Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether or not the blockade of sympathetic efferents by epidural anaesthesia blunts the normal increase in plasma renin activity in response to hypotension, we assessed the effect of hypotensive thoracic epidural anaesthesia with widespread sympathetic blockade on plasma renin activity. Plasma renin activity and vasopressin concentration, arterial pressure, and serum osmolality were measured in 17 patients before and after random epidural injection of either 6.7 ml of 0.75% bupivacaine (n = 7) or the same volume of saline (n = 10). As an indicator for efferent sympathetic drive, skin temperatures were measured on the hand and foot. A decrease in mean arterial pressure by more than 25% of baseline values was prospectively defined as hypotension requiring intervention. Thoracic epidural anaesthesia induced a decrease in mean arterial pressure of 24 mmHg (range 16-47) from 101 mmHg to 77 mmHg (P less than 0.001 vs. saline). Despite hypotension, plasma renin activity remained unchanged [medians 2.9 ng ml-1 h-1 (0-9.1) vs. 3.4 ng ml-1 h-1 (0-13.8)]. In contrast, vasopressin concentrations increased from a median of 3.8 pg ml-1 (0.5-8.2) to 6.0 pg ml-1 (4.2-33.6; P = 0.025). Both hand and foot skin temperatures increased significantly indicating widespread extent of sympathetic blockade. Serum osmolality did not change. With epidural saline, variables remained unchanged. Thus, during hypotension induced by widespread attenuation of efferent sympathetic drive through thoracic epidural anaesthesia, renin activity did not change, whilst vasopressin concentrations increased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sympathetic blockade by thoracic epidural anaesthesia suppresses renin release in response to hypotension, but activates the vasopressin system. 173 99

We examined the responses of vasopressin-neurons (VP-neurons) and oxytocin-neurons (OT-neurons) to acute salt-loading in a group of conscious rats (CON, n = 8) and rats under sodium pentobarbital (NEM, 50 mg/kg, i.p., n = 8) or urethane (URE, 1.6 g/kg, i.p. n = 8) anesthesia. Fifteen minutes following the induction of anesthesia, sodium pentobarbital produced an increase in basal plasma osmolality (Posm, 290 +/- 2 to 296 +/- 3 mosm/kg H2O, p less than 0.007) while urethane did not change basal Posm (287 +/- 2 to 289 +/- 2 mosm/kg H2O). Neither anesthetic agent resulted in any significant changes in basal plasma levels of vasopressin-associated neurophysin (VP-RNP) and oxytocin-associated neurophysin (OT-RNP). In response to intravenous infusion of 18% saline, all three groups of rats had similar rises in Posm. The slopes of the relationship between the rise in plasma VP-RNP and the rise in Posm were markedly reduced in both groups of anesthetized animals compared to that observed for conscious animals (CON = 2.54 +/- 0.5; NEM = 1.22 +/- 0.18; URE = 1.17 +/- 0.24 fmol.ml-1.mosm-1.kg H2O-1 p less than 0.0126). The slopes of the relationship between the rise in plasma OT-RNP and the rise in Posm were not significantly (p less than 0.4478) different between the CON group and the NEM group, while the slope for the URE group was significantly (p less than 0.05) smaller than that for the CON group (CON = 10.9 +/- 1.5; NEM = 9.3 +/- 1.5; URE = 6.3 +/- 0.7 fmol.ml-1.mosm-1.kg H2O-1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of pentobarbital and urethane on release from magnocellular neurons. 174 63

The authors analyze the results of measuring the content of vasopressin, renin, angiotensin II and aldosterone coupled with the results of studying hemodynamics, acid-base state, and lactate in the arterial blood during operations on the heart in 32 patients with different acquired heart diseases. The main attention was concentrated on studies into the nature of humoral changes during extracorporeal circulation in three types of anesthesia. In group I, anesthesia was maintained by fentanyl given in a dose of 5-6 micrograms/kg/h, diazepam (0.1 mg/kg/h), and arduan (0.02 mg/kg/h). In the second observation group, at the beginning of perfusion the patients were administered trimetotan (artonad) (0.2 mg/kg), and in group III, the dose of fentanyl was raised during perfusion to 10-12 micrograms/kg/h. It is concluded that during extracorporeal circulation, it is desirable that the dose of fentanyl be increased to attain more adequate anesthesia in that period of heart surgery. The magnitude of humoral changes occurring in the body during extracorporeal circulation served as a criterion for anesthesia adequacy.
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PMID:[Endocrine response to extracorporeal circulation]. 178 Dec 13

