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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a previous study (Wang, W., J. S. Chen, and I. H. Zucker. Circ. Res. 68: 1294-1301, 1991), we showed a depression in baroreflex gain in dogs with pacing-induced heart failure. This depression was not accompanied by a decrease in the central gain (carotid sinus nerve stimulation vs. renal nerve activity). These previous experiments were carried out on animals that were vagotomized and aortic denervated. In the present study these experiments were repeated, and the data were analyzed both in the intact and vagotomized state. Dogs were cardiac paced at 250 beats/min until heart failure was noted. Sham dogs were used as controls. The carotid sinuses were isolated, and the aortic nerves were sectioned. Activity from a renal sympathetic nerve (RSNA) was recorded with arterial pressure and carotid sinus pressure (CSP) during bilateral step increases in CSP from 25 to 300 mmHg. Mean arterial pressure (MAP) and RSNA responses to carotid sinus pressurization and to carotid sinus nerve stimulation were tested before and after bilateral vagotomy, and curves describing these relationships were constructed. Before vagotomy, the peak response relating stimulation frequency to MAP was significantly depressed in dogs with heart failure (-18.3 +/- 4.7 vs. -37.0 +/- 2.2%, P < 0.001). In addition, the CSP-MAP curves were depressed in dogs with heart failure. Frequency-RSNA curves were not altered in heart failure. There were no significant changes in the baroreflex gain responses to pressurization or electrical stimulation after vagotomy in either sham or heart failure groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of vagotomy on the baroreflex sensitivity in anesthetized dogs with experimental heart failure. 823 19

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.
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PMID:Characterization of baroreflex impairment in conscious dogs with pacing-induced heart failure. 823 15

It has been shown that alcohol administration causes baroreceptor reflex inhibition. The site of action of alcohol could reside anywhere within the baroreceptor reflex arc. Therefore, the goal of this study was to determine the effects of acute administration of alcohol on carotid sinus baroreceptor discharge characteristics. In pentobarbital-anesthetized dogs, the carotid sinus was isolated and perfused. Single unit baroreceptor discharge was recorded from the carotid sinus nerve along with carotid sinus diameter using sonomicrometry. Carotid sinus pressure-baroreceptor discharge and carotid sinus pressure-diameter curves were constructed. Perfusion of the carotid sinus with alcohol (100 mmol/L) significantly decreased the pressure threshold from 91.1 +/- 2.8 to 86.4 +/- 2.9 mm Hg (p < 0.05) and increased the peak discharge rate from 45.8 +/- 3.4 to 52.8 +/- 3.6 spikes per second (p < 0.01). The same phenomenon was seen during perfusion of the carotid sinus with acetaldehyde (2.5 mmol/L) but was not seen during perfusion with acetate (2.5 mmol/L). During perfusion of the carotid sinus with alcohol, the carotid sinus pressure-carotid sinus diameter relation did not change. The baroreceptor sensitization induced by alcohol is not an endothelium-dependent mechanism, because endothelial denudation did not block this alcohol-induced effect. Measurement of the duration of postexcitatory depression of carotid sinus baroreceptors, which is related to Na+,K(+)-ATPase activity, showed that perfusion of the carotid sinus with alcohol or acetaldehyde significantly reduced the duration of postexcitatory depression, indicating that the alcohol- and acetaldehyde-induced effect on baroreceptor discharge is most likely mediated by an inhibition of Na+,K(+)-ATPase.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acute alcohol administration stimulates baroreceptor discharge in the dog. 849 3

