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S M Hilton

Publications and source records attributed to S M Hilton.

At least 37 records · Page 2Linked to original sources

Inhibition of the baroreceptor reflex on stimulation in the brain stem defence centre.

1. In anaesthetized cats, the pattern of cardiovascular response characteristic of the defence reaction has been elicited by localized electrical stimulation within the appropriate region of the hypothalamus. The baroreceptor reflex response has been elicited by raising the pressure in a blind sac preparation of the carotid sinus or by electrical stimulation of the sinus nerve.2. In addition to arterial blood pressure, heart rate and regional blood flows, activity was recorded in cardiac and renal sympathetic nerves, to assess more precisely the cardiomotor and vasomotor changes during interactions between brain stem stimulation and baroreceptor activation.3. The sympatho-inhibitory and depressor effects of carotid sinus stimulation or electrical stimulation of the sinus nerve could be completely suppressed by stimulation within the hypothalamic defence area, as could the reflex bradycardia. It is concluded that this suppression is effected through the central nervous system.4. Stimulation at points in the hypothalamus close to, but outside, the defence area, and which elicited increases in arterial pressure and sympathetic activity of similar magnitude to those from the defence area itself, did not abolish the sympatho-inhibitory or depressor effects of baroreceptor activation, though the reflex bradycardia was usually inhibited. It is suggested that this less localized change results from augmentation of the central inspiratory drive which inhibits the vagal outflow to the heart.

Action Potentials↗

Possible mediators of functional hyperaemia in skeletal muscle.

1. (a) In experiments on gastrocnemius muscles of the cat performing external work, the work was graded, either by altering the intensity of motor nerve stimulation or by changing the load. Only under the former conditions was the steady-state increase in blood flow conductance at all consistently related to the work performed. (b) In such experiments, efflux of inorganic phosphate and of potassium were closely correlated with the increase in vascular conductance, in the form of a typical dose-response curve. There was no significant relationship between changes in plasma osmolarity and conductance. 2. (a) Whereas most soleus muscles in the cat exhibit virtually no functional vasodilation, those with a relatively low resting flow tend to do so. (b) There was a relationship between the vasodilation, if any, and release of phosphate in fifteen out of seventeen experiments on soleus muscles. No relationship was found between any release of potassium or change of plasma osmolarity, and absence or extent of functional vasodilation. 3. (a) Terminal arterioles and collecting venules in the rat's spinotrapezius muscle were observed in vivo under low power magnification while the muscle was bathed in various test solutions, so that the vasodilator properties of hyperosmolar solutions, potassium and phosphate could be studied. (b) The dilator effect of hyperosmolar solutions was much the weakest: solutions of 340 m-osmole/kg elicited the largest responses, but these seldom exceeded 50% mM-K+ and 3.2--6.4 mM-Pi (as NaH2PO4) elicited 25--50% of maximum dilation, while 9--10 mM-K+ and 16--20 mM-Pi dilated arterial vessels fully. The latency to onset of dilation was shortest (5 sec) with Pi and longest (15 sec) with K+. 4. These findings, together with those already in the literature, lead to the conclusions that (a) hypersomolarity is unlikely to be in an important factor initiating or maintaining functional hyperaemia in skeletal muscle, (b) while K+ release may contribute in fast muscle it can hardly be the factor initiating the response, and (c) inorganic phosphate is the only substance tested so far whose efflux is consistently related to the vascular response in all muscles under a variety of experimental conditions, and whose efficacy as a vasodilator seems adequate.

Animals↗

Evidence for phosphate as a mediator of functional hyperaemia in skeletal muscles.

Maximal twitch contractions of fast muscles of the cat caused an increase in phosphate concentration in the venous plasma from them: this efflux was greater as the contraction frequency was increased. At any given frequency of contraction, the phosphate efflux from contracting gastrocnemius was less than that from tibialis anterior and extersor digitorum longus, which have a higher proportion of fast fibres and exhibit greater functional hyperaemia. Soleus muscles, when contracting, released hardly any additional phosphate, except in the one experiment in which the muscle exhibited a functional hyperaemia. There was thus a consistent relationship between the extent of functional hyperaemia and phosphate efflux in different muscles and within any one group of muscles. Inorganic phosphate, given close arterially as NaH2PO4, was shown to be vasodilator.NaH2PO4 was much more potent than Na2HPO4, though this did not seem due simply to the associated change of pH. The functional hyperaemia of fast muscles could be matched, qualitatively and quantitatively, by injections or infusions of NaH2PO4. The possibility is discussed that the contraction hyperaemia of fast muscles is functionally related to phosphate release into the interstitial fluid during contractions.