Twelve patients undergoing total hip replacement, with regional anaesthesia and with dextran infusion for plasma expansion and thromboprophylaxis, were given the vasopressin analogue desmopressin (DDAVP) or placebo in a randomized, double-blind prospective study. In controls (n = 6) we found a prolongation of the bleeding time, low factor VIII (FVIII) and von Willebrand factor (vWF) and a decrease in antithrombin III to levels known to be at risk for venous thrombosis. Desmopressin shortened postoperative bleeding time, gave an early FVIII/vWF complex increase, prevented antithrombin III from falling to critically low values and appeared to activate the fibrinolytic system, both by tPA increase and PAI-1 decrease. Thus in the controls we found changes in both coagulation and fibrinolysis indicating a haemorrhagic diathesis as well as a risk for thromboembolism. Desmopressin induced factor changes that possibly reduce both risks.
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PMID:Effects on coagulation and fibrinolysis of desmopressin in patients undergoing total hip replacement. 179 9

Animal experiments have shown that severe haemorrhage often is characterized by an initial general increase in sympathetic activity leading to an increase in heart rate and a subsequent vagally mediated, reversible decrease in heart rate. It is likely that the decrease in heart rate is triggered by mechanoreceptors situated in the left ventricle. The receptors are supposed to be activated by a reduction in end-systolic volume occurring as a result of a decrease in venous return concomitant with the initial increase in heart rate. SA vago-vagal reflex elicited from and returning to the heart is thereby activated, resulting in a slowing of the heart. It has been hypothesized that the left ventricular receptors are activated when the ventricle contracts around an almost bloodless chamber. The decrease in heart rate may allow for an increased filling of the heart and an improved coronary perfusion. However, these experimental observations are in clear contradiction to the general description of the regulatory mechanisms operating during haemorrhagic shock in man as presented by authoritative medical, surgical and anesthesiological textbooks. Until now the (over-simplified) notion has been, that progressive haemorrhage results in an increased activation of the sympathetic nervous system leading to an increase in heart rate and that the occurrence of bradycardia was a sign of irreversible shock. The present systematic measurements in patients in haemorrhagic shock showed that the heart rate during severe haemorrhage often was normal (mean value 73 beats/min, range 46-98 beats/min). Simultaneous measurements of plasma concentrations of pancreatic polypeptide (an index of vagal activity) indicated that organs other than the heart also were exposed to increased vagal activity. A marked increase in the plasma concentration of vasopressin was not a constant finding as it was during the experimental-induced hypotensive central hypovolemia. This difference may be due to a decline in the release of vasopressin during prolonged haemorrhage. In order to elucidate essential regulatory mechanisms behind the clinical observations, central hypovolemia was induced experimentally by "head-up tilt", "lower-body negative pressure", "venous tourniquets of the thighs plus haemorrhage", and by epidural anesthesia. The initial stage of central hypovolemia was characterized by an increase in sympathetic nervous activity resulting in an increase in heart rate. Activation of the renin-angiotensin-aldosterone system occurred prior to marked increases in plasma concentrations of vasopressin. During progression of the central hypovolemia a qualitative shift in the regulatory mechanisms was evident.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Heart and endocrine changes during central hypovolemia in man. 180 34

Microalbuminuria is known to increase in various diseases with potential repercussion on the kidneys and indicates an increase in glomerular intracapillary pressure or changes in permeability characteristics. In this study, we measured whether albumin excretion is affected in patients undergoing anesthesia and surgery, which are both known to induce dramatic changes in renal function and in the release of vasoactive substances such as catecholamines, vasopressin, angiotensin, and prostaglandins. Seven patients with normal renal function and physiological microalbuminuria prior to surgery were studied. Urine samples were collected before anesthesia, just before the beginning of surgery, and thereafter 30 min following incision, and 30 min after the end of surgery. Anesthesia induced a significant increase in microalbuminuria, which further increased during surgery. After the end of surgical procedure, microalbuminuria decreased but remained significantly higher than control. This phenomenon may be due to an increase in intracapillary glomerular pressure and/or an alteration in glomerular permeability induced by a direct effect of drugs, or to the action of vasoactive substances on the glomerular structure.
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PMID:Microalbuminuria is acutely increased during anesthesia and surgery. 186 71

Deliberate hypotension may induce secretion of stress hormones. In the present study, the effects of hypotension induced by labetalol with isoflurane or plasma renin activity, plasma concentrations of adrenaline, noradrenaline, vasopressin, and aldosterone were investigated in eight adult patients undergoing middle-ear surgery. The mean arterial pressure was 50 mmHg (6.7 kPa) during hypotension. Plasma renin activity rose significantly during anaesthesia before hypotension, being similar during hypotension and before hypotension, and in returned postoperatively to the initial level. Plasma adrenaline fell significantly during hypotension and rose after anaesthesia to the preanaesthetic level. Plasma noradrenaline rose slightly during hypotension and after anaesthesia, but not significantly. Plasma vasopressin rose significantly after anaesthesia. Plasma aldosterone increased slightly throughout the study, but not significantly during any phase. In conclusion, labetalol with isoflurane-induced hypotension seems to attenuate the stress response in these operations. During hypotension, plasma renin activity is not an essential compensatory mechanism, which antagonises the decrease of blood pressure. Plasma vasopressin has no role in regulating blood pressure during labetalol-induced hypotension.
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PMID:Plasma renin, catecholamines, vasopressin and aldosterone during hypotension induced by labetalol with isoflurane. 189 44

