beta-endorphin and Brain-Injuries

To compare the efficacy of dextraldexmede (DEX) and propofol on sedation and β-endorphin (β-EP) in patients with moderate and severe traumatic brain injury (TBI).. Ninety patients with moderate and severe TBI with Glasgow coma score (GCS) 6-13 were randomly divided into three groups according to the order of admission of odd and even numbers. In group A (DEX/+morphine), DEX load 0.5-1.0 μg/kg was injected within 30 minutes, and maintaining at 0.2-0.6 μg×kg⁻¹ × h⁻¹ for 24 hours; and in group B (propofol/+ morphine), propofol load 0.5-2.0 mg/kg was injected within 10 minutes, and maintaining at 1-3 mg×kg⁻¹×h⁻¹ for 72 hours. Patients with poor efficacy were added with morphine intravenously. In group C, intramuscular injection of pethidine and other temporary medication was injected. The comprehensive assessment was conducted according to the Riker sedation and agitation score, combined with the physiological body reaction positive indicator elimination. The vital signs was monitored, and blood white blood cell (WBC) count, blood sugar, cortisol and β-EP before and after administration were determined.. (1) The sedation efficiency rate of the group A, B, C were 84.38% (27/32), 80.64% (25/31), 77.78% (21/27), respectively. The booster dose of morphine in group A was less than that in group B (24 h dosage: 16.23 ± 3.45 mg vs. 21.34 ± 5.55 mg). (2) Blood pressure and heart rate were significantly affected in the group A. The mean arterial pressure (MAP) in 0.5 hour of reaching loading dose in group A was significantly lower than that in group B and C (75.50 ± 9.35 mm Hg vs. 87.90 ± 8.05 mm Hg, 85.70 ± 7.10 mm Hg, both P<0.05). (3) WBC and cortisol levels showed downwards trends after treatment in group A and group B; WBC fell more in the group A compared with group B, cortisol level fell more in group B compared with group A, and the WBC and cortisol level began to decline after 24 hours in group C. (4) There were no significant differences in blood sugar and β-EP levels before and after treatment in group B, but β-EP had an increasing tendency in group A and group C, and the amplification in group C was more obvious than that in group A.. The sedation efficacy of DEX was superior to propofol in moderate and severe TBI, and was able to control excessive stress response after TBI better, and with more effect on blood pressure. Plasma β-EP was elevated during the early phase of brain injury by DEX, which was considered as its positive role in the regulation of early stress.

Topics: Adult; beta-Endorphin; Blood Pressure; Brain Injuries; Dexmedetomidine; Female; Humans; Hypnotics and Sedatives; Male; Middle Aged; Propofol

Pial artery constriction following fluid percussion brain injury (FPI) is associated with elevated CSF dynorphin and beta-endorphin concentration in newborn pigs. Additionally, dynorphin is a dilator under control conditions and a vasoconstrictor under decreased cerebrovascular tone conditions. Vasopressin contributes to beta-endorphin-induced pial constriction and the constrictor potential for dynorphin. Recently, it has been observed that FPI reverses vasopressin from a dilator to a constrictor. The present study was designed to characterize the effect of FPI on beta-endorphin-induced constriction and the role of vasopressin in that constriction as well as in the reversal of dynorphin's vascular response following FPI. Brain injury of moderate severity (1.9 - 2.3 atm) was produced in anesthetized newborn pigs equipped with a closed cranial window. Dynorphin in physiologic and pharmacologic concentrations (10(-10), 10(-8), 10(-6) M) was reversed from a dilator to a constrictor following FPI (7 +/- 1, 11 +/- 1, and 16 +/- 1 vs -4 +/- 1, -7 +/- 1, and -11 +/- 1% before and after FPI, respectively). Dynorphin-induced vascular changes were accompanied by increased cortical periarachnoid CSF vasopressin and these biochemical changes were potentiated following FPI (24 +/- 4 vs 134 +/- 7 and 53 +/- 7 vs 222 +/- 14 pg/mliter for control and dynorphin (10(-6) M) before and after FPI, respectively). In contrast, in animals pretreated with the vasopressin receptor antagonist [1-(beta-mercapto-beta beta-cyclopentamethylene propionic acid) 2-(O-methyl)-Tyr-AVP] (MEAVP, 5 micrograms/kg iv), dynorphin-induced constriction following FPI was attenuated (6 +/- 1, 12 +/- 1, and 16 +/- 1, vs -2 +/- 1, -4 +/- 1, and -7 +/- 1% before and after FPI, respectively). Additionally, beta-endorphin-induced pial constriction was potentiated following FPI (-7 +/- 1, -10 +/- 1, -15 +/- 1 vs -10 +/- 1 -15 +/- 2, and -21 +/- 2% for beta-endorphin (10(-10), 10(-8), 10(-6) M) before and after FPI, respectively). beta-endorphin-induced CSF vasopressin release was similarly potentiated following FPI. Further, MEAVP blunted the augmented constrictor responses to beta-endorphin observed following FPI (-5 +/- 1, -9 +/- 1, -14 +/- 1 vs -2 +/- 1, -5 +/- 1, and -8 +/- 1% before and after FPI, respectively). These data indicate that FPI potentiates beta-endorphin-induced pial construction and reverses dynorphin from a dilator to a constrictor. Additionally, these data show that vasopressin contribu

Topics: Animals; Arteries; beta-Endorphin; Brain Injuries; Cerebrovascular Circulation; Dose-Response Relationship, Drug; Dynorphins; Female; Male; Swine; Vasopressins

