Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Current research suggests that the secretion of beta-endorphin from the pituitary gland may be associated with the refractory hypotension seen in patients with septic shock. Extensive animal research and a few clinical studies have demonstrated that naloxone, a narcotic antagonist, can increase MAP, cardiac output, and cardiac contractility and improve survival in victims of endotoxic shock. The ability of naloxone to improve MAP, however, appears to decrease with prolonged persistent hypotension (greater than eight hours). Studies also suggest that a synergistic effect exists between naloxone and the steroid methylprednisolone in improving the hemodynamics of these patients. In the future, naloxone may prove to be essential in the management of patients in the early stages of septic shock, but more complete clinical trials are warranted. It is imperative that nurses be involved in this type of clinical research.
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PMID:Naloxone and its use in neonatal septic shock. 214 Aug 71

Administration of 20, 4 or 2.5 micrograms/kg of atriopeptin III (AT III) into the fourth ventricle of the brain of spontaneously hypertensive rats produced a 13, 14 and 7 mm Hg decrease in MAP respectively, while 1 microgram/kg had no effect on MAP and was significantly different from 20 or 4 micrograms/kg (p less than 0.025). In contrast, injection of AT III 20 micrograms/kg into the lateral ventricle did not produce a change in MAP. To examine an interaction of AT III with the opioidergic system, the opiate antagonist, naloxone HCl, 10 micrograms, was given by ICV injection 10 minutes prior to AT III, and significantly prevented the depressor response to AT III (p less than 0.025 compared with AT III alone). Injection of specific anti-sera to beta-endorphin failed to prevent the AT III-induced depressor response. Our results demonstrate that AT III can act within the central nervous system to decrease the MAP of rats, most likely at a locus in proximity to the fourth ventricle of the brain. Further, an interaction with the central opioidergic nervous system underlies the central effects of AT III.
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PMID:Central nervous system mediated vasodepressor action of atrial natriuretic factor. 252 18

The effect of hypoxic hypoxia (HH) and carbon monoxide hypoxia (COH) on adrenal medullary (MQ) and cortical (CQ) blood flow (radiolabeled microsphere technique) was studied in pentobarbital sodium-anesthetized, mechanically ventilated dogs. Animals were exposed to 60 min of hypoxia (arterial O2 content 8 vol%) induced by adding either nitrogen (HH, n = 6) or carbon monoxide (COH, n = 6) to the inspired gas. Whole adrenal Q and CQ increased by 70 and 50%, respectively, with HH but were unchanged during COH. MQ, however, increased threefold during both HH and COH. HH and COH both increased arterial levels of epinephrine, corticosteroids, and adrenocorticotropic hormone (ACTH). To determine whether the increase in CQ during HH was because of HH-induced increases in mean arterial blood pressure (MAP, approximately 20 mmHg), an additional group of animals (n = 6) was exposed to HH but had MAP maintained at control levels using a pressurized-bottle system. MAP control did not alter the CQ response to HH. We conclude that MQ appears to be associated with medullary secretory activity during hypoxia and that HH and COH stimulate adrenal medullary secretion equally. In contrast, CQ increases only with HH, despite similar increases in ACTH and corticosteroid levels during HH and COH, suggesting that an alternative mechanism is responsible for increased cortical blood flow during HH.
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PMID:Regional adrenal blood flow during hypoxia in anesthetized, ventilated dogs. 253 47

The effect of intracerebroventricular injections of arginine vasopressin (AVP) on burn shock in the rat and its possible mechanism were explored in this study. AVP was administered intraventricularly at 30 min intervals (50 ng) in the burned rats. The arterial pressure and electrocardiogram (ECG) were recorded with a multipurpose polygraph before and after burn. Compared with the control, the MAP of the rats in the AVP group was elevated at the initial stage and fell dramatically at the late stage of burn shock with a higher mortality. The ECG of the rats in the AVP group also displayed earlier changes such as elevation of S-T segment, inversion of T wave, and ventricular fibrillation. These findings suggest an unfavorable role of AVP in burn shock. The plasma, hypothalamic, and anterior and posterior pituitary levels of beta-endorphin 3 hr after burn were measured by radioimmunoassay. The increased level of beta-endorphin in the plasma after AVP treatment indicates the possible involvement of beta-endorphin in the deteriorating effect of AVP on burn shock.
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PMID:Possible involvement of beta-endorphin in the deteriorating effect of arginine vasopressin on burn shock in rats. 259 Oct 29