This study was undertaken to investigate the influences of halothane and isoflurane as well as different extubation techniques on the endocrine stress response during recovery from general anesthesia. Forty patients scheduled for herniorrhaphy and cholecystectomy were randomly allocated to 4 groups: 20 received halothane and 20 received isoflurane anesthesia. Within the halothane and isoflurane groups, 10 patients each were extubated during anesthesia (1/2 MAC) and a further 10 had awake extubation. Premedication, induction of anesthesia, and intraoperative anesthetic management were standardized in all groups. Plasma levels of endocrine stress parameters as well as mean arterial pressure (MAP), heart rate (HR), and arterial oxygen saturation (SaO2) were measured at nine time points up to 60 min after extubation. Biometric data and duration of operation and anesthesia were comparable in all groups. In the recovery period, epinephrine levels were higher in the isoflurane groups than in the halothane groups (P = 0.02). With respect to time course, earlier and more marked increases of epinephrine, norepinephrine, and antidiuretic hormone (ADH) levels were observed in the isoflurane groups compared to the halothane groups (P less than 0.01), representing the more rapid elimination of isoflurane. The sympathoadrenergic stress response was more pronounced in patients with extubation during anesthesia than in those with awake extubation: epinephrine levels were slightly higher and group levels of norepinephrine were significantly increased (P = 0.02). No influence of the extubation techniques was observed on ADH, ACTH, and cortisol levels or on MAP, HR, or SaO2. In summary, extubation during anesthesia did not reduce the endocrine stress response. It is concluded that awake extubation should be preferred unless the operation or the patient's condition requires extubation during anesthesia.
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PMID:[The stress reaction in the recovery phase from halothane and isoflurane anesthesia]. 195 37

To determine whether nalbuphine might replace fentanyl as the principal opioid for anesthesia during coronary artery bypass surgery, 20 patients undergoing myocardial revascularization were anesthetized with flunitrazepam and with a continuous infusion of either nalbuphine (an opioid agonist-antagonist) or fentanyl (a pure opioid agonist) in equipotent dosage ratio of 333:1. During endotracheal intubation, all patients given nalbuphine, but only one given fentanyl (P less than 0.05), required nitroglycerin to control arterial blood pressure. Two minutes after tracheal intubation, plasma values of epinephrine, norepinephrine, vasopressin, and cortisol did not change in the fentanyl group compared with the awake (baseline) levels, whereas catecholamines and vasopressin significantly increased with nalbuphine compared with the baseline and with the values in the fentanyl group. A steady state of anesthesia (30 min after intubation), when compared with the baseline, was characterized by unchanged systemic and pulmonary blood pressures and increased systemic vascular resistance with nalbuphine, by decreased systemic and pulmonary pressures and resistances with fentanyl, and by comparably decreased cardiac index with both opioids. Hormone values returned to baseline levels but norepinephrine remained significantly higher in the nalbuphine than in the fentanyl group. A bolus injection of either nalbuphine (2.5 mg/kg) or fentanyl (7.5 micrograms/kg) given during the steady-state period of anesthesia provoked only minimal hemodynamic changes. Before skin incision, 7 of 10 patients receiving nalbuphine required nitroglycerin to control arterial blood pressure. After sternotomy, both groups required nitroglycerin, but additional antihypertensive drugs were necessary mainly in the nalbuphine group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of nalbuphine and fentanyl anesthesia for coronary artery bypass surgery. Hemodynamics, hormonal response, and postoperative respiratory depression. 195 30

The effects of various stressful conditions on the levels of oxytocin (OT) and vasopressin (VP) in plasma and cisternal cerebrospinal fluid (CSF) of male rats were investigated. Three experimental models were used: exposure to a novel environment for 5 min, immobilization for 15 min, and ether inhalation for 10 min resulting in anaesthesia. Novelty and immobilization induced a slight but significant increase in OT levels in the CSF immediately after the stress. The effect of ether was considerably more pronounced. The concentration of VP in the CSF was elevated only by ether stress. In plasma, the level of OT was increased immediately following immobilization and ether stress but not after novelty stress, whereas VP only showed a delayed response 20 min after immobilization. These results indicate a rapid preferential release of OT in the periphery in response to physical and pharmacological stress. In addition, they provide evidence that release of OT into the CSF is triggered by physical, pharmacological as well as emotional stress, while the central release of VP is rather resistant to emotional stress. The data suggest that OT is a stress hormone in the central nervous system.
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PMID:Differential effects of emotional and physical stress on the central and peripheral secretion of neurohypophysial hormones in male rats. 200 57


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