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)

The responses to work-test in ischemia (tourniquet technique), before and after I.V. injection of naloxone (2 mg) or saline, were investigated in healthy volunteers and patients suffering from various types of headache. The patients were examined during both painful and painless periods. We found that only the subjects suffering from migraine showed a significantly shortened pain tolerance at work-test in ischemia, after injection of naloxone, and only during painful periods. Psychogenic headache patients and migraine patients in painless periods showed responses during work-test similar to those in healthy volunteers, even after injection of naloxone. We believe that hyperalgesic effect of naloxone is due to involvement of beta-endorphin systems only during organic pain.
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PMID:Headache patients: different responses induced by naloxone during work-test. 715 Nov 48

There is substantial evidence that cardiac opioid receptors are activated during arrhythmias induced by administration of opioid peptides or myocardial ischemia, supporting the hypothesis that endogenous opioid peptides (EOP) are involved in myocardial infarction. This prospective clinical trial is designed to determine whether the ischemia-induced arrhythmias and extent of the infarct are related to the release of the EOP beta-endorphin in patients with acute myocardial infarction. Two groups were included in the study, patients with acute myocardial infarction, and healthy volunteers who served as controls. The results indicate that, compared to the controls, there was augmentation of ischemic arrhythmias and ischemic damage as assessed by serum creatine kinase activity, accompanied by an elevated level of beta-endorphin, in patients with acute myocardial infarction. The above data strongly indicate that EOP are indeed involved in the pathophysiology of myocardial infarction, and suggest these peptides have an important role in ischemic heart disease.
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PMID:Plasma levels of endogenous opioid peptides in patients with acute myocardial infarction. 747 58

Plasma met-enkephalin-like immunoreactivity (MLI) levels were determined in cats before, during and after 90 min of intestinal ischemia followed by reperfusion and compared with the levels in control cats. Blood pressure and heart rate were registered and small intestinal mucosal lesions were graded. In control animals, the circulation was stable and there were no mucosal injuries. In the shock group, blood pressure decreased, heart rate increased and severe mucosal lesions were found. The circulating MLI levels were significantly higher 30 min after reperfusion of the ischemic intestine in the shock group than in the control group. There were correlations between MLI and tachycardia and hypotension respectively. Met-enkephalin was released in shock animals after reperfusion of the ischemic intestine and may explain naloxone responsiveness in intestinal shock models.
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PMID:Changes in circulating plasma met-enkephalin concentrations in feline intestinal ischemia--reperfusion. 805 60

The differences between diabetic and nondiabetic patients with silent myocardial ischemia were investigated. Based on the results of previous exercise testing, a total of 110 patients (15 diabetic and 95 nondiabetic) with exercise-induced myocardial ischemia were divided into the following 3 groups: 15 diabetics with silent myocardial ischemia, 49 nondiabetics with silent myocardial ischemia, and 46 nondiabetics with anginal symptoms. All patients underwent treadmill exercise testing and 24-hour ambulatory electrocardiographic recording. Before and during exercise, blood samples from the antecubital vein were obtained to determine the plasma beta-endorphin levels, and the pain threshold of each patient was measured with the electrical skin stimulation test. Furthermore, with regard to the ambulatory electrocardiographic recording, the mean of the SDs of all normal sinus RR intervals during successive 5-minute recording periods over 24 hours was analyzed and considered as an index of the autonomic function. The plasma beta-endorphin level during exercise was significantly greater in nondiabetic patients with silent ischemia than in diabetic ones. The SD mean was significantly less in the diabetic group than in the 2 nondiabetic ones. The findings suggest that the role of beta endorphin in diabetic patients with silent myocardial ischemia may be less significant than in nondiabetic ones; therefore, a diabetic neuropathy that affects the autonomic pain fibers that innervate the heart may be involved in the mechanism of silent myocardial ischemia in diabetics.
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PMID:Usefulness of plasma beta-endorphin level, pain threshold and autonomic function in assessing silent myocardial ischemia in patients with and without diabetes mellitus. 832 73

