pituitrin and Constriction--Pathologic

Ventricular failure is accompanied by a series of neurohormonal responses that result in vasoconstriction. Vasoconstriction develops and is mediated by norepinephrine, angiotensin II, and vasopressin. Vasoconstriction maintains blood pressure but contributes to deterioration in ventricular function. Baroreceptor dysfunction contributes to the syndrome by failing to ameliorate the sympathetic overstimulation. Drug therapy has historically included positive inotropes until recent data suggested that these drugs contributed to worsened survival. The role of digitalis glycosides in patients with ventricular failure who are in normal sinus rhythm remains a subject of scrutiny. Thus far, no long-term oral positive inotrope has replaced digoxin. Vasodilator therapy and interference with the neurohormonal response have become the major approaches to pharmacologic management of ventricular failure. Angiotensin-converting enzyme inhibitors have shown convincingly that they improve survival, slow the course of disease progression, and block the neurohormonal response to ventricular failure. New treatments for ventricular failure must be directed at long-term gain rather than short-term hemodynamic results.

Topics: Angiotensin II; Angiotensin-Converting Enzyme Inhibitors; Constriction, Pathologic; Digoxin; Heart Failure; Heart Ventricles; Hemodynamics; Humans; Norepinephrine; Survival Rate; Vasodilator Agents; Vasopressins

Topics: Adrenal Medulla; Animals; Autonomic Fibers, Preganglionic; Blood Pressure; Constriction, Pathologic; Electric Stimulation; Heart Rate; Male; Myocardial Contraction; Phenylephrine; Rats; Rats, Wistar; Receptor, Cannabinoid, CB1; Vasopressins

We studied the role of cardiac and arterial baroreceptors in the reflex control of arginine vasopressin (AVP) and renin secretion during graded hypotension in conscious dogs. The dogs were prepared with Silastic cuffs on the thoracic inferior vena cava and catheters in the pericardial space. Each experiment consisted of a control period followed by four periods of inferior vena caval constriction, during which mean arterial pressure (MAP) was reduced in increments of approximately 10 mmHg. The hormonal responses were measured in five dogs under four treatment conditions: 1) intact, 2) acute cardiac denervation (CD) by intrapericardial infusion of procaine, 3) after sinoaortic denervation (SAD), and 4) during combined SAD+CD. The individual slopes relating MAP to plasma AVP and plasma renin activity (PRA) were used to compare the treatment effects using a 2 x 2 factorial analysis. There was a significant (P < 0.01) effect of SAD on the slope relating plasma AVP to MAP but no effect of CD and no SAD x CD interaction. In contrast, the slope relating PRA and MAP was increased (P < 0.05) by SAD but was not affected by CD. These results support the hypothesis that stimulation of AVP secretion in response to graded hypotension is primarily driven by unloading arterial baroreceptors in the dog.

Topics: Animals; Arginine Vasopressin; Arteries; Blood Pressure; Constriction, Pathologic; Denervation; Dogs; Female; Heart Conduction System; Hemodynamics; Hypotension; Male; Pressoreceptors; Reference Values; Renin; Sinus of Valsalva; Vasopressins; Vena Cava, Inferior

Extracellular single-unit recording experiments were done in pentobarbital sodium-anesthetized rats to investigate the effects of electrical stimulation of afferent renal nerves (ARN) and renal vein (RVO) or artery (RAO) occlusion on the discharge rate of putative arginine vasopressin (AVP) and oxytocin (Oxy) neurons in the paraventricular nucleus of the hypothalamus (PVH). PVH neurons antidromically activated by electrical stimulation of the neurohypophysis were classified as either AVP or Oxy secreting on the basis of their spontaneous discharge patterns and response to activation of arterial baroreceptors. Ninety-eight putative neurosecretory neurons in the PVH were tested for their response to electrical stimulation of ARN: 44 were classified as putative AVP and 54 as putative Oxy neurons. Of the 44 AVP neurons, 52% were excited, 7% were inhibited, and 41% were nonresponsive to ARN stimulation. Of the 54 Oxy neurons, 43% were excited, 6% inhibited, and 51% were not affected by ARN. An additional 45 neurosecretory neurons (29 AVP and 16 Oxy neurons) were tested for their responses to RVO and/or RAO. RVO inhibited 42% of the putative AVP neurons and 13% of the putative Oxy neurons. On the other hand, RAO excited 33% of the AVP and 9% of the Oxy neurons. No AVP or Oxy neurons were found to be excited by RVO or inhibited by RAO. These data indicate that sensory information originating in renal receptors alters the activity of AVP and Oxy neurons in the PVH and suggest that these renal receptors contribute to the hypothalamic control of AVP and Oxy release into the circulation.

