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At least 631 records · Page 35Linked to original sources
PubMed1990

Disturbances in ocular sympathetic function and facial blood flow in unilateral migraine headache.

The relationship between thermographic asymmetry in various parts of the face and indices of ocular sympathetic outflow was examined in 80 patients with unilateral migrainous headache. Both during and between episodes of headache, the pupil on the symptomatic side dilated more slowly and less extensively in darkness than the opposite pupil, indicating that ocular sympathetic outflow was compromised in some patients. In such cases the upper forehead and orbital region were warmer on the symptomatic side during migraine. In contrast to these signs of a reduction in cervical sympathetic outflow, eyelid separation was greater on the symptomatic side in patients with headache on the side that was usually affected. During the headache-free interval no consistent thermographic asymmetry was detected and eyelid separation was similar on both sides. These findings suggest that extracranial vascular changes and ocular sympathetic dysfunction during migraine are secondary to activation of trigeminal-vascular reflexes or to antidromic release of vasoactive substances from trigeminal nerve terminals. A secondary deficit in the sympathetic pathway to the symptomatic pupil could also prevent the expression of an increase in sympathetic outflow during headache.

Adult↗
PubMed1976

Cerebral blood flow and brain function during hypotension and shock.

In conclusion, the reviewed results clearly suggest that vital functions of the brain -in spite of the well-developed autoregulatory mechanisms-are impaired during long-lasting hypovolemic and other shock conditions. The insufficiency of the cerebrocortical and hypothalamic regulatory mechanisms can contribute to the development of the irreversible shock. In other words, failure of the body suffering from shock to restore the homeostatic equilibrium can be attributed to the inadequacy of the central nervous servocontrol system. According to the available results, the regional cerebral microcirculatory defect develops through sludge formation. The unevenly distributed local brain damage could be the background of the functional impairment. The focal appearance suggest that, in addition to generalized (bloody borne) changes, local factors play an important role in the production of patchy ischemic areas in the brain.

Acetylcholine↗
PubMed1978

Relation between cholinergic and histaminergic components in reflex vasodilatation in the dog.

Previous studies have shown that phentolamine is able to reverse the reflex vasodilatation produced by transitory baroreceptor stimulation by blocking sympathetic, histaminergic, and cholinergic components. A direct anticholinergic action of phentolamine has never been described; however, since it is known that this drug is capable of inhibiting histamine release during the reflex vasodilatation, it is possible that its ability to block the cholinergic component of the reflex is related to the latter property. Therefore, this study was undertaken in an attempt to identify possible relationships between cholinergic and histaminergic components of the reflex vasodilatation. Accordingly, in mongrel dogs the gracilis muscle was isolated and perfused and then loaded with 14C-labeled histamine. A transitory systemic hypertension was induced by intravenous injection of norepinephrine; this produced a reflex vasodilatation, shown by the fall in perfusion pressure, which was accompanied by an increase of histamine release from the muscle. Vagal block induced by atropine pretreatment reduced the fall in perfusion pressure induced by the systemic hypertension and produced a reduction of histamine release during the vasodilatation. In another group of animals a vasodilatation in the perfused muscle was induced by injection of acetylcholine. This response was accompanied by an increase in histamine release from the gracilis muscle. Alpha-receptor blockade, which has been shown to inhibit histamine release, reduced this acetyl-choline-induced vasodilatation. These results, while confirming the participation of the cholinergic system in the reflex vasodilatation elicited by transitory stimulation of the arterial baroreceptors, seem to demonstrate that this component is mediated almost exclusively by histamine release.

Acetylcholine↗
PubMed1978

Mechanisms of vascular changes in skeletal muscle during asphyxia in the cat.

