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Biomedical subjects

V G Watson

Publications and source records attributed to V G Watson.

4 recordsLinked to original sources

Plasma beta-endorphin concentration in infants with apneic spells.

In an attempt to determine whether plasma beta-endorphin (beta-ED) concentrations correlate with occurrence of apnea in preterm infants, measurements were made in three groups of infants. The control group consisted of 11 infants with a mean (+/- SEM) gestational age of 30.5 +/- 0.8 weeks, a mean (+/- SEM) birthweight of 1650 +/- 180 g, and a mean (+/- SEM) postnatal age of 1.3 +/- 0.5 days. Eight infants with apnea, bradycardia, and associated hypotension had a mean (+/- SEM) gestational age, birthweight and postnatal age of 30 +/- 0.9 weeks, 1165 +/- 90 g, and 7.8 +/- 1.9 days, respectively. The third group consisted of eight infants experiencing apnea alone without bradycardia and had a mean (+/- SEM) gestational age, birthweight, and postnatal age of 31 +/- 0.8 weeks, 1380 +/- 125 g, and 2.6 +/- 0.9 days, respectively. The last two groups of infants suffered varying degrees of apnea, but differed in their severity. The plasma endorphin concentrations (+/- SEM) were 26.9 +/- 2, 68.0 +/- 9.0, and 39.6 +/- 2.0 pg/ml, respectively, for the previously described three groups. Significant elevation in beta-ED concentration was observed in the severely apneic infants with bradycardia when compared to the other two groups. The association of increased plasma beta-ED release with severe apneic spells may suggest that these endogenous opiates play a role in the pathophysiology of apnea of prematurity.

Apnea

Plasma beta-endorphin concentrations in neonates associated with acute stress.

Plasma beta-endorphin concentrations were measured in two groups of neonates. The control group (group 1) consisted of 20 infants with a mean gestational age of 31.5 +/- 0.6 weeks and a mean birth weight of 1,720 +/- 135 g. Blood samples were collected at a mean postnatal age of 1.0 +/- 0.3 days. Group 2 consisted of 23 infants with clinical evidence of acute illness and associated significant stress who had a mean gestational age of 33.2 +/- 1.1 weeks and a mean birth weight of 2,075 +/- 225 g. Their blood samples were collected at a mean postnatal age of 3.4 +/- 1.3 days. The mean beta-endorphin concentration in group 1 was 27.8 +/- 6 pg/ml and 63.9 +/- 4.2 pg/ml in group 2 (p less than 0.05). No correlation was observed for gestation or birth weight and beta-endorphin concentrations in group 1; however, in group 2 a positive correlation was seen for gestational age and plasma beta-endorphin concentrations (r = 0.4411) suggesting an increased release of plasma beta-endorphin with increasing gestation when faced with significant clinical stress.

Acute Disease

Hypoxic-ischemic encephalopathy and plasma beta-endorphin.

In an attempt to determine whether hypoxic-ischemic encephalopathy in and of itself or its associated pathologic conditions lead to increased concentrations of plasma beta-endorphin (beta-ED), measurements were made in three groups of term infants. Group 1 (control) consisted of 8 infants with a mean gestation of 38.6 +/- (SE) 0.4 weeks, a mean birth weight of 3,420 +/- 150 g, and a mean postnatal age of 1.4 +/- 0.7 days. Group 2 consisted of 10 infants with a mean gestational age, birth weight and postnatal age of 40.1 +/- 0.5 weeks, 3,310 +/- 80 g and 3,9 +/- 1.1 days, and group 3 included 6 infants with a mean gestational age, birth weight and postnatal age of 40.4 +/- 1 weeks, 3,650 +/- 310 g, and 2.8 +/- 1 days, respectively. The group 2 and 3 infants suffered clinical and neurological evidence of hypoxic-ischemic brain injury from perinatal asphyxia; however, the infants in group 2 suffered additional problems such as meconium aspiration, persistent fetal circulation with ongoing hypoxemia as measured by transcutaneous or umbilical arterial oxygen monitoring. The group 3 infants were normoxemic after resuscitation. The mean plasma beta-ED concentrations were 19 +/- (SE) 2.7, 103 +/- 35.7 and 25 +/- 4.5 pg/ml in groups 1, 2 and 3, respectively. A significant elevation of plasma beta-ED concentration was observed in group 2 when compared to groups 1 and 3. The association of increased plasma beta-ED concentration in infants with hypoxic-ischemic encephalopathy associated with ongoing hypoxemia suggests that hypoxemia may act as a strong stimulus for plasma beta-ED release in term infants.

Asphyxia Neonatorum