Fatty acid transport and incorporation into human erythrocytes in vitro.

When human erythrocytes were incubated in vitro with (14)C-labeled free fatty acids bound to serum albumin, labeled fatty acids were incorporated into erythrocyte triglycerides and phospholipids. The first step in this reaction was the transfer of free fatty acids from the albumin to the cells. This transfer was rapid and reversible. The acids were distributed between albumin and cells according to the relative quantities of albumin and cells present. Each acid had a different distribution coefficient. At equilibrium, relatively larger fractions of the stearic and palmitic acids and smaller fractions of the oleic and linoleic were associated with the cells. All these fatty acids were then slowly incorporated into phospholipids and triglycerides. The rate of incorporation of each was a function of its concentration in the cells, but larger fractions of the oleic and linoleic were incorporated than of the stearic, palmitic, myristic, or lauric. The two processes of transfer and incorporation thus had almost opposite selectivities for the different fatty acids. As a result, the fatty acids incorporated into triglycerides and phospholipids resembled in composition the fatty acids on the albumin except for moderately less stearic acid.

Hypoglycemia-induced prolactin release.

Recent advances in neurosurgical techniques have made it possible to remove pituitary adenomata with minimal morbidity and mortality. These developments have focused attention on early recognition of pituitary tumors, before the onset of visual disturbances or endocrine dysfunction. We have studied the prolactin response to insulin-induced hypoglycemia as an aid in the evaluation of patients with hypothalamic and pituitary disease. Regular insulin 0.1 units/kg was administered intravenously to normal subjects, to patients with pituitary tumors, and to patients with idiopathic galactorrhea. While the normal subjects regularly showed a prolactin response to hypoglycemia, this was observed infrequently in the other groups. It is possible that prolactin nonresponsiveness to insulin hypoglycemia may reflect nonspecific pituitary damage or may represent an abnormality specific to patients with galactorrhea. Our data suggest that the prolactin response to insulin hypoglycemia is a sensitive index of hypothalamic-pituitary dysfunction.

Pathophysiological correlates of thallium-201 myocardial uptake in experimental infarction.

The pathophysiological correlates of thallium-201 (201TI) myocardial uptake were studied in a 24-hour-old closed-chest canine infarct model. Reduction in regional 201Tl uptake correlated well with the magnitude of tissue creatine phosphokinase depletion and microsphere estimates of transmural blood flow. In low flow endocardial regions 201Tl occasionally under-estimated the magnitude of flow reduction. Even slight reductions of 201Tl uptake (less than 0.86 of normal) were associated with histopathological and histochemical evidence of necrosis.

The effects of opiate agonist and antagonist on serum prolactin in primates: possible role for endorphins in prolactin regulation.

Intravenous administration of the opiate receptor antagonist naloxone produced a significant reduction in basal serum PRL concentrations in four male Macaca arctoides. Significant decreases from basal levels were found 15, 30, 45, 60, 90, 120, 150, and 180 min after the iv injection of 0.05 and 0.25 mg/kg naloxone. The iv administration of 0.4 mg/kg morphine produced rapid and significant increases in PRL levels, while 0.04 mg/kg morphine or saline produced no change. Both the dopamine receptor-stimulating agent apomorphine (0.15 mg/kg) and naloxone (0.25 mg/kg) decreased basal serum PRL and blocked the morphine-induced increases in serum PRL. These data support the hypothesis that endorphins are involved in the stimulation of PRL secretion.

Effect of piperoxane on serum prolactin: possible role of epinephrine-mediated synapses in the inhibition of prolactin secretion.

Intravenous administration of 2,5 mg/kg piperoxane produced a rapid and significant increase in serum PRL concentrations in four non-human primates. This PRL increase was maximal 15 min after piperoxane infusion and significant, when compared with baseline levels, in the +15, +30, +45, +60, and +90-min samples. The iv administration of 5 mg/kg piperoxane also produced a rapid and significant increase, whereas saline 0.5 mg/kg or 1.0 mg/kg, did not change serum PRL levels. The iv administration of 10 microgram/kg clonidine, but not saline, produced a rapid and significant reduction in serum PRL levels. PRL levels were significantly reduced +15, +30, and +60 min after the clonidine infusion. Pretreatment with a bolus of 10 microgram/kg clonidine at -15 min caused a significant attenuation of the piperoxane-induced elevation in serum PRL in two monkeys. These data support the hypothesis that alpha-adrenergic receptors are involved in the inhibition of PRL secretion. These data are compatible with noradrenergic or adrenergic mechanisms which remain to be defined.

