Hypophysectomy does not alter the effects of somatostatin or growth hormone on canine splanchnic biogenic amine release.

We have demonstrated previously that growth hormone (GH) and somatostatin (somatotropin release inhibitory factor, SRIF) exert comparable effects on the release of splanchnic biogenic amines. The purpose of the present investigation was to study further the response of the two hormones and see whether the similarity persists in dogs completely deprived of endogenous GH. Experiments were conducted in seven hypophysectomized dogs fitted with an indwelling portal catheter.

Secretory pattern of canine growth hormone.

Our aim was to define the secretory pattern of growth hormone (GH) under basal conditions in fasted, conscious, male dogs accustomed to handling. Blood samples were withdrawn from a cephalic vein at 15-min intervals. In this way, any ultradian rhythms, if present, could be detected within the frequency range of 0.

The effect of beta-endorphin on biogenic amines, insulin, and glucagon levels in the hepatic portal circulation of normal and pancreatectomized dogs.

The effect of peak concentrations of beta-endorphin on hepatic portal and peripheral levels of plasma catecholamines, free serotonin, glucose, insulin, and glucagon was studied in trained, conscious, normal adult dogs fitted with an indwelling portal catheter. An injection of synthetic human beta-endorphin (20 micrograms/kg BW) into a cephalic vein produced a significant rise in the portal concentration of dopamine, norepinephrine, and epinephrine. The rise was accompanied by a reduction of portal free serotonin levels.

Insulin dependence of the actions of growth hormone and somatostatin on splanchnic biogenic amines of the dog.

It is known from studies previously conducted in this laboratory that an iv injection of ovine growth hormone (GH, 100 micrograms/kg BW) or an equimolar amount of somatostatin (SRIF, 7.5 micrograms/kg BW), given to normal conscious dogs into a saphenous vein, leads to a significant increase in hepatic portal plasma serotonin and a simultaneous decrease in the concentrations of dopamine, norepinephrine and epinephrine. The changes take place within 12 minutes after the injection and are observed only in the portal circulation.

Somatostatin mediates the effect of growth hormone surges on splanchnic biogenic amines.

Experiments were conducted in trained, conscious dogs fitted with an indwelling portal catheter. Radioenzymatic methods were employed for the quantitative measurement of plasma-free serotonin and catecholamines. An injection of ovine growth hormone (GH, 100 micrograms/kg) or an equimolar amount of somatostatin (somatotropin release inhibitory factor, SRIF, 7.

The effect of tryptophan on biogenic amines in the hepatic portal circulation of the dog.

Mongrel dogs were fitted with indwelling hepatic portal catheters. After recovery from surgery, experiments were conducted in fasting, unrestrained, fully conscious, normal dogs which were accustomed to handling and withdrawal of blood samples. L-Tryptophan, a specific serotonin precursor, was injected into a saphenous vein, 10 microM/kg body weight, dissolved in saline.

Secretory patterns of glucoregulatory hormones in prehepatic circulation of dogs.

The temporal organization of patterns of secretion of insulin, glucagon, and somatostatin was studied in basal conditions in normal or pancreatectomized dogs fitted with an indwelling hepatic portal catheter. Portal and peripheral blood samples were collected at a 7.5- or 15-min frequency, which covered the medium range of the ultradian period.

The effect of growth hormone on biogenic amines in the hepatic portal circulation of the dog.

The effects of a spike concentration of growth hormone (GH) on hepatic portal and peripheral levels of free serotonin and catecholamines were studied by improved radioenzymatic methods in trained, conscious, normal, adult dogs fitted with an indwelling portal catheter. An injection of ovine GH (6 or 100 micrograms/kg) into a cephalic vein produced in the hepatic portal circulation a transient, statistically significant rise of serotonin and a concomitant significant reduction in the concentration of dopamine, norepinephrine, and epinephrine. No change was found in the peripheral circulation, partly because the amines were conjugated to sulfates and glucuronides and these derivatives are not detectable by our assays.

Rapid changes in hepatic glucose output after a pulse of growth hormone in dogs.

In response to a single intravenous injection of bovine growth hormone (GH, 100 micrograms/kg) the non-steady-state turnover of glucose, as well as portal levels of insulin (IRI), glucagon (IRG), somatostatin (SRIF), and glucose were determined in normal conscious dogs. Using the two-compartment model validated to calculate rapid turnover changes and tracer infusion methods, the rate of hepatic output of glucose [Ra(t)] was found to be increased, reaching a maximum of 224 mg/min, 7.4 times the basal rate, 4 min after injection of GH.

A new technique for hepatic portal sampling in the conscious dog.

A technique for implantation of a silastic catheter into the portal vein is described. The central end of the catheter is passed through a puncture hole into a tributary of the portal vein. The peripheral free end, occluded by a rubber membrane, is passed through the abdominal wall and buried under the skin.

The effect of glucagon on the glycosaminoglycan content of canine arteries.

Hypophysectomized young beagles were treated for 21 days with pharmacological doses of glucagon, administered intramuscularly in two daily injections of 0.5 mg each. Hyaluronic acid, heparan, dermatan and isomeric chondroitin sulphates were determined in aorta, carotid, iliac, renal, mesenteric and coronary arteries.

Growth hormone stimulates serotonin secretion into the hepatic portal circulation.

Hepatic portal plasma concentrations of free serotonin were found to be transiently but significantly elevated in normal dogs following a single injection of ovine growth hormone into a peripheral vein. The data are consistent with the concept that spike concentrations of growth hormone are capable of altering the splanchnic concentration of agents that are concerned with glucose homeostasis.

