Sympathetic Control of Cerebral Blood Flow in Acute Arterial Hypertension

The cervical sympathetic chain on one side was stimulated electrically at 10–20 Hz and an acute rise in arterial blood pressure was produced by: intravenous injection of angiotensin, ligation of the thoracic aorta, or ligation of the aorta combined with injection of metaraminol. The blood flow through the cerebrum and the cerebellum was determined by using labelled microspheres. At high blood pressures there was multifocal breakdown of the blood-brain barrier in the cerebrum as indicated by leakage of Evans blue. The breakdown was restricted to the control side or much more marked on that side than on the stimulated side. Sympathetic stimulation prevented also breakdown of the blood-aqueous barrier. The blood flow through the cerebrum on the control side was higher than that on the stimulated side in all experiments. Regions with breakdown of the blood-brain barrier had flow rates which were about 10 times normal values. Cerebellar blood flow was less affected by the hypertension and did not react significantly to sympathetic stimulation. The results indicate that stimulation of the sympathetic nerves to the brain tends to prevent forced dilatation of the arterioles with a resulting regional overperfusion with blood and breakdown of the blood-brain barrier. It is concluded that one role of the sympathetic nerves supplying the brain is to extend the pressure region with autoregulation in its upper part under conditions of a general increase in sympathetic vasomotor activity.     

Sympathetic control of cerebral blood flow in acute arterial hypertension.

The cervical sympathetic chain on one side was stimulated electrically at 10-20 Hz and an acute rise in arterial blood pressure was produced by: intravenous injection of angiotensin, ligation of the thoracic aorta, or ligation of the aorta combined with injection of metaraminol. The blood flow through the cerebrum and the cerebellum was determined by using labelled microspheres. At high blood pressures there was multifocal breakdown of the blood-brain barrier in the cerebrum as indicated by leakage of Evans blue. The breakdown was restricted to the control side or much more marked on that side than on the stimulated side. Sympathetic stimulation prevented also breakdown of the blood-aqueous barrier. The blood flow through the cerebrum on the control side was higher than that on the stimulated side in all experiments. Regions with breakdown of the blood-brain barrier had flow rates which were about 10 times normal values. Cerebellar blood flow was less affected by the hypertension and did not react significantly to sympathetic stimulation. The results indicate that stimulation of the sympathetic nerves to the brain tends to prevent forced dilatation of the arterioles with a resulting regional overperfusion with blood and breakdown of the blood-brain barrier. It is concluded that one role of the sympathetic nerves supplying the brain is to extend the pressure region with autoregulation in its upper part under conditions of a general increase in sympathetic vasomotor activity.     

Cerebral circulation in acute arterial hypertension—protective effects of sympathetic nervous activity

The cervical sympathetic chain was stimulated electrically at 6 or 3 Hz on one side in anesthetized cats. Acute arterial hypertension was induced by ligation of the aorta. Evans blue was given as tracer for protein leakage. The regional blood flow in the brain was determined by using labelled microspheres. At high blood pressures there was a multifocal breakdown of the blood-brain barrier. The regions with breakdown had 10–20 times the normal flow rates. With a maintained hypertension regions which were overperfused at 5 min were still overperfused at 10 min, but there was little addition of new overperfused areas. Normalization of the pressure resulted in almost twice the normal flow rates in previously overperfused regions. The breakdown of the blood-brain barrier was restricted to the non-stimulated side, or more marked on that side. The protective effect of the sympathetic stimulation lasted more than 10 min. The results indicate that acute arterial hypertension tends to cause forced and long-lasting vasodilation in some areas in the brain but regions which are resistant to the acute rise have an increase in the vascular tone. Sympathetic activity helps in developing this tone. Normalization of the blood pressure results in partial recovery of the vascular tone in previously overperfused regions and normalization in other areas.     

