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At least 19 recordsLinked to original sources
PubMed1977

Cardiopulmonary baroreflexes: effects of pulmonary congestion and edema.

Systemic vasodepressor reflexes were initiated in pump-oxygenator perfused dogs by separately pressurizing the pulmonary vessels and the left cardiac chambers. Pulmonary vascular pressurization caused transient systemic vasodilation of a magnitude proportional to stimulus pressure over the range 0-65 cmH2O. The sensitivity of this reflex was sigificantly less than that of the left heart baroreflex. Mild pulmonary edema produced by a period of sustained congestion, and moderate edema, caused by sustained congestion in the presence of alloxan, had no discernible effect on systemic vasomotor tone or on subsequent pulmonary vascular baroreflexes. By comparison of these results with earlier studies in similar preparations I concluded that pulmonary arterial baroreflexes could alone produce the response obtained by pressurizing the entire pulmonary vascular bed. Although it was anticipated that type-J, irritant, and stretch receptors would be affected by congestion, no systemic vascular effects attributable to them were seen.

Animals↗
PubMed1975

An adrenergic component of the nervous apparatus of the aortic reflexogenic zone.

The structural organization of the adrenergic (sympathetic) component of the autonomic innervation of the depressor zone of the cat aortic arch was studied by luminescence microscopy of the catecholamines. A terminal adrenergic plexus, branching extensively in the connective-tissue basis of the depressor area of the aortic arch, was discovered. The participation of vessels supplying blood to the depressor area was established. Adrenergic neurons were found in the territory of the depressor zone of the aortic arch. It is postulated that the adrenergic component of the depressor zone of the aortic arch participates in the peripheral mechanism of the regulatory effects of the sympathetic nervous system on the baroreceptor apparatus.

Animals↗
PubMed1975

[Kidney in heart failure (author's transl)].

The adaptability of the kidney in heart-failure is restricted. This is due to a sympathetically mediated renal vasoconstriction, forming part of a sympathetically induced general rearrangement of haemodynamics. This is reflected in a rise of the total peripheral vascular resistance and of the right auricular pressure and can be normalized to a large extent by sympathetic gamma-blockade. The renal vasoconstriction reduces the glomerular filtration rate and, thus, the tubular sodium load. Simultaneously, possibly by the same sympathetic stimulus, more renin is liberated from the juxtaglomerular apparatus. This increases the production of angiotensin and in turn, raises the production of aldosterone. By the combined effect of the reduced glomerular sodium load and aldosterone-mediated increase in tubular reabsorption of sodium, sodium and water will be retained in the body. During the night-rest the load on the circulatory system diminishes. In the early stages of heart-failure this emergency circulatory reaction, therefore, subsides and the rise of the renal fraction of the cardiac output leads to the excretion of the retained fluid and is the basis of nocturia.

Blood Proteins↗
PubMed1976

Relation of efferent impulse activity in splenic nerve to reflexly induced reactions of resistance and capacitance vessels to spleen.

Constrictory responses of splenic resistance vessels arising under pressor reflexes were abolished by hexonium (2 mg/kg) as well as the high amplitude (above 15 muV) impulses in sympathetic splenic nerves. Constrictory and dilatory responses of splenic capacitance vessels were preserved after administration of the same dose of hexonium and correlated as to the directivity with the changes of the low amplitude (15 muV and lower) impulsation in the splenic nerve.

Animals↗
PubMed1977

Dopamine receptors in the femoral vascular bed of the dog as mediators of a vasodilator and sympathoinhibitory effect.

ET 495 and apomorphine, injected in small doses (0.1--1 microng/kg) into the femoral artery, induced a dose-dependent increase in femoral blood flow. This dilator effect was abolished by section of the ipsilateral femoral nerve and sciatic nerve, transection of the spinal cord, alpha-adrenoceptor blockade, ganglionic blockade and guanethidine. In addition, the increase in blood flow was inhibited by intravenous administration of haloperiol (2 mg/kg i.v.) or pimozide (2 mg/kg i.v.) and by injection of small doses (10--50 microng/kg) of these drugs into the femoral artery. It was concluded that a dopaminergic component located in the femoral vascular bed of the dog may be involved in the local vasodilator and sympathoinhibitory effect of apomorphine and ET 495.

Animals↗
PubMed1977

Electrical activity in sympathetic fibres to hind limb muscles of the cat produced by hypothalamic stimulation.

