PubMed Health⌕ Search

Biomedical subjects

H M Snow

Publications and source records attributed to H M Snow.

At least 73 records · Page 4Linked to original sources
PubMed1972

A reflex increase in heart rate from distension of the junction between the superior vena cava and the right atrium.

1. Localized distension of the junction between the superior vena cava and the right atrium without obstructing venous return caused an increase in heart rate.2. This increase in heart rate was a reflex response; the afferent path was in the vagi and the efferent solely in the sympathetic nerves.3. The receptors most likely to be stimulated by the distension of the junction between the superior vena cava and the right atrium are the right atrial receptors located on the endocardial surface of the intrapericardial portion of the superior vena caval-right atrial junction.

Animals↗
PubMed1972

The effect of distending the atrial appendages on urine flow in the dog.

1. Distension of the atrial appendages resulted in a diuresis, an increase in the rate of Na(+) excretion and an increase in heart rate.2. Both the urinary and heart rate responses to distension of the appendages were either abolished or much reduced by crushing the bases of the appendages.3. The diuresis in response to distension of the atrial appendages is similar to that previously described in response to distension of the pulmonary vein-atrial junctions by Ledsome & Linden (1968).4. It is concluded that stimulation of nerve endings within the atrial appendages results in a reflex increase in urine flow and heart rate.

Animals↗
PubMed1972

The effect of stretching the superior vena caval-right atrial junction on right atrial receptors in the dog.

1. Action potentials were recorded from fibres in the right cervical vagus, the receptor endings of which were localized to the endocardial surface of the superior vena caval-right atrial junction.2. Stretching the junction between the superior vena cava and the right atrium without obstructing venous return caused an increase in the discharge of these fibres. This increase in impulse frequency was similar to that caused by small changes in mean right atrial pressure (range 0-13.5 cm H(2)O).3. This evidence supports the earlier suggestion that stimulation of the right atrial receptors by stretching the superior vena caval-right atrial junction causes a reflex increase in heart rate.

Action Potentials↗
PubMed1971

The inotropic and chronotropic effects of catecholamines on the dog heart.

1. The chronotropic and inotropic responses of the denervated dog heart to intravenous infusions of noradrenaline, adrenaline and isoprenaline were studied.2. The maximum rate of rise of pressure in the left ventricle of the heart, (dP/dt max) measured at a constant heart rate and mean systemic arterial pressure during each series of infusions, was used as an index of inotropic changes (Furnival, Linden & Snow, 1970).3. The order of potency of the catecholamines in producing both chronotropic and inotropic effects was isoprenaline > adrenaline > noradrenaline.4. For the same increase in heart rate produced by an infusion of a catecholamine, noradrenaline caused a greater inotropic effect than adrenaline, which in turn caused a greater increase than isoprenaline.5. The chronotropic and inotropic effects of noradrenaline were potentiated by an intravenous injection of cocaine HCl (5 mg/kg), whereas those of isoprenaline were unchanged.6. The relative difference between the responses to noradrenaline and isoprenaline was abolished by an intravenous injection of cocaine HCl.7. It is concluded that the different relative chronotropic and inotropic effects of isoprenaline and noradrenaline are due to the greater uptake of noradrenaline by sympathetic nerve endings in the sinu-atrial node than in the muscle of the left ventricle.

Animals↗
PubMed1971

Reflex effects on the heart of stimulating left atrial receptors.

1. Stimulation of left atrial receptors, by distension of the pulmonary vein/left atrial junctions, is known to cause a reflex increase in heart rate; the efferent pathway is known to be solely in the sympathetic nerves.2. In expectation of a concomitant positive inotropic response the effect of stimulating the left atrial receptors on the inotropic state of the left ventricle was studied, using as a known sensitive index of inotropic changes the maximal rate of rise of pressure in the left ventricle (dP/dt max).3. Stimulation of left atrial receptors resulted in an increase in heart rate but there were no significant concomitant changes in dP/dt max.4. It is concluded that activity in this discrete efferent pathway does not include an inotropic effect on the left ventricle and therefore the reflex involves only those sympathetic nerves which innervate the sinu-atrial node.5. The possible function of atrial receptors in the regulation of heart volumes is discussed.

Animals↗
PubMed1971

Depression of the reflex tachycardia from the left atrial receptors by acidaemia.

1. The effects are described of an acidaemia, produced either by the inhalation of carbon dioxide or by an intravenous infusion of hydrochloric acid, on the reflex increase in heart rate which results from stimulation of the left atrial receptors in the anaesthetized dog.2. The results show that during acidaemia the reflex increase in heart rate from stimulation of the left atrial receptors is reduced. The extent of the reduction is related to the degree of the acidaemia.3. It is suggested that it is necessary to monitor and correct changes in the pH of arterial blood in experiments which involve reflex changes in heart rate, especially if the efferent pathway involves the sympathetic nerves.4. It is also suggested that the occurrence of such an acidaemia in anaesthetized surgically traumatized animals may be a factor contributing to the variability in results from investigations involving reflex changes in heart rate in response to stimulation of the left side of the heart.

Acidosis↗
PubMed1970

Inotropic changes in the left ventricle: the effect of changes in heart rate, aortic pressure and end-diastolic pressure.

1. Under conditions where heart rate, mean aortic pressure and enddiastolic pressure in the left ventricle are held constant, the intravenous infusion of isoprenaline is accompanied by large changes in dP/dt max in the left ventricle.2. Under similar conditions, during stepwise increments in the rate of infusion of isoprenaline the changes in dP/dt max (measured at a constant paced heart rate) were proportional to changes in the free (intrinsic) heart rate. It is concluded that dP/dt max is a quantitative index of inotropic changes in the left ventricle.3. In comparison to dP/dt max, three other variables which have been used to indicate inotropic changes in the heart (peak pressure in the left ventricle, duration of systole and stroke work at constant end-diastolic pressure), were shown to be unreliable indices of inotropic changes.4. Using dP/dt max to indicate inotropic changes, alteration in the heart rate while mean aortic pressure and end-diastolic pressure in the left ventricle were held constant, and in mean aortic pressure while heart rate ane end-diastolic pressure in the left ventricle were held constant, were each shown to be accompanied by small inotropic changes in the heart.5. Under similar conditions, changes in end-diastolic pressure in the left ventricle alone were not accompanied by inotropic changes as indicated by dP/dt max.

Animals↗