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Biomedical subjects

I R Innes

Publications and source records attributed to I R Innes.

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

Potassium and the recovery of splenic capsular smooth muscle after cold storage.

Cat spleen capsular smooth muscle, depleted of potassium and enriched with sodium by cold storage in a potassium free medium, relaxed and underwent transient reduction in responsiveness to noradrenaline when potassium was introduced into the bathing medium. Both these effects could be blocked by ouabain, lithium substitution for sodium or low ambient temperature, suggesting possible involvement of the sodium pump. In the continued presence of potassium, relaxation was maintained but sensitivity to noradrenaline increased, possibly due to restoration of normal intracellular sodium and potassium concentrations.

Animals↗
PubMed1975

Utilization of calcium pools during pharmaco or electromechanical coupling in smooth muscle.

Isometric contraction of cat spleen capsule due to noradrenaline had a fast and a slow phase. These phases were due to a tightly and a loosely bound (or extracellular) pool of calcium, respectively. Depolarization due to high potassium caused mainly a reduction of the slow phase. In sodium-loaded spleen strips recovering from potassium deprivation, the sodium pump is electrogenic and the muscle cells are probably hyperpolarized. In this situation also the slow phase of noradrenaline response is reduced. It is concluded that both depolarization and hyperpolarization affect the utilization of loosely bound calcium and that tightly bound calcium may be released during 'pharmacomechanical coupling' in splenic smooth muscle.

Animals↗
PubMed1973

Effect of cocaine on the affinity of -adrenoceptors for noradrenaline.

1. Doses of cocaine which cause specific or unspecific supersensitivity in cat spleen did not alter the blocking effect of phenoxybenzamine on the responses of isolated cat spleen strips to noradrenaline.2. The same doses of cocaine did not increase the protection of alpha-adrenoceptors given by noradrenaline during a standard exposure to phenoxybenzamine.3. It is concluded that cocaine does not change the affinity of the alpha-adrenoceptor for noradrenaline, and therefore changes in affinity are not responsible for the potentiating action of cocaine.

Animals↗
PubMed1973

Further observations on mesenteric vasoconstriction, survival and the clotting defect after endotoxin administration.

1. The initial response after endotoxin administration (3 mg/kg) in cats involved pulmonary vasoconstriction. This was not seen when endotoxin was given by slow infusion and it could be prevented after a bolus injection of endotoxin by pretreatment of the cats with aspirin (10 mg/kg). Intense mesenteric vasoconstriction occurred in all the cats.2. The mesenteric vasoconstriction was a specific response of the mesenteric blood vessels. At the time the mesenteric bed constricted, the renal bed dilated, the hepatic arterial bed remained unchanged and the smooth muscle of the intestinal wall relaxed.3. Arterial blood from cats with a fully developed mesenteric vasoconstriction after endotoxin administration was perfused through a normal intestine. No immediate vasoconstriction developed but the perfused intestine constricted slowly over 60 minutes. This suggests that mesenteric constriction was not due to circulating vasoconstrictor factors or the intestinal innervation, but involved a slow local mechanism within the intestine. It could not be prevented or reversed by a variety of pharmacological agents.4. These observations suggest that endotoxin caused a unique type of mesenteric vasoconstriction in cats by a local mechanism which took up to 60 min to develop, was sufficiently potent to reduce mesenteric flow to <30% control, and was maintained until death of the cats. Blood from these animals did not clot when placed in a glass tube.5. The mesenteric constriction and the clotting defect could be prevented by repeated administration of aminophylline and dextran solution before and after a bolus intravenous injection of endotoxin. Arterial pressure and mesenteric flow were maintained for at least 10 h in these experiments. Inadequate treatment intensified rather than reduced the intestinal mucosal damage.6. Cats were treated with aspirin, endotoxin and the optimal regimen for prevention of the mesenteric constriction and allowed to recover from the anaesthetic agent. In this series, 63% survived indefinitely compared to 25% after aspirin and endotoxin treatment and 0% after endotoxin alone.7. The possible mechanisms of action of aspirin and aminophylline-dextran solution are discussed. Our failure to obtain 100% survival is probably due to pulmonary damage which develops 10-24 h after endotoxin administration. This delayed pulmonary action of endotoxin is not prevented by aspirin treatment and it seems unlikely that aspirin will be of any value in the treatment of the pulmonary lesion in man.

Aminophylline↗
PubMed1973

The role of sodium pump in the inhibition of smooth muscle responsiveness to agonists during potassium restoration.

1. Isometric contractions of cat splenic capsular smooth muscle in response to noradrenaline and histamine were recorded.2. Removal of potassium from the bathing medium did not change the resting tension or the responsiveness to noradrenaline. Restoration of potassium inhibited responses to noradrenaline or histamine only if the muscles were stimulated with an agonist while in the K-free medium.3. This inhibition of responses to the agonists due to potassium was reversed rapidly by removing the ion or reversed slowly by prolonged exposure to the ion. The inhibition was also blocked by procedures or agents which block the sodium pump (ouabain, substitution of NaCl by LiCl), inhibit active processes (low ambient temperature) or prevent intracellular accumulation of sodium (substitution of choline for sodium).4. It is proposed that under special circumstances such as when there is an increase in internal sodium concentration, the sodium pump is probably electrogenic and causes relaxation when activated by external potassium. In the normal muscle the pump is probably electrically neutral.

Animals↗
PubMed1972

Influence of sodium pumping on smooth muscle contraction.

Isolated capsular muscle from cat spleen did not contract on exposure to a potassium-free bathing fluid. After exposure to conditions favouring downhill sodium and potassium movement (i.e. stimulation by noradrenaline in the absence of external potassium), subsequent reactivation of the sodium pump inhibited responses to noradrenaline. Under these special conditions, but not normally, the sodium pump may be behaving in an electrogenic manner.