Sympathetic effects on cerebral and ocular blood flow in rabbits pretreated with indomethacin

The effects of unilateral stimulation of the cervical sympathetic chain on cerebral and ocular blood flow was investigated in 8 rabbits anesthetized with pentobarbital sodium and pretreated with indomethacin in order to inhibit the formation of prostaglandins. Blood flow determinations were made with the labelled microsphere method during normotension and acute arterial hypertension. Hypertension was induced by ligation of the thoracic aorta. Evans blue was given as a tracer for protein leakage during hypertension. Sympathetic stimulation had no significant effect on the blood flow in the brain under the two conditions studied. In the uvea marked effects of sympathetic stimulation were obtained at normotension as well as at hypertension. There were no indications of breakdown of the blood-brain barrier or the blood-aqueous barrier. Thus, there was no evidence for any prostaglandin-mediated inhibition of sympathetic effects in the brain or the eye.     

Effects of sympathetic nerves on cerebral vessels in dog, cat, and monkey.

Cerebral vascular responses to sympathetic stimulation and denervation were examined in three species during acute severe hypertension as well as normal conditions. Cerebral blood flow (CBF) was measured with microspheres after the superior cervical sympathetic trunk was cut and during electrical stimulation of the superior cervical sympathetic ganglion. Sympathetic denervation did not increase CBF in anesthetized cats or monkeys. Under normal conditions, sympathetic stimulation decreased CBF significantly in monkeys (-26 +/- 3%) (mean +/- SE) but not in cats. During acute severe hypertension, decreases in CBF due to sympathetic stimulation were greatly augmented in cats (-29 +/- 7%, compared to -3 +/- 3%), only modestly augmented in dogs (-9 +/- 3%, compared to -1 +/- 2%), and not augmented in monkeys (-17 +/- 3%, compared to -23 +/- 4%). Disruption of the blood-brain barrier during hypertension was reduced by sympathetic stimulation. We conclude that 1) sympathetic tone to cerebral vessels is minimal because denervation does not increase CBF; 2) sympathetic stimulation decreases CBF under normal conditions in monkeys and during severe hypertension in cats, dogs, and monkeys, and it reduces disruption of the blood-brain barrier; and 3) there is an important species difference in responses to sympathetic stimulation under normal conditions and during acute hypertension.     

Effect of sympathetic nerves on cerebral vessels during seizures.

The purpose of this study was to determine the effect of activation of sympathetic pathways during seizures on cerebral blood flow and integrity of the blood-brain barrier. We measured cerebral blood flow with microspheres and disruption of the blood-brain barrier with labeled albumin in cats. One cerebral hemisphere was denervated by cutting the superior cervical sympathetic trunk on one side. During bicuculline-induced seizures, superior cervical sympathetic nerve activity increased about threefold. Blood flow to the innervated hemibrain was significantly lower than flow to denervated hemibrain. However, in relation to the total increase in flow, this effect of nerves was minor. Blood-brain barrier permeability increased about sixfold during seizures, but there was no difference between the innervated and denervated sides of the brain. We conclude that sympathetic nerves attenuate the increase in cerebral blood flow during seizures, despite the increase in metabolism, but this effect is small. Activation of sympathetic nerves does not reduce disruption of the blood-brain barrier during seizures.     

Hemodynamic,renal, and hormonal responses to changes in dietary potassium in normotensive and hypertensive man: Long-term antihypertensive effect of potassium supplementation in essential hypertension

