in blood pressure. It was concluded that the pressor action of yohimbine in conscious dogs was central in origin via the sympathetic nervous system. The different pattern of cardiovascular responses in the dog, cat and rat may be related to differences in the balance between medullary effects and effects on higher brain centres of the three species.

Adrenergic alpha-Antagonists↗
PubMed1974

Ergometrine and apomorphine as selective antagonists of dopamine in the canine renal vasculature.

1 Increases in renal blood flow were produced by intra-arterial injections of dopamine (5-50 mug) in anaesthetized dogs pretreated with alpha- and beta-adrenoceptor antagonists.2 Intra-arterial administration of ergometrine (0.5 mg) or apomorphine (1 mg) produced a depression of the renal dilator responses to dopamine, without affecting renal dilatations in response to intra-arterial acetylcholine (0.1-1 mug) or histamine (2-50 mug).3 The depression of dopamine responses lasted 10-15 min, and was greater with ergometrine than with apomorphine.4 It is concluded that both ergometrine and apomorphine can be used as specific blocking agents at vascular dopamine receptors. Ergometrine is the preferred drug for this purpose.

Acetylcholine↗
PubMed1974

Thermoregulatory responses to the injection of monoamines, acetylcholine and prostaglandins into a lateral cerebral ventricle of the echidna.

1. The putative neurotransmitter substances 5-hydroxytryptamine (5-HT), noradrenaline (NA), acetylcholine (ACh) and prostaglandins E(1) (PGE(1)) and E(2) (PGE(2)) have been injected into a lateral cerebral ventricle of the conscious echidna (Tachyglossus aculeatus); thermoregulatory responses in thermoneutral (ambient dry bulb temperature, T(db), of approximately 22 degrees C), cool (T(db) of approximately 14 degrees C) and warm (T(db) of approximately 26 degrees C) environments were determined.2. Under all conditions, all of the drugs tested either caused deep body temperature to fall or else had no effect; the fall was brought about by peripheral vasodilatation and/or reduced metabolic rate due to a decrease in shivering or to general relaxation.3. Responses of the many placental mammals to 5-HT, NA and ACh vary widely, and the echidna, a monotreme, appears to exhibit responses most like those of the rat.4. Placental mammals tested to date invariably exhibit a hyperthermic response to prostaglandins, and the hypothermic responses of this monotreme is therefore unique. The present study included the confirmation of a hyperthermic response to PGE(1) and PGE(2) in cats and rats.5. It is concluded that the concept of thermoregulation by amines and other substances in the hypothalamus of placental mammals may also be applicable to the monotremes which have evolved separately from the marsupials and placental mammals for about 180 million years.

Acetylcholine↗
PubMed1973

Cardiovascular responses to injections of cholinomimetic drugs into the cerebral ventricles of unanaesthetized dogs.

1. The cardiovascular and behavioural effects of cholinomimetic drugs injected through a cannula chronically implanted into a lateral cerebral ventricle were examined in unanaesthetized dogs.2. Acetylcholine (ACh) (10-20 mug) produced an increase in arterial pressure and heart rate, the dogs became more alert, moved their heads, licked and swallowed and then became drowsy.3. The responses to ACh were potentiated by intraventricular physostigmine (5 mug), were abolished by intraventricular atropine (100 mug) but were unaffected by intraventricular mecamylamine (250 mug). The responses to ACh were reproducible on any one day if injections were given again after a 30 min interval but tolerance developed when ACh was injected repeatedly over periods of several days.4. Methacholine (40 mug) produced similar behavioural and cardiovascular effects to ACh but of a longer duration. The responses to methacholine were abolished by intraventricular atropine (100 mug).5. Nicotine (20-60 mug) produced a biphasic cardiovascular response of an initial brief pressor response and tachycardia followed by a secondary increase in arterial pressure and heart rate which was greater in magnitude and duration. The secondary cardiovascular effects were associated with restlessness and vomiting.6. The responses to nicotine were abolished by prior injection of mecamylamine (250 mug) but were unaffected by atropine (100 mug). The responses to nicotine were not reproducible if injections were repeated on the same day but could be again produced if a few days were allowed to elapse between injections.7. An increased heart rate occurred during the pressor response to the cholinomimetic drugs but when a comparable pressor response was produced by intravenous infusion of noradrenaline in the same unanaesthetized dogs pronounced reflex bradycardia resulted.8. The results indicate that the activation of both muscarinic and nicotinic cholinergic mechanisms leads to cardiovascular and behavioural effects in the conscious dog although the site of action and peripheral mechanisms have not been determined.

Acetylcholine↗
PubMed1970

Effects of monoamine oxidase inhibitors and amphetamine on hypothermia produced by halothane.

1. In cats, the effects of tranylcypromine and pheniprazine, two monoamine oxidase (MAO) inhibitors with strong amphetamine-like actions, of pargyline, an inhibitor without amphetamine-like actions, and of amphetamine itself, were examined on the hypothermia produced by a 2 hr period of halothane inhalation.2. The hypothermia was prevented by intraperitoneal injections of the three MAO inhibitors. Tranylcypromine and pheniprazine acted in doses of a few milligrams, pargyline in doses of over 100 mg.3. The hypothermia was prevented by injections into the cerebral ventricles of tranylcypromine and pheniprazine, in doses which were effective also on intraperitoneal injection; intraperitoneal injections were sometimes more effective. The large doses of pargyline needed to prevent the hypothermia when injected intraperitoneally were not tested by the intraventricular route, as the injections had to be made in a volume of 0.1 ml. In smaller doses intraventricular pargyline was not effective.4. The hypothermia was prevented by an intraperitoneal or intraventricular injection of amphetamine in a dose as little as 1 mg; intraperitoneal injections were sometimes more effective.5. The effects of tranylcypromine and pargyline given intraperitoneally, and of amphetamine given intraventricularly as well, were also examined on the hypothermia produced by an intraventricular injection of 200 mug noradrenaline. The two MAO inhibitors and amphetamine prevented the hypothermia, or greatly reduced it.6. It is concluded (a) that even on intraventricular injection the MAO inhibitors must first be absorbed into the blood stream before they can prevent the hypothermia of a halothane anaesthesia; (b) that their action may not be solely on the anterior hypothalamus; and (c) that they may not act only through MAO inhibition.

Amphetamine↗