In patients with prior shock and liver injury, mechanical circulatory assist still has a high risk of hepatic failure. The purpose of this study was to evaluate the effect of mechanical circulation using pulsatile or nonpulsatile blood pumps on shock organs, particularly shock liver. In 14 dogs, a shock liver model was produced by clamping the descending aorta above the diaphragm. After 60 minutes of ischemia, left atrial-femoral artery bypass (LHB) was started while the clamp remained in place. A pneumatic pulsatile pump (Toyobo; Tokyo, Japan) was used in seven dogs (Gr-PP) and a centrifugal pump (Biomedicus; Minneapolis, MN) in seven (Gr-NPP). In both groups the mean arterial pressure was maintained at 80 mmHg. The mean bypass flow was 96 +/- 14 ml/kg/min for Gr-PP, and 95 +/- 35 ml/kg/min for Gr-NPP. In both groups the bile flow and arterial ketone body ratio decreased significantly after ischemia, and recovered to normal after 120 min of LHB. There was no significant difference between the two groups in this model. The other parameters (glutamic oxaloacetic transaminase [GOT], glutamic pyruvic transaminase, lactate dehydrogenase, mitochondrial GOT) were independent of the period of ischemia and reperfusion, and there was no difference between the two groups. In conclusion, these results suggest that nonpulsatile circulatory assist may not be disadvantageous for the circulatory support and recovery of liver function in the setting of shock liver.
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PMID:Comparison between pulsatile and nonpulsatile circulatory assist for the recovery of shock liver. 857 74

Release of met-enkephalin-like immunoreactivity (MLI) into the circulation was investigated during feline intestinal ischemia-reperfusion in relation to the mass of ischemic tissue and in correlation to the sympathoadrenergic, response as gauged by plasma norepinephrine (NE) and epinephrine (E) levels. Chloralose anesthetized cats were randomized to a control group (C, n = 7), 20 cm segmental (S, n = 7), or complete intestinal ischemia (l, n = 7) for 90 min followed by reperfusion for 180 min. MLI and NE/E concentrations were assayed by radioimmunoassay and chromatography, respectively. Severe mucosal lesions and cardiovascular decompensation were observed in l animals in association with increased MLI and NE levels in femoral venous and portal venous plasma, whereas no such responses were observed in the S or C groups. MLI and NE concentrations were consistently higher in portal venous than in femoral venous plasma in 1 animals and correlations between MLI and NE levels were found during reperfusion in the portal, but not the systemic, circulation. Concentrations of E remained unchanged in all groups and did not correlate to MLI release. We conclude that: 1) intestinal MLI release and sympathetic activation occur only when the ischemic insult is sufficient to cause circulatory collapse, characteristic of an "on-off" rather than a "dose-response" pattern; and 2) intestinal MLI and NE release at reperfusion are correlated whereas MLI and E release do not appear to be related events.
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PMID:Met-enkephalin and catecholamine release during feline intestinal ischemia-reperfusion. 879 56

We observed that the pro-opiomelanocortin-derived neuropeptide, gamma 2-melanocyte-stimulating hormone (gamma 2-MSH), has various peripheral and central hemodynamic effects in the rat, including a marked enhancing effect on cerebral blood flow. This hemodynamic profile might be of interest in the pharmacotherapeutic approach to acute cerebral ischemia. Being an adrenocorticotropin (ACTH) analogue, gamma 2-MSH might also possess direct neuronal protective properties. Therefore, in two rat models of focal cerebral ischemia we studied the effects of gamma 2-MSH, with nimodipine, a Ca2+ channel antagonist, as a reference compound, on parasagittal laser-Doppler-assessed cortical blood flow and infarction volume. In isoflurane-anesthetized Wistar and F344 rats i.v. bolus infusions (four in total) of gamma 2-MSH or nimodipine or their vehicle controls were given 1 h before, 1 min after, and 1 h and 2 h after occlusion of the middle cerebral artery. We used both an intravasal and an extravasal middle cerebral artery occlusion technique because pilot experiments had shown differences in the severity of ischemia with the two techniques. gamma 2-MSH (100 nmol/kg in 1 min) increased cortical blood flow significantly but transiently, both pre- and post-ischemically, whereas nimodipine (20 micrograms/kg in 1 min) increased cortical blood flow only pre-ischemically in both models of middle cerebral artery occlusion. gamma 2-MSH had no effect on cortical and striatal infarction volume, while nimodipine caused a significant reduction of cortical infarction volume in the extravasal middle cerebral artery occlusion model. To conclude, despite its hemodynamic and possible neuroprotective properties, gamma 2-MSH did not prevent ischemic neuronal damage after middle cerebral artery occlusion in rats. This might be partly due to the short half-life of the peptide, leading to a transient increase in cortical blood flow and short neuronal exposure time, suggesting that prolonged infusion of the neuropeptide might be required. The results with nimodipine support the notion that it attenuates cortical ischemic damage, independently of effects on cerebral hemodynamics.
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PMID:The effects of gamma 2-melanocyte-stimulating hormone and nimodipine on cortical blood flow and infarction volume in two rat models of middle cerebral artery occlusion. 881 23