Summary The hemodynamic, hormonal, and renal responses to alterations in dietary potassium were studied in normotensive and hypertensive subjects. In a short-term study, nine normotensive and nine hypertensive young men received a normal diet and low potassium, high potassium, and high potassium/low sodium diets for 1 week, each. The long-term effect of potassium supplementation (normal diet plus 96 mmol KCl/d for 8 weeks) was evaluated in 17 patients with essential hypertension. Blood pressure did not change significantly during short-term alterations of potassium intake but decreased during long-term supplementation (from 152.2±3.5/99.6±1.9 mm Hg to 137.4±2.9/89.1±1.4 mm Hg). High dietary potassium induced a significant but transient natriuresis. Plasma potassium concentration was increased during long- but not during short-term high potassium intake. In contrast to plasma renin activity (PRA) and aldosterone, urinary kallikrein was consistently stimulated during long-term potassium supplementation. The plasma concentrations of adrenaline and noradrenaline were significantly higher in hypertensive than in normotensive subjects and were not markedly altered by the dietary changes. It is concluded that long- but not short-term potassium supplementation lowers blood pressure in patients with essential hypertension. The antihypertensive effect may be mediated by potassium-induced natriuresis, by a stimulation of Na-K-ATPase secondary to increased plasma potassium levels, and/or by a modulation of the renin-angiotensin-aldosterone, kallikrein-kinin, and sympathetic nervous systems.Abbreviations MAP mean arterial pressure - Na-K-ATPase sodium-potassium ATPase - PRA plasma renin activity The study was supported in part by the Ministerium für Wissenschaft und Forschung, Nordrhein-Westfalen (FA-92/14)     

Effects of sympathetic stimulation on cerebral and ocular blood flow. Modification by hypertension, hypercapnia, acetazolamide, PGI2 and papaverine

The effect of unilateral, electrical stimulation of the cervical sympathetic chain in rabbits anesthetized with pentobarbital sodium and vasodilated by hypercapnia, acetazolamide, papaverine or PGI2 was investigated to determine to what extent the sympathetic nerves to the brain and the eye cause vasoconstriction and prevent overperfusion in previously vasodilated animals. Evans blue was given as a tracer for protein leakage. Blood flow determinations were made with the labelled microsphere method during normotension and acute arterial hypertension. Hypertension was induced by ligation of the thoracic aorta and in some animals metaraminol or angiotensin was also used. Acetazolamide caused a two to threefold increase in cerebral blood flow (CBF) and hypercapnia resulted in a fivefold increase. CBF was not markedly affected by papaverine or PGI2. In the choroid plexus, the ciliary body and choroid, papaverine and hypercapnia caused significant blood flow increases on the control side. Sympathetic stimulation induced a 12% blood flow reduction in the brain in normotensive, hypercapnic animals. Marked effects of sympathetic stimulation at normotension were obtained under all conditions in the eye. In the hypertensive state the CBF reduction during sympathetic stimulation was moderate, but highly significant in hypercapnic or papaverine-treated animals as well as in controls. Leakage of Evans blue was more frequently seen on the nonstimulated side of the brain. In the eye there was leakage only on the control side except in PGI2-treated animals where 2 rabbits had bilateral leakage. The effect of sympathetic stimulation on the blood flow in the cerebrum and cerebellum in vasodilated animals seems to be small or absent if the blood pressure is normal. In the eye pronounced vasoconstriction occurs under these conditions. In acute arterial hypertension sympathetic stimulation protects both the cerebral and ocular barriers even under conditions of marked vasodilation.     

Effects of sympathetic stimulation on cerebral and ocular blood flow Modification by hypertension,hypercapnia, acetazolamide,PGI2 and papaverine