Hypercalcitoninemia in acute pancreatitis.

Calcitonin was measured in four patients with acute pancreatitis with hypocalcemia. A marked elevation of this hormone was noted in each case and persisted over several days. The peak level of calcitonin preceded the maximum fall in calcium. Among the various factors affecting calcium balance in pancreatitis, calcitonin probably plays an important role.

Dopamine infusion acutely inhibits the TSH and prolactin response to TRH.

Ten normal males were given 100 mug TRH, and blood samples obtained for serum TSH and serum prolactin. After a period of at least one week, the TRH test was repeated while the patients were receiving a dopamine infusion. Both the TSH and prolactin response to TRH were inhibited by dopamine. Dopaminergic neurons may act through the pituitary-portal system to play a role in the regulation of TSH and prolactin secretion.

The effect of aspirin and indomethacin on the TRH response in man.

A double-blind study of the effect of two inhibitors of prostaglandin synthesis on the TRH stimulation of serum TSH and prolactin was carried out in 35 normal males. The subjects were evaluated before and after the administration of indomethacin or aspirin for one week. Both indomethacin and aspirin lowered plasma prostaglandin E and F levels significantly. Indomethacin treatment had no effect on the serum TSH or prolactin response to 100 mug TRH or the serum T3 and T4 levels. In contrast, aspirin treatment significantly decreased the serum TSH response to TRH and significantly lowered mean total serum T3 (RIA) and T4 (D). There was no effect on the prolactin response to TRH. These findings suggest that aspirin blocks TRH responsiveness by a mechanism other than the inhibition of prostaglandin synthesis, probably by its previously demonstrated effect on increasing the fraction of unbound thyroid hormone.

In vitro pituitary responsiveness to gonadotropin-releasing hormone (LH-RH) in intact and castrated male and female rats.

The in vitro response of pituitaries isolated from both normal and 18-21 day post-castration male and female intact rats to incremental doses of synthetic gonadotropin-releasing hormone (LH-RH) has been investigated. Intact male pituitaries released luteinizing hormone (LH) maximally at the smallest dose of LH-RH (0.1 ng/ml) whereas intact female pituitaries released LH in a dose-response fashion. FSH release from intact male pituitaries was considerably greater than that from intact female pituitaries. As with LH, intact male pituitaries appeared maximally stimulated at 0.1 ng/ml of LH-RH. Intact female pituitaries did not release FSH until a 10 ng/ml dose of LH-RH was used. Male and female castrate pituitaries were more susceptible to LH-RH-induced LH and FSH release than were their intact counterparts, although this was more pronounced with regard to LH release. In addition castrate male pituitaries were more sensitive to lower doses of LH-RH than were castrate female pituitaries, this being most pronounced regarding LH release. Castrate female pituitaries released less FSH at the 100 ng/ml dose than at the 10 ng/ml dose, possibly indicating inhibition at these higher doses. In addition, pituitary extraction and serum from normal and castrate male and female rats were examined for LH and FSH content. LH content of castrated rat pituitaries of both sexes was considerably greater than that of their intact counterparts, as expected. However, castrate male pituitaries contained significantly less FSH than intact male pituitaries, whereas the opposite was true for the female groups. Serum LH and FSH levels were increased in the castrate groups with no difference between sexes. Serum from intact males contained considerably more FSH than did the serum from intact females.

Hypercalcitoninemia in infancy.

Immunoreactive calcitonin (iCT) was measured in 19 infants with neonatal hypocalcemia. The infants had a variety of neonatal diseases and stresses. iCT levels were generally elevated to two to 20 times the adult values. Poor correlation existed between the infant age and the level of iCT or between iCT alone and the serum calcium. However, there was significant correlation between the serum calcium and the ratio of the iCT to infant age from conception, suggesting that both infant age and iCT levels in combination may be related to hypocalcemia. Also, it appears that a variety of neonatal stresses may be associated with increased sensitivity to the hypocalcemic effect of iCT, as well as increased levels of iCT.