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Biomedical subjects

G H Greeley

Publications and source records attributed to G H Greeley.

At least 145 records · Page 8Linked to original sources
PubMed1984

Physiologic role of cholecystokinin in the intestinal phase of pancreatic polypeptide release.

Release of pancreatic polypeptide (PP) after a meal is biphasic, with an early transient peak believed to be under cholinergic control, and a secondary, prolonged intestinal phase thought to be mediated by hormones. Endogenous release of PP was stimulated by intraduodenal oleate (6.8 mmol/hr) or by intravenous administration of pure cholecystokinin-33 (CCK-33, 0.1 micrograms/kg/hr) in five dogs. Radioimmunoassay measurements of plasma concentrations of PP and CCK-33 were compared by linear regression analysis before and after vagotomy. Correlations between plasma concentrations of PP and CCK-33 before vagotomy (r = 0.83 [oleate], r = 0.97 [IV-CCK-33]) and after vagotomy (r = 0.92 [oleate], r = 0.92 [IV-CCK-33]) were highly significant. Changes in plasma concentrations of PP relative to a particular increment in plasma CCK-33 (before vagotomy) were similar, whether stimulated by oleate or by exogenous CCK-33. After vagotomy, less PP was released relative to a change in plasma CCK-33 (stimulated by oleate or by exogenous CCK-33), but the PP response relative to a change in plasma CCK-33 induced by the two stimuli remained remarkably similar. These results provide evidence that the intestinal phase of physiologic release of PP is mediated to a large extent through release of CCK.

Animals↗
PubMed1984

Intracerebroventricular administration of cholecystokinin-8 elevates plasma pancreatic polypeptide levels in awake dogs.

The effect of intracerebroventricular (ICV) administration of cholecystokinin-8 (CCK-8) (0.5, 1.0, 2.0, 4.0 micrograms) on plasma levels of pancreatic polypeptide (PP) was studied in conscious dogs. ICV administration of CCK-8 (1.0, 2.0, 4.0 micrograms) produced a rapid and transient elevation in plasma concentrations of PP. Peripheral muscarinic receptor blockade with atropine or truncal vagotomy abolished PP secretion induced by ICV CCK-8. Pretreatment with ICV atropine also prevented the elevation in plasma PP induced by CCK-8. Plasma levels of CCK-33/39, CCK-8, and gastrin were not affected by ICV CCK-8. Our results indicate that central administration of CCK-8 selectively elevated plasma PP concentration. Since the effect of CCK-8 on plasma PP was abolished by central and peripheral atropine pretreatment, as well as by vagotomy, central and peripheral vagal cholinergic mechanisms appear to participate in release of PP that is induced by CCK-8 given by ICV injection.

Animals↗
PubMed1984

Release of cholecystokinin in response to food and intraduodenal fat in pigs, dogs and man.

The present study was done to compare endogenous cholecystokinin-33 release in response to physiologic stimuli (meal, fat) in pigs, dogs and man. Plasma levels of cholecystokinin-33 were monitored using a radioimmunoassay for cholecystokinin which detects only cholecystokinin-33 and cholecystokinin-39. Ingestion of a meal caused release of cholecystokinin-33 within five, 20 and 120 minutes in man, pigs and dogs, respectively. Intraduodenal administration of corn oil resulted in a significant release of cholecystokinin-33 within 20 minutes in dogs, pigs and man.

Adult↗
PubMed1984

Role of neurotensin in pancreatic secretion.

The objective of this study was to examine the effect of neurotensin (NT) on pancreatic exocrine secretion in awake dogs (n = 5) with chronic gastric and pancreatic fistulas. Intravenous (IV) infusion of NT (1 microgram/kg/hr) alone significantly stimulated pancreatic secretion of protein and bicarbonate without causing release of secretin or cholecystokinin-33 (CCK-33). IV NT potentiated the secretory response of pancreatic bicarbonate to the intraduodenal (ID) infusion of HCl alone and to ID infusions of the amino acids, phenylalanine and tryptophan (AA) alone, as well as to an ID mixture of AA plus HCl. IV NT acted in an additive manner with ID AA, ID HCl, or ID AA plus HCl in the stimulation of pancreatic protein output. The addition of IV NT to each luminal secretagogue (ID AA, ID HCl, or ID AA plus HCl) failed to elevate plasma concentrations of CCK-33 or secretin over those observed during ID infusion of each secretagogue alone. ID corn oil (Lipomul) stimulated the simultaneous release of CCK-33, NT, and secretin significantly; IV infusion of NT (0.5 microgram/kg/hr) resulted in plasma NT levels that were similar to levels observed after ID Lipomul. These studies provide evidence that endogenous NT, CCK, and secretin may interact in the physiologic regulation of pancreatic exocrine secretion.

Amino Acids↗
PubMed1984

Comparison of cholecystokinin release and gallbladder emptying in men and in women at estrogen and progesterone phases of the menstrual cycle.