The present study evaluated a protocol for drawing large volumes of blood over an acute time frame in conscious cannulated rats with blood from cannulated donor rats simultaneously infused to maintain isovolemia. During time control (n = 6), three successive 1.5-ml blood samples were drawn at 10-min intervals with equal volumes of donor blood infused simultaneously. One milliliter of blood was drawn quickly and saved for analysis followed by an additional 3 ml of blood withdrawal to total a 15-ml/kg hemorrhage. Two subsequent 1.5-ml samples were replaced with autologous (hemorrhage) blood. During hypoxia inspired O2 was decreased to 10% after the first sample-transfusion. The sampling-transfusion protocol (time control) had no effect on blood pressure (MAP), hematocrit (Hct), blood gases, renin, or adrenocorticotropic hormone (ACTH). Hemorrhage resulted in a significant decrease in MAP, Hct, base excess, and arterial PCO2 and an increase in arterial PO2, renin activity, and ACTH. Ten percent O2 resulted in significant hypoxemia, respiratory alkalosis, and a small degree of hypotension at the 20-min sample with no change in renin and a moderate increase in ACTH. The consistency of the results with previous studies confirms the utility and efficiency of large sample-transfusion protocols for the study of blood gas and endocrine dynamics in conscious rats.
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PMID:Evaluation of a blood sample-transfusion protocol in rats: blood gases, renin, and ACTH. 284 65

The endogenous opiate beta-endorphin is released concomitantly with adrenocorticotropin from the pituitary during stress. In the present study we investigated the possible involvement of opiate receptors in the cardiovascular depression associated with hypovolemic shock in the nonhuman primate. Changes in circulating levels in beta-endorphin were monitored during hemorrhagic shock in 18 female baboons. Plasma levels of beta-endorphin increased significantly during hemorrhagic shock and were significantly correlated with a decrease in cardiac output (P less than 0.05). Single bolus administration of the opiate receptor antagonist naloxone (2 or 5 mg/kg) produced a transient but significant improvement in cardiac output (P less than 0.05) and mean arterial pressure (P less than 0.05). Hemodynamic improvement was maintained with a constant infusion of naloxone. Opiate receptor blockade with the longer acting antagonist naltrexone (2 or 5 mg/kg) significantly increased mean arterial pressure (MAP; P less than 0.05), and CO (P less than 0.05), and decreased heart rate. Our results suggest that the baboon is an excellent model for the study of hemorrhagic shock and provide further evidence for endogenous opiate involvement in the cardiovascular pathophysiology of hemorrhagic shock.
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PMID:Endorphins in primate hemorrhagic shock: beneficial action of opiate antagonists. 293 29

Chemical antagonists were used to assess the role of beta-endorphin and arginine-vasopressin (AVP) in canine endotoxin shock. Fifteen awake dogs were given Escherichia coli endotoxin IV. Within 5 min, CO decreased to 28%, LV dP/dt to 46%, and MAP to 52% baseline. Fifteen minutes after endotoxin, five dogs each received naloxone, AVP antagonist, or no treatment. Control (untreated) animals exhibited persistent cardiovascular depression, with CO 49%, LV dP/dt 69%, and MAP 91% of baseline after 45 min. Naloxone improved CO to 69%, LV dP/dt to 94%, and MAP to 91% by 30 min after treatment. AVP blockade improved CO to 105%, LV dP/dt to 107%, and MAP to 95% of baseline by 30 min after treatment, and caused significant tachycardia. Plasma cortisol and AVP increased markedly in all groups after endotoxin administration. AVP antagonist treatment increased mean survival from 1.4 to 4 days. These data suggest that abnormally elevated AVP contributes to cardiovascular depression in canine endotoxin shock and that AVP blockade is therapeutic in the animal model studied.
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PMID:The role of endorphins and vasopressin in canine endotoxin shock. 294 95

