Effect of opiate receptor blockade by naloxone on development of ischemic cardiac arrhythmias

1989 ◽  
Vol 107 (5) ◽  
pp. 598-600
Author(s):  
G. I. Kositskii ◽  
S. D. Mikhailova ◽  
S. L. Gorozhanin ◽  
T. M. Semushkina
Keyword(s):  
Cardiac Arrhythmias ◽  
Opiate Receptor ◽  
Receptor Blockade ◽  
Ischemic Cardiac Arrhythmias

Opiate Receptor Blockade and Diurnal Pituitary and Adrenal Hormone Levels

1985 ◽  
Vol 17 (02) ◽  
pp. 86-89 ◽  
Author(s):  
R. D. G. Leslie ◽  
R. W. G. Prescott ◽  
P. Kendall-Taylor ◽  
D. Cook ◽  
D. Weightman ◽  
...  
Keyword(s):  
Opiate Receptor ◽  
Receptor Blockade ◽  
Hormone Levels ◽  
Adrenal Hormone

Effect of opiate-receptor blockade on normoglycemic and hypoglycemic glucoregulation

1986 ◽  
Vol 250 (3) ◽  
pp. E236-E242 ◽  
Author(s):  
K. M. el-Tayeb ◽  
P. L. Brubaker ◽  
H. L. Lickley ◽  
E. Cook ◽  
M. Vranic
Keyword(s):  
Plasma Glucose ◽  
Glucose Production ◽  
Opiate Receptor ◽  
Receptor Blockade ◽  
Endogenous Opiates ◽  
Counterregulatory Hormones ◽  
Beta Endorphin ◽  
Initial Decrease ◽  
Pituitary Adrenal Axis ◽  
Naloxone Treatment

By use of the opiate antagonist naloxone, we have examined the hormonal and metabolic responses to opiate-receptor blockade under basal conditions and during insulin-induced hypoglycemia in normal dogs. Naloxone treatment had no measurable effect on glucose concentration, turnover, and norepinephrine levels, but stimulated plasma epinephrine, glucagon, and cortisol and inhibited insulin release. Insulin (7 mU X kg-1 X min-1) decreased plasma glucose to 42 +/- 4 mg/dl due to an initial decrease in glucose production and an increase in glucose disappearance. Glucose production then increased, and plasma glucose plateaued. After 50 min of insulin infusion, epinephrine levels increased 26-fold (P less than 0.05), norepinephrine and glucagon 3-fold (P less than 0.02), and cortisol 4-fold (P less than 0.01). Similarly, plasma beta-endorphin and adrenocorticotropin (ACTH) were elevated (6-fold, P less than 0.01, and 16-fold, P less than 0.05, respectively). When naloxone was given during insulin-induced hypoglycemia, there was earlier release of epinephrine, glucagon, beta-endorphin, ACTH, and cortisol as well as a greater release of glucagon (P less than 0.001) and cortisol (P less than 0.0001). This resulted in a greater increase in glucose production (P less than 0.01), thus lessening the insulin-induced hypoglycemic excursion. In conclusion, in the dog, endogenous opiates may play a small role in the regulation of basal insulin and glucagon release and can inhibit the pituitary-adrenal axis under basal conditions and during hypoglycemia. Thus increased glucose production in response to insulin-induced hypoglycemia is consistent with the excessive response of counterregulatory hormones during opiate-receptor blockade.

The Effects of Selective mu1 Opiate Receptor Blockade on Breathing Patterns in the Fetal Lamb

1991 ◽  
Vol 30 (2) ◽  
pp. 202???206
Author(s):  
PETER Y. CHENG ◽  
JOHN A. DECENA ◽  
DUN-LI WU ◽  
Y I CHENG ◽  
HAZEL H. SZETO
Keyword(s):  
Opiate Receptor ◽  
Receptor Blockade ◽  
Breathing Patterns ◽  
Fetal Lamb

CEREBROCORTICAL AND MEDULLARY BLOOD FLOW CHANGES AFTER GENERAL OPIATE RECEPTOR BLOCKADE DURING HEMORRHAGIC SHOCK IN CATS

Shock ◽  
1997 ◽  
Vol 7 (4) ◽  
pp. 288-293 ◽  
Author(s):  
Katalin Komjáti ◽  
Peter Sandor ◽  
Norbert Sandor ◽  
Laszlo Szirmai ◽  
Maria H-Velkei ◽  
...  
Keyword(s):  
Blood Flow ◽  
Hemorrhagic Shock ◽  
Opiate Receptor ◽  
Receptor Blockade ◽  
Medullary Blood Flow ◽  
Flow Changes
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