It is well known that the baroreceptor reflex is blunted in the heart failure state. However, the mechanisms for this depression are not well understood. The aim of the present study was to determine if carotid sinus nerve fiber density is decreased in the heart failure state. Experiments were carried out in pacing-induced heart failure and normal dogs. The carotid sinus nerve (CSN) was dissected and the CSN discharge responses to changes in arterial pressure with nitroglycerin (25 micrograms/kg, i.v.) or phenylephrine (10 micrograms/kg, i.v.) were recorded. Thereafter, the carotid sinus area was isolated and perfused with oxygenated Krebs-Henseleit solution. Carotid sinus baroreceptor single-unit activity was recorded and a carotid sinus pressure-discharge curve was constructed using either static or pulsatile pressure. Finally, the carotid sinus nerve was removed and fixed at its in situ length in 3% glutaraldehyde. The fixed carotid sinus nerve was cut transversely in 0.5-1.0-micron sections and prepared for electron microscopy. A photographic collage of the CSN was then analyzed at 4000 x magnification. The total number, diameter and area of myelinated and non-myelinated fibers were measured with a digitizer and the density and diameter distribution were calculated. Carotid sinus nerve discharge responses to change in arterial pressure were significantly blunted in dogs with pacing-induced heart failure. Furthermore, single-unit baroreceptor responses to both static and pulsatile pressurization were markedly depressed in dogs with heart failure. However, there was no change in either fiber density or the ratio of myelinated fibers to unmyelinated fibers in the carotid sinus nerve in heart failure. In addition, there was no change in the distribution of either fiber diameter or cross-sectional area in the carotid sinus nerve in dogs with heart failure. These data indicate that there is no significant change in the number or type of fibers in the CSN of dogs with heart failure. Therefore, the depressed baroreceptor reflex in heart failure is not due to structural changes in fibers of the CSN. The depressed baroreflex is most likely due to desensitization of individual baroreceptors.
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PMID:Depressed baroreflex in heart failure is not due to structural change in carotid sinus nerve fibers. 886 92

The physicochemical properties of water enable it to act as a solvent for electrolytes, and to influence the molecular configuration and hence the function--enzymatic in particular--of polypeptide chains in biological systems. The association of water with electrolytes determines the osmotic regulation of cell volume and allows the establishment of the transmembrane ion concentration gradients that underlie nerve excitation and impulse conduction. Fluid in the central nervous system is distributed in the intracellular and extracellular spaces (ICS, ECS) of the brain parenchyma, the cerebrospinal fluid, and the vascular compartment--the brain capillaries and small arteries and veins. Regulated exchange of fluid between these various compartments occurs at the blood-brain barrier (BBB), and at the ventricular ependyma and choroid plexus, and, on the brain surface, at the pia mater. The normal BBB is relatively permeable to water, but considerably less so to ions, including the principal electrolytes Brain fluid regulation takes place within the context of systemic fluid volume control, which depends on the mutual interaction of osmo-, volume-, and pressure-receptors in the hypothalamus, heart and kidney, hormones such as vasopressin, renin-angiotensin, aldosterone, atriopeptins, and digitalis-like immunoreactive substance, and their respective sites of action. Evidence for specific transport capabilities of the cerebral capillary endothelium, for example high Na+K(+)-ATPase activity and the presence at the abluminal surface of a Na(+)--H+ antiporter, suggests that cerebral microvessels play a more active part in brain volume regulation and ion homoeostasis than do capillaries in other vascular beds. The normal brain ECS amounts to 12-19% of brain volume, and is markedly reduced in anoxia, ischaemia, metabolic poisoning, spreading depression, and conventional procedures for histological fixation. The asymmetrical distributions of Na+ K+ and Ca2+ between ICS and ECS underlie the roles of these cations in nerve excitation and conduction, and in signal transduction. The relatively large volume of the CSF, and extensive diffusional exchange of many substances between brain ECS and CSF, augment the ion-homeostasing capacity of the ECS. The choroid plexus, in addition to secreting CSF principally by biochemical mechanisms (there is an additional small component from the extracellular fluid), actively transports some substances from the blood (e.g. nucleotides and ascorbic acid), and actively removes others from the CSF. In contrast with CSF secretion, CSF reabsorption is principally a biomechanical process, passively dependent on the CSF-dural sinus pressure gradient. Pathological increases in intracranial water content imply development of an intracranial mass lesion. The additional water may be distributed diffusely within the brain parenchyma as brain oedema, as a cyst, or as increase in ventricular volume due to hydrocephalus. Brain oedema is classified on the basis of pathophysiology into four categories, vasogenic, cytotoxic, osmotic and hydrostatic. The clinical conditions in which brain oedema presents the greatest problems are tumour, ischaemia, and head injury. Peritumoural oedema is predominantly vasogenic and related to BBB dysfunction. Ischaemic oedema is initially cytotoxic, with a shift of Na+ and CI- ions from ECS to ICS, followed by osmotically obliged water, this shift can be detected by diffusion-weighted MRI. Later in the evolution of an ischaemic lesion the oedema becomes vasogenic, with disruption of the BBB. Recent imaging studies in patients with head injury suggest that the development of traumatic brain oedema may follow a biphasic time course similar to that of ischaemic oedema. Hydrocephalus is associated in the great majority of cases with an obstruction to the circulation or drainage of CSF, or, occasionally, with overproduction of CSF by a choroid plexus papilloma. In either case, the consequence is a ris
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PMID:The normal and pathological physiology of brain water. 907 71


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