Animals↗

The ponto-medullary area integrating the defence reaction in the cat and its influence on muscle blood flow.

1. In anaesthetized cats the effects were investigated of electrical stimulation of regions in the caudal mesencephalon, pons and medulla on muscle blood flow, skin blood flow and arterial blood pressure.2. It was found that within the dorsal part of the well known pressor area there is a narrow strip, 2.5 mm lateral from the mid line, starting ventral to the inferior colliculus and ending in the medulla close to the floor of the IV ventricle, from which vasodilatation in skeletal muscles is selectively obtained. This strip is quite separate from the more ventral, efferent pathway for active vasodilatation running from the hypothalamic and rostral mesencephalic ;defence centre'.3. As in the case of the hypothalamic and rostral mesencephalic ;defence centre', the muscle vasodilatation obtained from the caudal strip is accompanied not only by a rise of arterial blood pressure, but also by tachycardia, vasoconstriction in the skin, pupillary dilatation and piloerection.4. Stimulation, restricted to the caudal strip, via implanted electrodes in unanaesthetized animals, produced a behavioural response resembling the defence reaction. The strip, therefore, is probably a caudal extension of the ;defence centre'.5. Unlike the vasodilatation elicited from the more rostral part of the ;defence centre' in the hypothalamus and mesencephalon, the muscle vasodilatation obtained on stimulation of the caudal strip was resistant to atropine, but was blocked by guanethidine.6. It is suggested that during naturally occurring defence reactions in the normal animal the ponto-medullary area is activated together with the hypothalamo-mesencephalic area, inhibition of vasoconstrictor tone then accompanying activation of the vasodilator nerve fibres in skeletal muscle.

Animals↗

The reflex nature of the pressor response to muscular exercise.

1. In anaesthetized cats tetanic contraction of the hind-limb muscles, elicited by stimulating the ventral roots L6-S1, caused a rise of arterial blood pressure, usually accompanied by small increases in heart rate and pulmonary ventilation: in decerebrate cats, all components of the response were much increased.2. With tetani of different strengths, obtained by stimulating with different intensities at the same frequency, the pressor response increased with increasing tension.3. When muscle contraction had been abolished by gallamine, or when dorsal roots L6-S1 had been sectioned, ventral root stimulation no longer caused a pressor response. The response is therefore a reflex, initiated in the exercising limb.4. The pressor response was not affected by section of all articular nerves to knee and ankle joints, or by section of the vagi. The stimulus therefore originates in the contracting muscles alone.5. The pressor response is potentiated by occluding the circulation through the working muscles. Reasons are discussed for concluding that the stimulus is chemical rather than mechanical, and that the ;metabolic receptors' for this exercise reflex are the free endings of group III and IV sensory nerve fibres located around the blood vessels.

Animals↗

Participation of the anterior hypothalamus in the baroreceptor reflex.

1. On the basis of discrete electrical stimulation in the pre-optic region and anterior hypothalamus of anaesthetized cats, a depressor area has been defined, stimulation of which elicits a fall of arterial blood pressure of 30-50 mm Hg and a bradycardia of some 25%, caused by inhibition of sympathetic vasomotor tone and by vagal activation respectively. These are accompanied by a reduction in rate and depth of respiration.2. The depressor area, from which this pattern of response is elicited, lies ventral and caudal to the anterior commissure, and extends caudally in the dorsal hypothalamus, dorsal to the fornix.3. The pattern of response elicited from identified points in the depressor area was shown to be indistinguishable from that to baroreceptor afferent stimulation.4. A lesion destroying the hypothalamic depressor area bilaterally reduced the response to baroreceptor afferent stimulation. Lesions in the medullary depressor area which spared a large part of the nucleus of the tractus solitarius also reduced, but did not abolish, the baroreceptor reflex response. The two lesions combined abolished the reflex.5. It is concluded that the whole brain-stem depressor area, from the hypothalamus through the mid-brain to the medulla, constitutes a functional unit which integrates the response to baroreceptor afferent stimulation.

Animals↗