The effect of unilateral, electrical stimulatio of the cervical sympathetic chain in rabbits anesthetized with pentobarbital sodium and vasodilated by hypercapnia, acetazolamide, papaverine or PGI₂ was investigated to determine to what extent the sympathetic nerves to the brain and the eye cause vasoconstriction and prevent overperfusion in previously vasodilated animals. Evans blue was given as a tracer for protein leakage. Blood flow determinations were made with the labelled microsphere method during normotension and acute arterial hypertension. Hypertension was induced by ligation of the thoracic aorta and in some animals metaraminol or angiotensin was also used. Acetazolamide caused a two to threefold increase in cerebral blood flow (CBF) and hypercapnia resulted in a fivefold increase. CBF was not markedly affected by papaverine or PGI₂. In the choroid plexus, the ciliary body and choroid, papaverine and hypercapnia caused significant blood flow increases on the control side. Sympathetic stimulation induced a 12 % blood flow reduction in the brain in normotensive, hypercapnic animals. Marked effects of sympathetic stimulation at normotension were obtained under all conditions in the eye. In the hypertensive state the CBF reduction during sympathetic stimulation was moderate, but highly significant in hypercapnic or papaverine-treated animals as well as in controls. Leakage of Evans blue was more frequently seen on the nonstimulated side of the brain. In the eye there was leakage only on the control side except in PGI₂-treated animals where 2 rabbits had bilateral leakage. The effect of sympathetic stimulation on the blood flow in the cerebrum and cerebellum in vasodilated animals seems to be small or absent if the blood pressure is normal. In the eye pronounced vasoconstriction occurs under these conditions. In acute arterial hypertension sympathetic stimulation protects both the cerebral and ocular barriers even under conditions of marked vasodilation.     

Regional,segmental, and temporal heterogeneity of cerebral vascular autoregulation

Autoregulation of cerebral blood flow is heterogeneous in several ways: regional, segmental, and temporal. We have found regional heterogeneity of the autoregulatory response during both acute reductions and increases in systemic arterial presure. Changes in blood flow are less in brain stem than in cerebrum during decreases and increases in cerebral perfusion pressure. Segmental heterogeneity of autoregulation has been demonstrated in two ways. Direct determination of segmental cerebral vascular resistance indicates that, while small cerebral vessels (<200 μm in diameter) make a major contribution to autoregulation during acute increases in pressure between 80 and 100 mm Hg, the role of large cerebral arteries (>200 μm) becomes increasingly important to the autoregulatory response at pressures above 100 mm Hg. Measurement of changes in diameter of pial vessels has shown that, during acute hypotension, autoregulation occurs predominantly in small resistance vessels (<100 μm). Finally, there is temporal heterogeneity of autoregulation. Sudden increases in arterial pressure produce transient increases in blood flow, which are not observed under steady-state conditions. In addition, the blood-brain barrier is more susceptible to hypertensive disruption after rapid, compared to step-wise, increases in arterial pressure. Thus, when investigating cerebral vascular autoregulation, regional, segmental, and temporal differences in the autoregulatory response must be taken into consideration.     

Redistribution of cardiac output after hypothalamic lesions and hemorrhage

Summary The effects of ablation of the anteroventral portion of the third cerebral ventricle (AV3V) on cardiac output and distribution of regional blood flows were determined in conscious rats using 15 m radiolabelled microspheres before, and 2 min and 15 min after hemorrhage (n=11 for each group). Prior to hemorrhage, cerebral blood flow was significantly greater (216±30 ml/min/100 g), and cerebral vascular resistance was lower (0.60±0.09 mm Hg/ml/min/ 100 g) in rats with AV3V lesions than in controloperated animals (132 ±16 ml/min/100 g; 0.92+0.1 mm Hg/ml/min/100 g, respectively), while mean arterial blood pressure, cardiac output, and regional blood flow to other organs were similar. Less blood was withdrawn from animals with AV3V lesions (4.4 ±0.6 ml) than from control-operated rats (6.0±0.5 ml) to reduce blood pressure to approximately 65 mm Hg. Hemorrhage decreased cerebral vascular resistance in control-operated animals (0.52±0.07 mm Hg/ml/min/100 g), but not in rats with AV3V lesions (0.48±0.1 mm Hg/ml/min/100 g). Cardiac output and regional blood flow to other organs were similar between rats with AV3V lesions and controloperated animals following hemorrhage. These data demonstrate that electrolytic ablation of the AV3V region results in a selective increase in cerebral blood flow and decreased cerebral vascular resistance, but does not alter the reflex changes in regional blood flow evoked by hemorrhage.     