Sixteen anesthetized foxhounds were instrumented for hemodynamic measurements. The adrenolumbar vein was cannulated, and hemorrhagic hypotension (MAP = 40 mmHg for 3h) was induced by bleeding. The plasma levels of beta-endorphin (beta-END), methionine-enkephalin (M-ENK), and leucine-enkephalin (L-ENK) were determined in systemic and adrenal venous blood by specific RIA. Five dogs received an i.v. bolus of naloxone (2 mg/kg) and a subsequent naloxone infusion of 2 mg/kg per hour 1 h after onset of hypovolemia. Eleven dogs served as controls and received equivalent volumes (1 ml/kg per hour) of saline. Hemorrhage resulted in a sharp increase in plasma concentrations of all measured opioid peptides, particularly of M-ENK (26-fold) and L-ENK (24-fold) in the adrenal effluent. Systemic beta-END levels remained 3-fold increased, whereas the ENK release decreased spontaneously. Naloxone treatment inhibited the spontaneous fall of adrenal ENK release during the hypotensive phase; the ENK values remained elevated 20- to 35-fold. Reinfusion of the autologous blood resulted in a normalization of the concentrations of all peptides in both groups. These data demonstrate that hemorrhagic hypotension will cause stimulation of release of endogenous opioid peptides. The high levels of ENK in the adrenal effluent indicate that the adrenal gland is the main source of these peptides in the circulation. In addition to beta-END, the ENK have therefore to be considered as possible factors perpetuating circulatory shock.
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PMID:Release of opioid peptides in canine hemorrhagic hypotension: effects of naloxone. 608 83

Naloxone has been used as a pharmacological tool to investigate the role of endorphins and opiate receptors in the cardiovascular pathophysiology of shock. It would appear that endorphins act on opiate receptors to contribute to the abnormalities found and that naloxone improves survival as well as cardiovascular function in shock. Preliminary studies in humans and the subhuman primate create cautious optimism regarding the clinical application of this information. Naloxone has served us well as a key to unlock the involvement of endorphins and opiate receptors in shock. However, further advances in our understanding may depend on the development and use of opiate receptor agonists and antagonists specific for the different opiate receptors described, each subserving different functions. Naloxone's disadvantage of increasing pain awareness may limit its clinical usefulness but might be overcome by using drugs that reverse the behavioral and neuroendocrine changes produced by beta-endorphin without altering pain relief. Thyrotropin-releasing hormone (TRH) is just such a "physiological" opiate antagonist which has been shown to increase MAP in experimental endotoxic and hemorrhagic shock [32].
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PMID:Naloxone in endotoxic shock: experimental models and clinical perspective. 630 74

Previous studies established that naloxone reverses hypotension in endotoxin, hemorrhagic, and spinal shock. We studied endotoxin shock in hypophysectomized (Hx) rats, which have little circulating beta-endorphin. Hx or intact rats received surgically implanted jugular catheters for drug injection and aortic catheters for arterial blood pressure (MAP) recording. On the second day after implantation, rats were pretreated with either naloxone or saline. Two minutes later each rat received endotoxin. Following endotoxin, all rats showed a brief biphasic hypertensive-hypotensive response followed by stabilization of MAP near baseline. Within 20 min, all Hx rats, regardless of pretreatment, and the saline-treated intact rats, showed progressive hypotension (P less than 0.005). Only the naloxone-pretreated intact rats maintained a stable MAP. Plasma endorphin measured at 20 min was undetectable in Hx rats in contrast to intact rats (P less than 0.001); plasma corticosterone levels were likewise suppressed in the Hx rats (P less than 0.01). Thus (1) naloxone protected only the rats with an intact pituitary-adrenal-sympathetic system, and (2) pituitary endorphin is not required to generate endotoxin shock in hypophysectomized rats.
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PMID:Endotoxin shock: prevented by naloxone in intact but not hypophysectomized rats. 632 Feb 13


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