Electrical stimulation of the "Defence Area" of the hypothalamus in anaesthetized cats was accomplished by stereotaxic placement of bipolar stainless steel electrodes; the spinal cord was sectioned at L4. The muscle blood flow in one hind limb was recorded with an electromagnetic flowmeter. Increases of between 100% and 300% were observed during hypothalamic stimulation. Electroneurographic recordings from small nerve filaments supplying tibialis anterior muscle revealed two populations of neurones whose activity was abolished by lumbar sympathectomy. It appears that the increased blood flow in skeletal muscle during stimulation of the hypothalamic "Defence Area" is brought about by a simultaneous inhibition of vasoconstrictor activity and increase in cholinergic vasodilator discharge.

Animals↗
PubMed1977

Coupling of signals to brown fat: alpha- and beta-adrenergic responses in intact rats.

The present study examines the effects of alpha- and beta-adrenergic antagonists (phentolamine and propranolol, respectively) and agonists (phenylephrine, isoproterenol) on the neurally induced temperature changes and membrane potentials of interscapular brown adipocytes. These studies, performed in vivo with anesthetized rats, indicate that both alpha- and beta-adrenergic components are associated with the biphasic temperature changes observed following sympathetic activation of the tissue. Specifically, the initial transient temperature decrease seen after brown fat stimulation appeared to reflect vasoconstriction mediated primarily via alpha-receptors, while the subsequent rise in tissue temperature was associated primarily (though perhaps not entirely) with beta-adrenergic pathways. In contrast, the redistribution of ions across the membrane of the brown adipocyte, a phenomenon manifested as a membrane depolarization, was elicited by phenylephrine (an alpha-agonist) as well as by isoproterenol (a beta-agonist), with the magnitude of the isoproterenol-induced depolarization being comparable to that of the phenylephrine-induced effect.

Adipose Tissue, Brown↗
PubMed1975

Adrenergic mechanisms in the rabbit ear artery. A review.

A number of factors which have been implicated in the response of the rabbit ear artery to adrenergic agents and stionstriction in the arterial smooth muscle; (b) the interrelationship between the intramural distribution of sympathetic nerves and muscle, and the influence of uptake and enzymic inactivation on the response to norepinephrine, and (c) the influence of presynaptic adrenergic and cholinergic receptors on the rwsponse to sympathetic nerve stimulation.

Acetylcholine↗
PubMed1977

Uptake of 3H-norepinephrine in rabbit mesenteric blood vessels.

The uptake of traited norepinephrine in isolated rabbit mesoduodenal blood vessels was measured. Neuronal uptake was estimated utilizing the inhibitory effect of cocaine, and expressed on the basis of wet and dry tissue weights as well as circumferential area of the vascular wall. This area was presumed to approximate the area of the adrenergic nerve terminal plexus. The wet weight of smaller tissues was apt to be underestimated due to excessive drying during weighing; dry weight was more consistent over a wide range of tissue size. Either on the basis of weight or circumferential are, neuronal uptake in arteries increased as the diameter diminished, but uptake was practically constant in all segments of the veins. Arterial uptake per unit circumferential area was greater than in the accompanying veins, but this was not necessarily the case when uptake was expressed per unit weight. Neuronal norepinephrine may be a useful index of adrenergic nerve density. On this basis it is suggested that the adrenergic neural vasoconstriction increases with decrease in diameter of both arteries and veins in rabbit mesoduodenum.

Adrenergic Fibers↗
PubMed1975

Effect of sympathetic nerve stimulation on cerebral and cephalic blood flow in dogs.

The effect of sympathetic stimulation (stellate ganglion) on dog cerebral and cephalic blood flows was studied via a cervical or a thoracic approach to the stellate ganglion under sodium pentobarbital or chloralose anesthesia. Two different stimulation voltages (3v and 5v) of monophasic pulses were applied for 1 minute. Venous outflow was measured at the confluence of the sagittal, straight and lateral sinuses with the lateral sinuses occluded and with them patent. When the lateral sinuses were occluded, stellate ganglion stimulation resulted in a marked decrease in common carotid blood flow to 38 plus or minus 2.5% (SE) of control and dilation of the ipsilateral pupil, but cerebral blood flow did not change. Similar effects were observed with each of the anatomic approaches, anesthetics, and voltages used and in dogs with low cerebral vascular tone induced by hypercapnia. When the lateral sinuses were kept patent, sympathetic nerve stimulation decreased the venous outflow to 89 plus or minus 2.9% of control and clamping both of the external jugular veins increased venous outflow to 120 plus or minus 2.7% of control. When the lateral sinuses were kept patent and the extracranial venous pressure was increased by clamping both of the external jugular veins, the decrease in venous outflow in response to sympathetic stimulation was even larger: venous outflow was only 65 plus or minus 4.9% of control. We conclude that stimulation of the stellate ganglion has no effect on the cerebral vasculature. Sympathetic stimulation significantly decreases venous blood flow measured at the confluence of the sinuses only when communications between the intracranial and extracranial venous vasculatures are present.

Animals↗