Short-Term Biomechanical Adaptation of the Rat Carotid to Acute Hypertension: Contribution of Smooth Muscle

The biomechanical adaptation of the arterial wall to hypertension has been studied extensively in recent years; however, the exact biomechanical contribution of vascular smooth muscle cells (VSMCs) during the adaptation process in conduit vessels is not known. We induced hypertension in 8 wk old Wistar rats by total ligation of the aorta between the two kidneys. Mean blood pressure increased from 92 ± 2 (mean ± SE)mm Hg to approximately 150 mm Hg. Rats were sacrificed 2, 4, and 8 d after surgery and the left common carotid artery was excised for analysis. Wall thickness increased by 18% in 8 d and the opening angle by 32% in 4 d. The elastic properties were measured under normal VSMC tone (i.e., the amount of VSMC tone under normal conditions also called basal VSMC tone or normal resting VSMC tone), under maximally contracted VSMC (NE, 5 × 10 ^-7mol/L) and under totally relaxed VSMC conditions (papaverine, 10^-4 mol/L). The most pronounced modifications were the changes in elastic properties related to normal VSMC tone. The functional contraction ratio at 100 mm Hg, defined as the relative contraction under normal conditions (normal VSMC tone), increased by 439% 4 d after the induction of hypertension. The total contraction capacity of the VSMC increased by 38% within 8 d. The changes in normal VSMC tone led to important changes in the mechanical properties of the arterial wall. Under normal VSMC conditions, compliance at mean pressure (148 mm Hg) increased by 159% within 8 d, whereas in the absence of VSMC tone, compliance did not increase significantly. We conclude that in conduit vessels, the VSMC, which is the sensing and effecting element of the adaptation process, is subjected to large-scale changes during the early phase of arterial adaptation to acute hypertension. © 2001 Biomedical Engineering Society. PAC01: 8719Rr, 8719Ff, 8719Uv, 8717-d     

Neurogenic modification of the vulnerability of the blood-brain barrier during acute hypertension in conscious rats

To study the possible influence of sympathetic adrenergic tone on the blood-brain barrier function during acute hypertension in conscious unrestrained rats with indwelling catheters in the aorta and a jugular vein the blood pressure was increased by noradrenaline, 6-hydroxydopamine (6-OHDA) or baclofen. One or 60 min later the rats were sacrificed and the extravasation of ¹²⁵I labelled albumin determined in the brain. After i. v. injection of noradrenaline the baroreceptor reflex will decrease the sympathetic tone whereas the blood pressure increase induced by the other two drugs is accompanied by an increased sympathetic activity. One minute after a corresponding rise in blood pressure the albumin content in the brain was considerably lower in rats given 6-OHDA than in those given noradrenaline. 60 min after the injection of 6-OHDA or baclofen the extravasation in the brain did not differ despite a considerably more rapid increase in pressure after 6-OHDA. Pretreatment with clonidine increased the blood-brain barrier dysfunction in rats given 6-OHDA but not in those given baclofen, probably because the slower rise in pressure facilitates myogenic autoregulation. It is concluded that neurogenic influences on vessel tone can modify the response of the blood-brain barrier during acute hypertension in conscious rats.     

Cerebrovascular sympathetic denervation and blood-brain barrier function in conscious rats

Electrical stimulation of the sympathetic nerves to the cerebrovascular bed enables the resistance vessels to better withstand a high blood pressure in terms of blood-brain barrier integrity. Sympathetic denervation could hence be expected to lead to a decrease in cerebrovascular tone and increased vulnerability of the blood-brain barrier. In the present study acute hypertension was induced in conscious unrestrained rats by administration of angiotensin or bicuculline. The albumin leakage into the brain, as studied by Evans blue-albumin and ¹²⁵I labelled human serum albumin. was not enhanced in acutely or chronically sympathectomized rats compared to controls.     