Previously, it has been observed that newborn pig pial artery constriction after fluid percussion brain injury was associated with elevated CSF dynorphin and beta endorphin concentration. Additionally, brain injury reversed dynorphin-induced pial artery vasodilation to vasoconstriction. The present study was designed to characterize the relationship between opioids and activation of phospholipase C (PLC) and protein kinase C (PKC) in brain injury-induced pial vasoconstriction. Anesthetized newborn pigs equipped with a closed cranial window were connected to a percussion device consisting of a saline-filled cylindrical reservoir with a metal pendulum. Brain injury of moderate severity (1.9-2.3 atm) was produced by allowing the pendulum to strike a piston on the cylinder. Brain injury decreased pial arteriolar diameter within 10 min of injury and continued to fall progressively for 3 h (130 +/- 5, 108 +/- 4 and 102 +/- 5 microns for 0, 10 and 180 min postinjury). In contrast, the PLC inhibitor, neomycin (10(-4) M), blunted brain injury-induced pial vasoconstriction (133 +/- 4, 129 +/- 4 and 135 +/- 5 microns for 0, 10 and 180 min postinjury, respectively). Similarly, staurosporine (10(-7) M), a PKC inhibitor, also blunted brain injury-induced vasoconstriction. beta endorphin (10(-8), 10(-6) M)-induced pial artery vasoconstriction was blunted by neomycin (12 +/- 1, 19 +/- 1 vs. 2 +/- 1, 4 +/- 2% constriction before and after neomycin, respectively). Staurosporine similarly blunted beta endorphin pial constriction (10 +/- 1, 15 +/- 1 vs. 1 +/- 1, 1 +/- 1% constriction before and after staurosporine, respectively). The constrictor potential for dynorphin was also inhibited by neomycin and staurosporine.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Animals, Newborn; beta-Endorphin; Blood Gas Analysis; Blood Pressure; Brain Injuries; Cerebral Arteries; Dynorphins; Enzyme Activation; Female; Male; Opioid Peptides; Protein Kinase C; Swine; Type C Phospholipases; Vasoconstriction

beta-endorphin-like immunoreactivity (beta-ELI) was measured in the cerebrospinal fluid (CSF) of 36 patients with acute head injury and 12 controls. The mean values of beta-ELI in CSF of controls and patients with moderate and severe acute head injury were 51.9 +/- 5.6 pg/ml, 110.5 pg/ml, and 173.8 +/- 20.1 pg/ml respectively, with significant difference between them (p less than 0.05). The results showed that beta-ELI increased in CSF of acute head injury patients.

Topics: Adolescent; Adult; Aged; beta-Endorphin; Brain Injuries; Child; Contusions; Female; Hematoma; Humans; Male; Middle Aged; Radioimmunoassay; Skull Fractures

Topics: Acute Disease; Adolescent; Adult; Aged; beta-Endorphin; Brain Injuries; Child; Female; Humans; Male; Middle Aged; Prognosis

beta-endorphin-like immunoreactivity (beta-ELI) was measured in cerebrospinal fluid (CSF) of 36 acute head-injured patients and 12 patients without head injury as controls. The mean level of beta-ELI in CSF of controls, mild cerebral contusions, and severe cerebral contusion patients were 51.9 +/- 5.6 pg/ml, 110.5 +/- 14.5 pg/ml, and 173.8 +/- 20.1 pg/ml respectively, with significant difference between them. The results also showed that beta-ELI may reflect the prognosis of acute head-injured patients.

Topics: beta-Endorphin; Brain Injuries; Craniocerebral Trauma; Female; Humans; Male; Reference Values

Delayed injury following trauma to the central nervous system (CNS) may be due to the release or activation of endogenous factors. Endogenous opioid peptides have been proposed as one such class of injury factors, based on pharmacological studies demonstrating a therapeutic effect of naloxone and other opiate receptor antagonists following CNS injury. However, changes in brain opioid concentrations following injury have not been evaluated. In the present study, we measured regional alterations in dynorphin (ir-Dyn), leucine-enkephalin (ir-Enk) and beta-endorphin immunoreactivity (ir-End) following low- (1.0-2.0 atmospheres (atm)) or high- (3.0-4.0 atm) level fluid-percussion brain injury in the cat. A significant decrease in ir-End was observed in the hypothalamus at 2 h following high- but not low-level injury. No changes were observed in tissue ir-Enk following either level of injury. Severe brain trauma but not low-level injury caused a significant increase in ir-Dyn in the striatum, frontal cortex, parietal cortex, pons and medulla. In the anterior pituitary, a significant increase in ir-End and a significant decrease in ir-Dyn was observed at 2 h following both levels of injury. Pathological damage to brain tissue after injury was most pronounced in those regions showing significant increases in ir-Dyn but not other opioids. In the medulla, the increase in ir-Dyn but not ir-End or ir-Enk was also significantly correlated with a fall in systemic mean arterial pressure (MAP) at 2 h following high- but not low-level injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; beta-Endorphin; Blood Pressure; Brain Injuries; Cats; Dynorphins; Enkephalin, Leucine; Osmolar Concentration; Radioimmunoassay; Tissue Distribution

The present study examined the role of endogenous opioid peptides in the pathophysiological sequelae of fluid percussion head injury in the cat. Two hours following injury, tissue concentrations of dynorphin-like immunoreactive material (ir-Dyn) were significantly elevated in specific brain regions where injury, as evidenced by histological examination, was most severe. Changes in ir-Dyn but not beta-endorphin-like immunoreactive material (ir-End) were significantly correlated with a fall in regional cerebral blood flow (CBF) that occurred 2 h following injury. Administration of the opiate antagonist WIN44,441-3 (with enhanced activity at kappa-receptors) stereospecifically increased cerebral blood flow to the injured regions.

Topics: Animals; Azocines; beta-Endorphin; Brain Chemistry; Brain Injuries; Cats; Cerebrovascular Circulation; Dynorphins; Female; Male; Narcotic Antagonists; Receptors, Opioid