Vascular responses in the hindlimb muscles of anesthetized paralyzed cats during systemic asphyxia were studied. The cats were ventilated with 10% O2-10% CO2-80% N2 for 10-20 min periods, while blood flow to the skinned hindlimb was monitored (electromagnetic flowmeter). Mean arterial pressure rose and hindlimb flow typically fell during asphyxia, implying increased vascular resistance. After sympathetic denervation of the hindlimb, resistance increased in some groups of animals, and did not change in others during asphyxia. Functional adrenalectomy did not alter these response characteristics. Resistance also did not changes significantly if the control resistance was first increased to the predenervation level by electrically pacing the lumbar sympathetic chain. In contrast, pronounced vasodilatation occurred during asphyxia after blocking of the alpha receptors in the hindlimb (phenoxybenzamine) or after systemic catecholamine depletion (reserpine). We conclude that the vasoconstriction in innervated muscle during asphyxia was caused in part by increased discharge of sympathetic constrictor nerves to the muscle vasculature, with augmentation from a humoral alpha agonist of nonadrenal origin, possibly norepinephrine released from sympathetic nerves throughout the body.

Adrenal Medulla↗
PubMed1978

Mechanisms underlying overshoot dilation after sympathetic denervation.

(1) 30--60 sec after transection of the sympathetic chain, the diameter of both femoral artery and vein dilates to approximately 120% of the control diameter ('overshoot dilation'). Vessel diameter subsequently decreases and stabilizes with 5--10 min at a value of 108% of the original ('stabilized dilation'). (2) After treatment with norepinephrine-uptake-blocking drugs (cocaine, imipramine), the transient overshoot dilation is abolished and the diameter 1 min after denervation is identical to that at stabilized dilation. (3) It is proposed that (a) the stabilized rather than the transient overshoot dilation represents the loss of sympathetic control following following denervation and (b) the overshoot dilation reflects a transient decrease in transmitter concentration within the vessel wall, associated with a temporarily undiminished rate of neural reuptake activity persisting even in the absence of transmitter release.

Animals↗
PubMed1978

Cardiovascular changes in awake dogs caused by suddenly induced aortic hypertension.

Cardiovascular adaptation to the sudden inflation of a balloon in the descending aorta was investigated in intact awake, standing dogs. The balloon inflation raised pressure in the arterial bed proximal from the balloon. Initially, it lowered heart rate and cardiac output. After 4 sec, heart rate and cardiac output began increasing again and within the next 14 sec, these functions returned almost to the control values. The restoration of cardiac output was associated with a further rise in aortic pressure. These findings are consistent with the hypothesis that the prime circulatory adaptation to a hindrance to arterial flow is restoration of blood flow even though this requires a further elevation of arterial pressure. The demands of the tissues for an adequate supply of blood appear to override the inhibitory baroreceptor reflexes. The circulatory changes observed under conditions of attenuated parasympathetic inhibition and under conditions of attenuated beta-adrenergic stimulation were consistent with this interpretation. The findings suggest that arterial hyertension may involve a comparable adaptation of cardiac output in patients whose blood flow is hindered by pathologically narrowed arterioles.

Animals↗
PubMed1975

Development and maintenance of renal hypertension in normal and guanethidine sympathectomized rats.

The sympathetic nervous system has been postulated to play a role in the maintenance of renal hypertension. Permanent peripheral sympathectomy was performed by treating newborn rats for 21 days with guanethidine. Sympathectomy was confirmed by (1) relative insensitivity to tyramine, (2) lack of responsiveness to renal nerve stimulation, and (3) absence of dopamine-beta-hydroxylase immunofluorescence in renal blood vessels. Placement of a clip on the left renal artery led to the development of two-kidney renal hypertension. No differences were observed between the two-kidney renal hypertensive normal and sympathectomized rats; both had elevated plasma renin activity and vasodepression with angiotensin antagonists which were maintained up to nine weeks. Furthermore, in normal rats chronic beta-adrenergic blockade with propranolol caused no change in the development of the two-kidney renal hypertension. Similarly, no differences were seen in blood pressure, plasma renin activity, or response to antagonists between the one-kidney renal hypertensive (clip plus contralateral nephrectomy) normal and sympathectomized rats. Both showed sustained low renin hypertension up to 12 weeks. The absence of the peripheral sympathetic nervous system did not affect the development or maintenance of hypertension in either model of hypertension.

Animals↗