Effects of cervical sympathetic stimulation on cerebral and ocular blood flows during hemorrhagic hypotension and moderate hypoxia

The effect of cervical sympathetic stimulation upon regional blood flows was investigated in albino rabbits during graded hemorrhagic hypotension and mild to moderate hypoxic hypoxia. Regional blood flows were determined using labelled microspheres. Cerebral blood flow (CBF) decreased in response to progressive hypotension and increased considerably during hypoxia (100–200%). Unilateral sympathetic stimulation did not change the ipsilateral cerebral flow responses under either condition. There was a greater tendency to autoregulate down to lower blood pressures in deep than in superficial cerebral structures. During hypoxia cortical gray matter blood flow increased relatively more than did white matter blood flow. Blood flow in different parts of the eye decreased during hypotension and tended to increase during hypoxia. Unilateral sympathetic stimulation reduced tlow rates on the stimulated side (10–50% of control side) under both conditions. The vasoconstrictory effect upon retinal blood flow tended. however, to be less during hypoxia. Dural blood flow showed a poor autoregulation and also no consistent vasodilatory response upon hypoxia. Sympathetic stimulation had a very marked effect. The results suggest that the cervical sympathetic nerves do not have any appreciable effect upon cerebral circulation during profound hypotensive and moderate hypoxic states. Dural and most ocular blood flows seem. however. to be clearly affected by sympathetic stimulation even under these extreme conditions.     

Peripheral blood flows during colorectal distension in anaesthetised dogs

Distension of the descending colon elicits reflex cardiovascular responses, including increases in heart rate and arterial blood pressure. To study the relative contribution of vasoconstriction in individual vascular beds to this reflex response, experiments were performed on seven dogs anaesthetised with chloralose and instrumented with electromagnetic flowmeters around the superior mesenteric, the left renal and the left external iliac arteries. The colorectal portion of the intestine was distended at constant pressure (36.6 mm Hg, 4.9 kPa mean; range 25–50 mm Hg, 3.3–6.7 kPa) with warm Ringer solution for periods of 2 min. After a set of control distensions, the experiments were performed whilst the reflex rise in arterial pressure was prevented by removal of blood from the arterial tree. In control distensions arterial pressure increased by 11.3±1.5 mm Hg, 1.51±0.12 kPa (mean±SEM). In distensions at constant arterial pressure, peripheral blood flows were altered to different extents in the three territories studied: vascular resistance increased by 30.8±5.6% (P<0.01) in the mesenteric, by 4.1±1.5% (P<0.03) in the renal, and by 15.2±6.8% (NS) in the external iliac bed. We conclude that colorectal distension may reflect activation of a function-specific pathway of the sympathetic nervous system, which leads to much greater vasoconstriction in the splanchnic circulation than in renal or musculocutaneous circulations.     

Barrier and uptake mechanisms in the cerebrovascular response to noradrenaline.

Cerebral blood flow (CBF) was measured in 20 baboons by the intra-arterial xenon-133 injection method. The CBF responses to intra-arterial infusions of noradrenaline (NA) were determined. These responses were normally found to be vasodilator and mediated by beta adrenoreceptors. After infusion of substances blocking extraneuronal uptake of NA or opening of the blood-brain barrier, this vasodilation was either abolished or converted to an alpha-receptor mediated vasoconstriction. This suggests that normally the cerebral circulation is protected against noradrenergic vasoconstriction by mechanisms reducing the concentration of NA in the tunica media to below threshold for alpha-adrenoreceptor stimulation.     