Why are gallstones more common in women than in men? To investigate this, we measured gallbladder emptying (by ultrasonography) and release of endogenous cholecystokinin (CCK) (by specific radioimmunoassay) in eight men and nine women in response to ingestion of corn oil (1 gm/kg). Each woman was studied on the fourteenth and twenty-first day of her menstrual cycle, estimated to be the estrogen (women [E] ) and progesterone (women [P] ) peaks, respectively. Fasting plasma concentrations of CCK were significantly higher in women (E) (135 +/- 7 pg/ml) than in men (99 +/- 13 pg/ml) but not significantly higher than in women (P) (113 +/- 11 pg/ml). The peak increase in CCK concentration over basal concentration and the integrated release of CCK were not significantly different from one group to another. Men had a larger fasting gallbladder volume (GBV) (21.4 +/- 3.2 ml) than did women (E) (12.4 +/- 2.1 ml) and women (P) (14.2 +/- 2.1 ml) and emptied more GBV in response to fat than did the women. The residual GBV and fractional emptying after ingestion of corn oil were not different among the three groups. Measurements of plasma CCK and GBV during the contraction phase were highly correlated in all groups. It appears, from these data, that the increased prevalence of gallstones in women relative to men cannot be explained on the basis of significant differences either in release of CCK or in gallbladder motility. Linear regression lines that were developed indicated that the mean change in GBV relative to a given change in plasma CCK was significantly higher in men than in women. Differences between men and women in this hormonal-motility relationship may contribute to the incidence of gallstones in premenopausal women.

Adult↗
PubMed1983

Biologic and radioimmunologic activity of cholecystokinin in regions of mammalian brains.

The distribution and heterogeneity of cholecystokinin (CCK) in different regions of the central nervous system (CNS) of 12 adult rats and six cows was determined by means of specific radioimmunoassays. In addition, the biologic activity of immunoreactive material was evaluated in a bioassay that used a rabbit gallbladder-strip preparation. High amounts of immunochemically detectable CCK-8 (20.2 +/- 1.5 pmol/g) and CCK-33 (33.7 +/- 3.3 pmol/g) and of biologically active CCK were found in the telencephalon, although concentrations decreased progressively from the rostral to the caudal portions of the brain. The distribution and biologic activity of CCK was similar in rat and cow brain. Ratios of biologic to immunologic activity ranged from 1.0 to 8,0 and were higher for CCK-8 than for CCK-33. The results indicate that (1) CCK-8 and CCK-33 immunoreactivity are widely distributed throughout the CNS in a unique and differential manner; (2) CCK is biologically active in all the regions of the brain, with a pattern of distribution similar to that found with radioimmunoassay; (3) measurable bioactivity was equal to or greater than measurable immunoreactivity in all areas of the brain in rat and cow; and (4) CCK is present in tissues without significant species differences between rat and cow.

Animals↗
PubMed1983

Release of cholecystokinin in conscious dogs: correlation with simultaneous measurements of gallbladder pressure and pancreatic protein secretion.

We have used an antibody that cross-reacts with cholecystokinin-33/39 to measure cholecystokinin release into plasma; this release was correlated with simultaneous measurements of gallbladder pressure and pancreatic protein secretion in response to intestinal administration of fat. Nine conscious dogs were prepared with chronic gastric, pancreatic, and gallbladder fistulas. Plasma cholecystokinin, gallbladder pressure, and pancreatic protein output were measured simultaneously before, and at intervals during, a 2-h intraduodenal infusion of sodium oleate. This infusion resulted in significant (p less than 0.05) elevations of plasma cholecystokinin (from 64 +/- 7 to 181 +/- 27 pg/ml), in gallbladder pressure (from 13 +/- 1 to 27 +/- 3 cmH2O), and in pancreatic protein output (from 65 +/- 7 to 148 +/- 21 mg/15 min); all measurements are from the basal state to 120 min after the onset of duodenal perfusion. Plasma concentrations of cholecystokinin were significantly correlated with gallbladder pressure (r = 0.91, p less than 0.05) and pancreatic protein output (r = 0.84, p less than 0.05). These data provide evidence that release of endogenous cholecystokinin, as measured by radioimmunoassay, can be correlated with the classic biologic actions ascribed to cholecystokinin.

Animals↗
PubMed1980

A delayed LH/FSH rise after gonadectomy and a delayed serum TSH rise after thyroidectomy in monosodium-L-glutamate (MSG)-treated rats.

The serum LH and FSH rise after gonadectomy and the serum TSH rise after thyroidectomy were examined in rats that received monosodium-L-glutamate (MSG) as neonates. The rise in serum gonadotrophins after gonadectomy was significantly delayed in both adult and peripubertal MSG-treated rats when compared to control castrates. Serum LH and FSH levels, however, eventually achieved levels in MSG-treated rats that were not significantly different than those of controls. The serum TSH rise after thyroidectomy was significantly delayed in adult female MSG-treated rats, but not in prepubertal female MSG-treated rats. Pituitary responsiveness to both exogenous LH-RH and TRH was unaffected by neonatal MSG treatment, with one exception: pituitary responsiveness to HL-RH of orchidectomized peripubertal males was blunted significantly. The results are discussed in terms of the possible neurotoxic effects of neonatal MSG treatment, as well as the altered hypothalamic sensitivity to gonadal steroids.