Topics: Afferent Pathways; Animals; Arterial Occlusive Diseases; Cardiovascular System; Constriction, Pathologic; Electric Stimulation; Kidney; Male; Neurons; Neurosecretory Systems; Oxytocin; Paraventricular Hypothalamic Nucleus; Rats; Rats, Wistar; Renal Artery; Renal Veins; Vascular Diseases; Vasopressins

Patients who smoke have higher complication rates than nonsmokers following many surgical procedures. It is not known if the adverse effects of smoking are caused by a nicotine effect or by some other potentially harmful agents that exist in tobacco smoke. It is also not known if these vasoactive effects are mediated through sympathetic nerve fibers (via nicotinic receptors in ganglia) or through elevated circulating levels of vasoactive hormones. We designed a 5-day protocol to measure relative blood flow both before and after a digital sympathetic block in the digits of subjects who were regular smokers following both smoking and wearing of a transdermal nicotine patch. Suitable pulse/wave tracings were recorded on 23 subjects. We also measured serum levels of nicotine, cotinine, vasopressin, norepinephrine, epinephrine, dopamine, and carboxyhemoglobin on each test day. Data for these serum levels were available in 30 test subjects. Digital sympathetic block had a significant beneficial effect in reversing the decreased digital blood flow that occurred after smoking (and also with use of the nicotine patch), despite the elevated circulating levels of vasopressin and norepinephrine seen with smoking. The vasoactive effects of smoking are probably due to the nicotinic effects on sympathetic fibers at the ganglionic levels.

Topics: Adult; Aged; Autonomic Nerve Block; Carboxyhemoglobin; Catecholamines; Constriction, Pathologic; Cotinine; Female; Fingers; Humans; Male; Middle Aged; Nicotine; Photoplethysmography; Receptors, Nicotinic; Smoking; Sympathetic Fibers, Postganglionic; Vasopressins

Continuous infusion of IV vasopressin have been widely used to lower portal pressure and reduce bleeding from esophageal varices. Recently, the combination of vasopressin and nitroglycerin has been noted to be superior to vasopressin alone. This is due to the ability of nitroglycerin to reduce the detrimental effects of vasopressin while preserving its beneficial effects. In September 1989 the authors initiated a protocol in the medical intensive care unit of a large university teaching center that directed caregivers in the simultaneous use of vasopressin and nitroglycerin for use in variceal bleeding.. To determine whether the protocol was being used correctly and whether the addition of nitroglycerin produced the desired cardiovascular effects.. Nineteen patients (25 separate episodes) assigned to the vasopressin/nitroglycerin protocol were monitored retrospectively over a 20-month period for a total of 1068 hours of vasopressin/nitroglycerin infusion. Twenty-four patients received nitroglycerin at 10 to 50 micrograms per minute, 13 at 50 to 100 micrograms per minute and 6 at 100 to 400 micrograms per minute.. Nitroglycerin dosage was not advanced appropriately in 78% of episodes despite evidence of bradycardia, hypertension and peripheral vasoconstriction.. Revision of the protocol, giving additional guidance to clinicians on assessment and nitroglycerin advancement, was necessary and was accomplished.

Topics: Bradycardia; Clinical Protocols; Constriction, Pathologic; Drug Monitoring; Drug Therapy, Combination; Esophageal and Gastric Varices; Gastrointestinal Hemorrhage; Heart Rate; Hemodynamics; Humans; Hypertension; Infusions, Intravenous; Nitroglycerin; Nursing Assessment; Nursing Evaluation Research; Nursing Records; Patient Care Planning; Practice Patterns, Physicians'; Retrospective Studies; Vasopressins

We determined, in urethan-anesthetized rabbits, whether pharmacological alteration of neuronal function in the ventrolateral medulla oblongata, including the A1 area, and in the nucleus tractus solitarii (NTS), alters plasma adrenocorticotropic hormone (ACTH) and vasopressin and whether inhibition of neuronal function in the ventrolateral medulla impairs the secretion of ACTH normally observed in response to hemorrhage or constriction of the inferior vena cava. We also tested whether the increase in plasma ACTH and vasopressin after pharmacological inhibition of neuronal function in the NTS is dependent on a pathway that synapses in the A1 area of the ventrolateral medulla. Activation of the A1 area with bicuculline increased both ACTH and vasopressin. Inhibition of the NTS with muscimol increased levels of both hormones, as did hemorrhage and constriction of the inferior vena cava. Inhibition of neuronal function within the A1 area with muscimol eliminated the secretion of vasopressin but did not significantly alter the secretion of ACTH, obtained by injecting muscimol into the NTS. Injection of muscimol into the A1 area eliminated the secretion of both ACTH and vasopressin in response to constriction of the inferior vena cava and, in the case of vasopressin, in response to hemorrhage. Although hemorrhage-initiated secretion of ACTH was significantly reduced by injection of muscimol into the A1 area, it was not completely eliminated by these injections or by injections of muscimol into a more rostrocaudally extensive region of the medulla oblongata. We conclude that the net output from the NTS tonically inhibits secretion of both ACTH and vasopressin, reflecting tonic baroreceptor tone. For vasopressin, the pathway from the NTS to the hypothalamus is dependent on a synapse in the A1 area. For ACTH, there are pathways to the hypothalamus that do not synapse in the A1 area, but neurons in this region do have an excitatory effect on secretion of ACTH.