The control of the circulation in skeletal muscle during arterial hypoxia in the rabbit

1. The effects of arterial hypoxia on muscle blood flow were examined in normal unanaesthetized rabbits in relation to simultaneously determined changes in cardiac output, arterial pressure and heart rate. Muscle blood flow was estimated from the difference between total limb flow (local thermodilution) and the estimated skin flow (using a calibrated heat conductivity method). The role of the arterial chemoreceptors and baro-receptors in the control of muscle blood flow was examined and the nature of the sympathetic efferent discharge analysed.2. In mild hypoxia (P(O2) > 35 mm Hg) in the rabbit, muscle blood flow did not change, although cardiac output increased. During moderate hypoxia (P(O2) 30-35 mm Hg) there was initial vasoconstriction in muscle, followed by a return to control values paralleling the changes in cardiac output. In severe arterial hypoxia (P(O2) < 30 mm Hg) the initial vasoconstriction was less marked, and during the ;steady state' there was a large vasodilatation and increase in muscle blood flow, at a time when the cardiac output was not elevated.3. The early vasoconstriction in arterial hypoxia is mediated mainly through sympathetic vasoconstrictor nerves as a result of strong arterial chemoreceptor stimulation.4. Increased secretion of adrenaline is an important factor in restoring muscle blood flow to control values during moderate arterial hypoxia, and in elevating the muscle blood flow above these values in severe hypoxia. The peripheral dilator (beta-) effects of adrenaline oppose the peripheral constrictor (alpha-) effects resulting from increased activation of sympathetic constrictor nerves during arterial hypoxia.     

Thyrotropin-releasing hormone (TRH) causes sympathetic activation and cerebral vasodilation in the rabbit

The effects of TRH on regional blood flow were studied in rabbits under urethane anesthesia. Four types of experiments were performed with the following results. (1) I.v. injection of 2 mg/kg b.w. TRH in animals with unilateral cervical sympathotomy caused a rise in mean arterial blood pressure from 10.0 +/- 0.5 to 13.3 +/- 0.5 kPa. Total cerebral blood flow, measured with labeled microspheres, increased from 75 +/- 5 to 126 +/- 16 g/min/100 g tissue on the intact side. There was a similar increase on the side with sympathotomy. The greatest increase, about 70%, was observed in cortical gray matter, caudate nucleus and thalamic region. There were marked reductions in blood flows in the spleen, gastric mucosa, skin and skeletal muscle. Mydriasis occurred on the side with an intact sympathetic supply. (2) I.v. infusion of 0.06 mg/kg b.w. per min TRH in animals with unilateral cervical sympathotomy and stabilized blood pressure increased total cerebral blood flow from 84 +/- 10 to 139 +/- 7 g/min/100 g. Blood flows to the masseter muscle, submandibular gland and facial skin but not to the eye or tongue were markedly reduced on the side with an intact sympathetic supply while little or no effect was observed on the side with sympathotomy. (3) Unilateral peripheral stimulation of the sympathetic chain at 1 Hz after bilateral sympathotomy caused a reduction in blood flows in the tongue, masseter muscle, submandibular gland and facial skin in animals with stabilized blood pressure. No potentiation of the stimulation effect was observed during TRH infusion. (4) The arteriovenous difference in oxygen saturation in the brain decreased from 39.1 +/- 2.8 to 26.4 +/- 3.7% after i.v. injection of 2 mg/kg b.w. TRH. The results indicate that TRH caused cerebral vasodilation in excess of that required by possible changes in cerebral metabolism. The vasoconstriction in the head region and the mydriasis was caused mainly by an increase in the activity of the cervical sympathetic nerves.     

Differences in cerebrovascular effects of phenoxybenzamine

Phenoxybenzamine differs in its effects on the blood supply in different vascular regions of the brain. It increases the blood supply in the vertebral arterial system whereas in the territory of the carotid arteries the blood flow is reduced. Meanwhile, phenoxybenzamine has a marked depriming effect on nervous regulation of the cerebral circulation. It depresses reflex responses of the intracranial vessels, reduces the changes in the cerebral blood flow induced by stimulation of the cervical sympathetic nerves, and has a protective effect after experimental disturbance of the cerebral circulation.Presented by Academician of the Academy of Medical Sciences of the USSR V. V. Zakusov.Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 79, No. 6, pp. 60–63, June, 1975.