Diurnal episodic pattern of insulin secretion in the dog.

Sampling portal blood every 15 min by means of indwelling cannulae, we have found evidence that basal insulin secretion in nonanesthetized dogs takes place in six or seven major secretory episodes over a 24-h period. Reproducible patterns were obtained in four experiments conducted on three normal animals. When frequency of peaks was plotted against the log of insulin concentration, a normal distribution was obtained (lognormal distribution).

Arterial glycosaminoglycans in diabetic dogs.

The glycosaminoglycan (GAG) composition of a number of large and medium-sized arteries was studied in 6 alloxan-diabetic beagles and was compared with 6 normal, age-matched controls. Diabetic animals were maintained on diet and insulin for 100 days. The aortic arch, thoracic and abdominal segments, external iliac, superior mesenteric, renal, common carotid and coronary arteries were analyzed for hyaluronic acid (HA) and for heparan (HS), dermatan (DS), and chondroitin (CS) sulphates.

Effect of growth hormone on acute glucagon and insulin release.

The aim was to clarify whether or not sudden spike concentrations of plasma growth hormone (GH) can affect the endocrine pancreas in vivo. The peaking of GH was reproduced by an injection (10 mg/kg iv) of bovine GH to anesthetized normal, pancreatectomized, and alloxan-diabetic dogs. In portal but not in peripheral blood, immunoreactive plasma glucagon (IRG), glucagon-like activity (GLI), and immunoreactive insulin (IRI), were significantly elevated within 10 min in normal and alloxan-diabetic dogs.

The relationship of hormones to arterial glycosaminoglycans and atherosclerosis.

Glycosaminoglycan fractions were measured in representative large and medium sized arteries of normal, hypophysectomized and hormone treated young beagles. Hyaluronate, heparan sulphate, dermatan sulphate and the isomeric chondroitin sulphates were determined in the aortic arch, thoracic and abdominal segments, in the external iliac, superior mesenteric, renal, common carotid and coronary arteries. The hormones used for replacement therapy of hypophysectomized animals were growth hormone, thyroxine, cortisone and the sex hormones testosterone, estrogen and progesterone.

Effect of hormones on the glycosaminoglycan content of canine renal arteries.

The effect of hypophysectomy and replacement therapy with individual hormones such as somatotropin, cortisone, estradiol, progesterone and testosterone on the glycosaminoglycan (GAG) composition of renal arteries was studied in young beagles. The renals from normal animals showed a uniformly low total GAG content of about two thirds of the value found for aorta and coronary arteries. Neither hypophysectomy nor hormone replacement altered the GAG content, with the exception of estradiol which showed a marked effect by raising the hyaluronic acid content to nearly double the normal value.

The effect of sex hormones on glycosaminoglycan content of canine aorta and coronary arteries.

Hyaluronate (HA), heparan sulfate (HS), dermatan sulfate (DS) and isomeric chondroitin sulfates (CS) were measured in vascular walls of 9-10 months old normal and hypophysectomized female beagles treated with sex hormones. Following hypophysectomy the animals were maintained for 8 weeks without any hormonal replacement therapy and then they were exposed for 3 weeks to parenteral treatment with sex hormones. One group received twice weekly 25 mg testosterone, another group was given the same amount of progesterone, and a third group received on day 1 and day 14, estrogens in 2 injections, consisting of a mixture of 10 mg short-acting estradiol-17-phenylpropionate and 2.

Failure of ergotamine to alter the lipolytic effect of somatotropin in dogs.

Hypophysectomized dogs were injected intravenously with bovine somatotropin (GH), and plasma free fatty acid (FFA) concentrations were measured over a period of 2 h. The response consisted of an initial reduction in the concentration of plasma FFA followed by a rebound and a delayed rise above baseline values. When the animals were given a single intravenous injection of ergotamine tartrate 30 min prior to the administration of GH, the biphasic pattern with the sluggish rise in plasma FFA was retained.

Effect of ergot alkaloids on sulfonylurea-stimulated insulin secretion in dogs.

The insulinogenic response to a standard i.v. dose of a sulfonylurea can be markedly augmented in normal, conscious dogs if they are given 30 min earlier a single i.

Lack of somatotropin effect on glycosaminoglycan content of canine coronary arteries.

Eight beagles, 10 months of age, were surgically hypophysectomized and subsequently maintained without hormonal replacement therapy for 8 weeks. Four of the animals then received daily injections of bovine somatotropin (0.2 mg/kg subcutaneously for 3 weeks), while the remaining 4 were treated with saline.

Lipolysis as a function of cell numbers and fat content: comparison between isolated rat and dog adipocytes.

The lipolytic responses to dihydroergotamine (5 mug/mi) of isolated rat adipocytes andto epinephrine (50 ng/m1 and 1 mug/m1) of both rat and dog adipocytes were measured over a period of two hours. Glycerol release was calculated as a function of either glycerol ester content or of cell number per incubation vial. The conventional calculation based on glyceride content gave the following results: a) epididymal fat cells from rats weighing less than 160 gm were more sensitive to dihydroergotamine and epinephrine than were fat cells from heavier animals weighing close to 200 gm; b) dog adipocytes from abdominal subcutaneous tissue were less sensitive to eipnephrine than were rat adipocytes.

Inhibition of sulphonylurea-stimulated insulin secretion by beta adrenergic blockage.

Normal dogs were injected i.v. with a single dose of 0.