Topics: 2-Amino-5-phosphonovalerate; Adrenocorticotropic Hormone; Animals; Cardiovascular System; Constriction, Pathologic; Hemorrhage; Hypercapnia; Hypoxia; Injections; Medulla Oblongata; Muscimol; Rabbits; Stimulation, Chemical; Vasopressins; Vena Cava, Inferior

The relative roles of cardiopulmonary and sinoaortic baroreceptors in the regulation of vasopressin and corticosteroid release were evaluated in conscious dogs. The dogs were prepared with inflatable cuffs around either the ascending aorta, proximal to the brachiocephalic trunk, or the pulmonary artery. Inflation of the cuffs was adjusted to cause a reduction of mean systemic arterial pressure (MAP) of 0, 5, 10, 20, or 30% of control for 1 h in separate experiments. In spite of the profound systemic hypotension caused by constriction of the ascending aorta, plasma vasopressin failed to increase and corticosteroids increased only in response to a 30% decrease in MAP. In contrast, a 5% reduction in MAP during pulmonary arterial constriction increased plasma vasopressin and corticosteroid concentrations significantly. The apparent paradox in these results is correlated with different effects of the two maneuvers on left atrial pressure. Left atrial pressure increased dose dependently during inflation of the ascending aortic cuff but decreased during inflation of the pulmonary arterial cuff. In contrast, graded inflation of the pulmonary arterial cuff caused dose-dependent increases in right atrial pressure, plasma vasopressin, and corticosteroids. Therefore, we conclude that powerful inhibitory signals, arising from the left heart, can inhibit vasopressin and hypotension release in response to systemic hypotension.

Topics: Adrenal Cortex Hormones; Animals; Aorta; Constriction, Pathologic; Dogs; Female; Heart Conduction System; Hypotension; Male; Pressoreceptors; Pulmonary Artery; Vasopressins

The purpose of this study was to test the role of carotid arterial mechanoreceptors in the control of vasopressin secretion in conscious 6- to 7-wk-old lambs. Bilateral carotid occlusion decreased lingual arterial pressure and stimulated reflex increases in heart rate and femoral arterial blood pressure but did not significantly alter plasma concentrations of vasopressin. Acute vagosympathetic blockade, produced by injection of 2% lidocaine onto the vagosympathetic trunks, did not significantly alter heart rate or blood pressure but did stimulate a slow increase in plasma vasopressin concentration, suggesting that afferent vagal fibers tonically inhibit vasopressin secretion. Bilateral carotid occlusion after vagosympathetic blockade stimulated a brisk increase in plasma vasopressin that was larger than the response to vagosympathetic blockade alone. These results suggest that vasopressin secretion in lambs is partially controlled by arterial mechanoreceptors in the carotid sinus and by extracarotid receptors with vagosympathetic afferent fibers.

Topics: Analysis of Variance; Animals; Blood Pressure; Carotid Arteries; Carotid Artery Diseases; Constriction, Pathologic; Heart Rate; Lidocaine; Sheep; Vasopressins

Five patients given vasopressin by infusion to reduce portal hypertension developed signs of cutaneous gangrene 18-24 hours after the start of the infusion. Four patients were treated by application of local dressings; in three cases the lesions healed, but the fourth patient died from variceal haemorrhage. The remaining patient required split skin grafting but died 48 hours after operation. The mechanism of this effect of vasopressin is not clear, but if local blanching of the skin is noted during infusion the catheter should be flushed immediately with a vasodilator in an effort to counteract the drug's vasoconstrictor effect.

Topics: Adult; Aged; Constriction, Pathologic; Esophageal and Gastric Varices; Female; Gangrene; Gastrointestinal Hemorrhage; Humans; Hypertension, Portal; Infusions, Parenteral; Male; Skin; Vasopressins

This report describes a case of massive gastric hemorrhage, initially controlled by selective arterial vasopressin infusion. Infusion was followed by extensive necrosis of the gastric wall which necessitated subtotal gastrectomy. Gastric necrosis following arterial infusion is rare and in this case appears to be due to migration of the infusion catheter into a peripheral branch of the left gastric artery in a patient whose gastric circulation had been compromised by prior surgery. The complications related to the use of arterial infusion for the control of gastric hemorrhage are discussed and the literature is reviewed.

Topics: Angiography; Catheters, Indwelling; Constriction, Pathologic; Female; Gastrectomy; Gastric Mucosa; Gastrointestinal Hemorrhage; Humans; Infarction; Infusions, Intra-Arterial; Middle Aged; Necrosis; Stomach; Vasopressins