Animals↗
PubMed1980

Studies of the neural mechanisms by which hypothyroidism decreases prolactin secretion in the rat.

These studies report that chronic hypothyroidism in the rat is accompanied by decreased serum prolactin. An investigation of those mechanisms by which hypothyroidism decreases prolactin secretion revealed the following findings: (1) activation of tyrosine hydroxylase in the median eminence (ME) and increase in the turnover-rate of dopamine (DA) in the ME; (2) a decreased content and in vitro release of prolactin by pituitaries from hypothyroid rats; (3) decreased [3H]spiroperidol binding to pituitary homogenates obtained from hypothyroid rats, and (4) normal increase of serum prolactin following administration of haloperidol. Comparison of the effects of hypothyroidism on dopaminergic terminals of the striatum with those of the ME was made and the following tentative conclusions proposed. Hypothyroidism presumably increases the release of DA into the pituitary portal system. A deficiency of thyroid hormone desensitizes the pituitary lactrotrope to inhibition by DA, decreases the total pituitary prolactin content and presumable also reduces the peripheral catabolism of prolactin. The overall net effect of hypothyroidism is, therefore, a decrease in serum prolactin levels which can increase normally following haloperidol. The mechanism by which a deficiency of thyroid hormone alters the function of the tuberoinfundibular and striatal dopaminergic systems is unknown.

Animals↗
PubMed1980

Prolactin in cerebrospinal fluid: a probable site of prolactin autoregulation.

The purpose of this study was to examine the thesis that increasing concentrations of prolactin within the cerebrospinal fluid (CSF) increase the activity of dopaminergic terminals within the median eminence and that this increased dopaminergic activity is temporally associated with a suppression of endogenous prolactin secretion. To avoid difficulties encountered in performing catecholamine turnovers in the undisturbed rat, the measurement of tyrosine hydroxylase was validated as an index of dopaminergic activity within the median eminence. In the median eminence, but not the medial preoptic area, parallel increases in the activity of tyrosine hydroxylase and the turnover of dopamine (but not norepinephrine) occurred following hyperprolactinemia. Twenty-six hours but not 2.5 h after the subcutaneous administration of ovine prolactin, the activity of tyrosine hydroxylase was increased in the median eminence, and endogenous prolactin secretion was inhibited. During a 26 h continuous intracerebroventricular (icv) infusion (88 ng/h) of rat prolactin, there was a complete suppression of endogenous prolactin secretion. Twenty-six but not 2.5 h after the initiation of the icv infusion of prolactin, there was an increase in tyrosine hydroxylase activity in the median eminence. The results of these studies suggest that: (1) measurement of tyrosine hydroxylase activity within the median eminence is a useful index of the activity of dopaminergic terminals; (2) increasing concentrations of prolactin within the CSF suppressed prolactin secretion by the anterior pituitary; (3) this suppression of prolactin is accompanied by an increased activity of dopaminergic terminals within the median eminence; (4) those neural structures concerned with the regulation of prolactin secretion respond directly to prolactin itself; (5) the autoregulation by prolactin of its own secretion manifests a certain latency more characteristic of a tonic rather than a phasic inhibitory control; and finally, (6) dopaminergic terminals in the median eminence but not the preoptic area appear uniquely sensitive to prolactin.

Animals↗
PubMed1980

Decreased serum 3,5,3'-triiodothyronine and thyroxine levels accompanying acute and chronic ritalin treatment of developing rats.

Basal serum levels of T3, T4, and TSH and the serum TSH increment after TRH are reported for rats chronically or acutely treated with ritalin. Serum levels of T3 and T4 are significantly reduced in rats chronically treated with ritalin twice daily for 21 days. Female rats appear to be more susceptible than males to the suppressive action of ritalin. Ritalin appears to accelerate the circulatory clearance of serum T3 and T4. Basal serum levels of TSH demonstrate graded elevations after sequentially higher doses of ritalin and, in most cases, hypophyseal responsivity (delta TSH) to TRH challenge appears to be marginally enhanced by chronic ritalin treatment. Thyroidal responsiveness is not adversely affected by chronic ritalin treatment. Serum T3 and T4 levels return to normal levels after chronic ritalin treatment is discontinued; however, the maturational rise of the basal serum level of TSH is permanently depressed in 35 and 100 mg/kg BW ritalin-treated males. Acute administration of ritalin (35 or 100 mg/k BW) results in a significant reduction of the serum levels of T3 and T4 within 5 h and depressed levels persist for 18 days.

Aging↗