Effects of Low-Dose Morphine and Fentanyl Infusions on Urinary and Plasma Catecholamine Concentrations during Scoliosis Surgery

Pathak, Kalindi S.; Anton, Aaron H.; Sutheimer, Craig A.

doi:10.1213/00000539-198505000-00011

Cited by 9 publications

(2 citation statements)

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“…Similar improvements in blood pressure and perfusion following naloxone have been observed in septic newborn humans (30) and neonatal piglets (31). In contrast, fentanyl, a potent opiate agonist, causes a dose-dependent inhibition of plasma NE and E in humans (32) and adult dogs (33) as well as decreases in heart rate, blood pressure, and cardiac output (33). The effect on NE is greater than E. These effects are all reversed by naloxone administration.…”

Section: Discussionmentioning

confidence: 69%

Neonatal Adaptation: Naloxone Increases the Catecholamine Surge at Birth

et al. 1987

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ABSTRACT. A marked increase in plasma catecholamines at birth has been described in animals and man. Because the factors that regulate catecholamine secretion are incompletely understood and because it has recently been suggested-that endogenous opiates are important in the regulation of catecholamine secretion, we designed studies to2etermine the influence of opiate receptor blockade prior to delivery on the increase in plasma catecholamines at birth. Term fetal sheep were delivered by cesarean section and randomly assigned to receive naloxone or vehicle. Naloxone was given just prior to umbilical cord cutting as a 2 mg/kg bolus followed by 2 mg/kg/h. Naloxone administration resulted in significantly greater peak levels of plasma norepinephrine (peak levels of 1.5 f 0.4 versus 0.9 f 0.1 ng/ml) and epinephrine (peak levels of 1.4 f 0.7 versus 0.9 f 0.3 ng/ml) and higher norepinephrine values throughout the study period. Naloxone administration was associated with significantly elevated heart rate (peak 184 f 12 versus 207 f 13 beats per min) and blood pressure (peak 95 f 6 versus 88 f 2 mm Hg). These studies demonstrate that opiate receptor blockade from birth markedly augments the neonatal sympathoadrenal response in the term newborn lamb. Fetal and newborn animals secrete catecholamines in response to a variety of stimuli including hypoxia (I), hemorrhage (2), hypothermia (3), labor (4), and delivery (5). The marked increase in catecholamine secretion at birth is particularly important because of the wide range of physiological changes which occur at birth and the importance of the sympathoadrenal system in modulating these changes. In the chronically catheterized fetal sheep, plasma catecholamines begin to rise in the last 3 h of Received September 30, 1986; accepted January 9, 1987 spontaneous labor prior to delivery (4). There is then a further augmentation in plasma levels of both NE and E following delivery and cord cutting (6). We were interested to extend our observations to study the factors that regulate catecholamine release at birth.Two levels of control of catecholamine release have been recognized, including oc 2 receptor-mediated presynaptic inhibition of NE release and inhibition by endogenous opiate peptides. BEND is secreted in response to stress (7) and degrees of hypoxia in fetal sheep known to produce marked catecholamine secretion result in markedly increased levels of circulating BEND (8).Catecholamines and ENK are costored and secreted by the adrenal medulla in response to cholinergic or splanchnic nerve stimulation (9-12). Opiate peptides inhibit catecholamine release by inhibition of neurotransmission in sympathetic ganglia (13,14) and inhibition of adrenal medullary catecholamine secretion (1 5). The physiological significance of these observations in vivo is unclear. In the present study, in order to investigate the role of endogenous opiates in vivo as modulators of sympathoadrenal activity at birth, we compared plasma catecholamine levels with and without continuous opiate receptor...

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Section: Discussionmentioning

confidence: 69%

Neonatal Adaptation: Naloxone Increases the Catecholamine Surge at Birth

et al. 1987

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“…In adult rats, the beneficial effects of naloxone during hemorrhagic shock are blocked by adrenalectomy (3 1). In contrast, fentanyl, a potent opiate agonist, causes a dose-dependent inhibition of plasma norepinephrine and epinephrine in humans (36,37) and adult dogs (38) as well as decreases in HR, blood pressure, and cardiac output. However, the effects of opiate peptides are complex and their excitatory or inhibitory effects depend on the site of administration, the concomitant use of anesthesia, the species studied, the type of receptor affected, and the dose administered (16).…”

Section: Martine Jz Et Almentioning

confidence: 99%

Naloxone Potentiates Epinephrine Release during Hypoxia in Fetal Sheep: Dose Response and Cardiovascular Effects

et al. 1988

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The effect of opiate receptor blockade on the plasma catecholamine response to hypoxemia was studied in seven chronically catheterized fetal lambs in utero. All animals underwent treatment with hypoxia alone, naloxone infusion alone (2 mg/kg) and hypoxia with naloxone at four different dosages (0.1, 0.5, 1.0, and 2.0 mg/kg). Maternal and fetal hypoxia was maintained for 20 min. There were no differences noted in the degree of hypoxemia or acidemia between the different hypoxia treatment groups. Hypoxia increased both norepinephrine and epinephrine plasma levels in all fetal sheep studied. We found a dose-dependent increase in plasma epinephrine levels in response to naloxone infusion during hypoxia. Plasma epinephrine level by 20 min of hypoxia with the 0.1 mg/kg naloxone dose (geometric mean 5366 pg/ml) was significantly more than with hypoxia alone (997 pg/ml). Naloxone at the other doses did not alter the epinephrine responses. There was no augmentation of plasma norepinephrine levels by naloxone at any dose studied. Thus, naloxone augmented the plasma epinephrine response to hypoxia in fetal sheep suggesting that the opiate peptides act as modulators of the sympathoadrenal system. The naloxone dose response differences observed in this study suggest this modulation is largely by antagonism of mu-receptors.

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