Animals↗
PubMed1971

Protection against induction of supersensitivity to catecholamines by cocaine.

1. Adrenaline, noradrenaline, isoprenaline, tyramine, phentolamine, pronethalol, histamine and acetylcholine were each tested for their ability to prevent cocaine from causing supersensitivity to catecholamines in cat spleen strips in vitro. A high concentration of one of these drugs was added to the bath 5 min before cocaine hydrochloride (10 mug/ml). The effect on subsequent responses to catecholamines was compared with the effect of cocaine in control strips in the absence of an interfering drug.2. Phentolamine completely abolished the potentiating effect of cocaine. Large doses of adrenaline or noradrenaline reduced, but did not completely prevent, potentiation. Tyramine, isoprenaline, pronethalol, histamine and acetylcholine did not prevent potentiation.3. The ability of these drugs to interfere with potentiation does not correlate well with their ability to interfere with uptake of noradrenaline. Interference with uptake by cocaine is therefore unlikely to account fully for potentiation.

Acetylcholine↗
PubMed1970

Dissociation of potentiation of isoprenaline by cocaine from inhibition of uptake in cat spleen.

1. Cocaine hydrochloride, 10 mug/ml, potentiated isoprenaline and noradrenaline in isolated spleen strips from normal cats and from cats treated with reserpine 24 h previously.2. Isoprenaline was taken up almost as well as noradrenaline by spleen strips from cats treated with reserpine.3. Cocaine blocked uptake of noradrenaline but did not reduce uptake of isoprenaline. Drug concentrations used in these studies were the same as in potentiation experiments.4. It is concluded that inhibition of uptake is not the mechanism by which cocaine potentiates the effect of isoprenaline on the spleen and might be only a contributory factor in the case of noradrenaline potentiation.

Animals↗
PubMed1969

Excitatory action of sympathomimetic amines on 5-hydroxytryptamine receptors of gut.

1. Twenty-two sympathomimetic amines were tested for excitatory activity on isolated guinea-pig ileum, rabbit jejunum, and rat stomach.2. Eight amines contracted all or almost all guinea-pig ileum preparations; five amines contracted half the preparations and relaxed the others. Nine amines were consistently relaxant. Structural requirements for excitatory activity were not clear.3. Six amines contracted rat stomach and only four contracted rabbit jejunum. Only beta-phenylethylamine and (-)-amphetamine contracted all three preparations.4. The excitatory effects of the sympathomimetic amines on guinea-pig ileum seem to be due to an action on 5-hydroxytryptamine receptors. This conclusion is based on evidence that their excitatory action is antagonized by 2-bromolysergic acid diethylamide, by morphine and by desensitization with 5-hydroxytryptamine, and that there is cross-protection between 5-hydroxytryptamine and the excitatory sympathomimetic amines against block by phenoxybenzamine.

Amphetamine↗
PubMedDate not supplied

Effect of carotid sinus baroreceptor reflex on responses to phenylephrine and nitroprusside in anesthetized cats.

This study attempted to measure the extent to which the carotid sinus baroreceptor reflex attenuates the acute changes in arterial pressure during infusions of phenylephrine and nitroprusside, and to express these effects as equations which could be used in a simple computer model of the circulation. Arterial pressure and cardiac output were measured in vagotomized cats anesthetized with chloralose or pentobarbital. The carotid arteries were perfused to allow sinus pressure either to follow changes in systemic arterial pressure or to be held at the preinfusion control level, thereby eliminating the effects of the reflex. There was a linear relationship between arterial pressure in the presence and absence of the reflex, and the changes in arterial pressure were attenuated to one-third by the reflex while cardiac output was not significantly changed. These effects are described by simple equations involving peripheral resistance, heart rate, and venous compliance. The activity of the reflex was not significantly different in cats anesthetized with pentobarbital or chloralose, and our data do not support the view that these anesthetic agents depress the vasomotor component of the carotid sinus reflex.

Anesthesia↗
PubMedDate not supplied

Effects of arteriolar vasodilators on hepatic venous compliance and cardiac output in anesthetized cats.

The effects of cumulative doses of seven arteriolar vasodilators were examined in cats anesthetized with pentobarbital. Cardiac output was measured by a thermodilution technique and hepatic venous compliance by plethysmography. All the drugs produced dose-related decreases in total peripheral resistance. Diazoxide, prazosin, and sodium nitroprusside produced no significant changes in hepatic venous compliance or cardiac output. Diazoxide and prazosin produced no change in right atrial pressure, while nitroprusside produced a small fall. It is concluded that these drugs do not alter hepatic venous tone, although nitroprusside may cause a small venodilator effect elsewhere. Epinephrine and dopamine produced marked decreases in hepatic venous compliance and increased cardiac output. This increased cardiac output can be explained on the basis of cardiac stimulation combined with no increase in afterload due to arteriolar vasodilatation and maintenance of preload by venoconstriction. Isoproterenol and hydralazine unexpectedly produced a similar pattern--marked decreases in hepatic venous compliance and increased cardiac output. With hydralazine, these effects preceded arterial hypotension. Possible mechanisms are discussed. These studies support our roterenol and hydralazine produce a beta-receptor-mediated cardiac stimulation and an indirect hepatic venoconstriction, which are not secondary to the hypotension. Possible mechanisms are discussed. These studies support our hypothesis that splanchnic venoconstriction is a necessary factor for the production of large sustained increases in cardiac output. A reduction in afterload per se doesnot increase cardiac output in normal anesthetized cats since a compensatory decrease in preload occurs. It is suggested that afterload influences cardiac output only in situations where the heart is on the flat portion of the Starling function curve.

Animals↗