beta-endorphin and Cardiovascular-Diseases

The effects of analgesia on plasma beta-endorphin (beta-E), serum cortisol and blood glucose responses were investigated in 20 distressed, mechanically ventilated neonates during the first 3 days of life. Morphine 0.1 mg/kg, meperidine 1 mg/kg or alfentanil 10 micrograms/kg were used for analgesia as clinically indicated. Plasma beta-E, serum cortisol and blood glucose were recorded before analgesia and 1 and/or 2, 12 and 24 h afterwards in the distress group and once in 20 healthy neonates (control group). beta-E, cortisol, and blood glucose before analgesia were significantly higher in the distress group than in the control group. Cortisol values had decreased significantly 2 h after analgesia and blood glucose within 12 h. Plasma beta-E values had decreased to the same level as in the controls 24 h after the start of analgesia. The results indicate that the stress response in the distressed neonates with cardiorespiratory problems, as assessed by beta-E, cortisol, and blood glucose, is attenuated by opioid medication, and it is concluded that these patients should be given adequate analgesia.

Topics: Analgesia; Apgar Score; Asphyxia Neonatorum; beta-Endorphin; Blood Glucose; Cardiovascular Diseases; Gestational Age; Heart Defects, Congenital; Humans; Hydrocortisone; Infant, Newborn; Persistent Fetal Circulation Syndrome; Respiration Disorders; Respiratory Distress Syndrome, Newborn

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.

Topics: Animals; Arginine Vasopressin; beta-Endorphin; Blood Pressure; Cardiac Output; Cardiovascular Diseases; Dogs; Endorphins; Endotoxins; Escherichia coli; Female; Heart Rate; Hydrocortisone; Kinetics; Male; Naloxone; Shock, Septic