Our previous studies indicate that function of ATP-dependent K+ channels (K(ATP)) in cerebral arterioles is suppressed after ischemia. In the current study, we examined pial arteriolar responses to forskolin, dibutyryl-cAMP, NS-1619, and methionine (met)-enkephalin, activators of calcium-dependent K+ channels (K(Ca)) before and 1 hour after 10 minutes of total, global ischemia in anesthetized piglets. Arteriolar diameters were measured using a closed cranial window and intravital microscopy. All pharmacologic agents were given topically. Baseline diameters were approximately 100 microm, and diameters had returned to normal by 1 hour after ischemia. Forskolin dilated arterioles by 9 +/- 3%, 18 +/- 4%, and 31 +/- 12% at 5 x 10(-8), 5 x 10(-7), and 10(-6) mol/L, respectively (P < 0.05, n = 10). In addition, dibutyryl-cAMP dilated arterioles by 8 +/- 2% at 10(-4) mol/L and 14 +/- 2% at 3 x 10(-4) mol/L (P < 0.05, n = 6). Also, NS-1619 increased diameter of arterioles by 9 +/- 2% at 10(-7) mol/L and 17 +/- 9% at 10(-5) mol/L (P < 0.05, n = 5). Finally, met-enkephalin dilated arterioles by 9 +/- 2% at 10(-8) mol/L and 16 +/- 3% at 10(-6) mol/L (P < 0.05, n = 5). At 1 hour after ischemia, arteriolar dilator effects to forskolin, dibutyryl-cAMP and NS-1619, and met-enkephalin were intact. Thus, in contrast to K(ATP), K(Ca) in cerebral arterioles are resistant to ischemic stress.
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PMID:Calcium-activated K+ channels in cerebral arterioles in piglets are resistant to ischemia. 939 Jun 46

The antiinflammatory effects of alpha-melanocyte-stimulating hormone (alpha-MSH) molecules, specifically alpha-MSH(1-13) and its COOH-terminal tripeptide alpha-MSH(11-13), are well established. The peptides have been effective in tests of all major models of inflammation, and more recent tests have been extended to include experimental inflammatory bowel disease, CNS ischemia/reperfusion injury, and bacterial endotoxin-induced inflammation within the brain. The broad effectiveness of alpha-MSH molecules in all major types of inflammation indicates that the peptides exert actions that are very basic to the inflammatory process. Three general mechanisms of antiinflammatory action of alpha-MSH molecules have been identified: inhibition of production of inflammatory mediators by, or inhibition of inflammatory actions of, peripheral host cells; inhibition of peripheral inflammation induced by actions on melanocortin receptors within the brain; inhibition of CNS inflammation by local action of the peptides. It appears that alpha-MSH molecules have multiple actions that modulate the primitive inflammatory response.
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PMID:Mechanisms of antiinflammatory action of the neuroimmunomodulatory peptide alpha-MSH. 962 64

The purpose of this study was to evaluate whether the synthetic adrenocorticotropin-(4-9) (ACTH-(4-9)) analogue ORG 2766, HMet(O2)-Glu-His-Phe-D-Lys-Phe-OH, which has been shown to have beneficial effects on both the recovery from experimentally induced lesions of the central nervous system and peripheral nerve degeneration, has a protective effect on focal ischemic neuronal damage. The NMDA receptor antagonist dizolcipine (MK-801), a very potent neuroprotective drug, was used as positive reference compound. Isoflurane-anesthetized rats had the middle cerebral artery occluded using either an intravasal or an extravasal technique, because pilot experiments had shown differences in the severity of ischemia for the two middle cerebral artery occlusion techniques. MK-801, 500 microg kg(-1) min(-1), or saline was administered i.v. 30 min after occlusion of the middle cerebral artery. In the ACTH-(4-9) analogue/saline group, 10 and 150 microg/kg of the analogue, or saline was injected s.c. both directly after and 24 h after occlusion. The ACTH-(4-9) analogue treatment had no effect on the infarction volume in either model of middle cerebral artery occlusion, whereas MK-801 caused a significant reduction in the volume of cortical infarction in both models. We conclude that, although ORG 2766 is known to enhance the recovery from experimentally induced lesions of the central nervous system through a neurotrophic action and has proven to have significant beneficial effects on peripheral nerve regeneration, it did not prevent ischemic neuronal damage after intravasal or extravasal middle cerebral artery occlusion in rats. The results with MK-801, which caused significant reductions in the volume of cortical infarction in both models of middle cerebral artery occlusion, with clearly the largest reduction in the intravasal middle cerebral artery occlusion model, again indicate that there are differences in the severity of the cerebral ischemia which the two models produce in the rat brain.
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PMID:The effect of the adrenocorticotropin-(4-9) analogue, ORG 2766, and of dizolcipine (MK-801) on infarct volume in rat brain. 965 55


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