Biomedical subjects

V L Go

Publications and source records attributed to V L Go.

At least 109 records · Page 6Linked to original sources

PubMed1987

Frequency and significance of serum alpha-fetoprotein elevation in severe hepatitis B surface antigen-negative chronic active hepatitis.

To determine the frequency and significance of alpha-fetoprotein elevation in severe hepatitis B surface antigen-negative chronic active hepatitis, 558 serum samples obtained from 83 patients were tested by an immunoenzymometric assay. All patients received corticosteroids and sampling occurred at 6-12-mo intervals during 96 +/- 6 mo of follow-up. Twenty-nine patients (35%) had an abnormal level. In 26 patients, the abnormality was at presentation. In 3 patients, the abnormality developed 11-127 mo later. Two of these patients had primary hepatocellular carcinoma. Serum aspartate aminotransferase levels were higher in patients with an alpha-fetoprotein elevation at presentation (p less than 0.02). After therapy, the alpha-fetoprotein level normalized and patients entering remission had lower levels than at entry (p less than 0.001). alpha-Fetoprotein levels, however, did not correlate closely with serum aspartate aminotransferase levels at entry nor did they distinguish patients with different patterns of histologic activity. Outcomes after therapy were similar in patients with and without alpha-fetoprotein elevation. Three patients (4%) developed primary hepatocellular carcinoma after 113 +/- 26 mo but only 2 had elevated alpha-fetoprotein levels. We conclude that elevation of the alpha-fetoprotein level occurs commonly at presentation. The abnormality frequently resolves after corticosteroid therapy and it does not have prognostic significance. An elevation that occurs after treatment suggests primary hepatocellular carcinoma.

Adolescent↗

PubMed1987

Gastric electromechanical and neurohormonal function in anorexia nervosa.

The gastrointestinal motor function in patients with anorexia nervosa is poorly understood, although it may be relevant to the pathophysiology of the disorder. We have undertaken a multidisciplinary study of 8 patients with anorexia nervosa and 8 age- and sex-matched controls. We have characterized their gastrointestinal and neurohormonal function by measuring (a) gastric electrical activity, (b) antral phasic pressure activity, (c) gastric emptying of solids and liquids, and (d) hormonal and autonomic function. Patients with anorexia nervosa at the time of the initiation of therapy presented with (a) increased episodes of gastric dysrhythmia (mean percentage of dysrhythmic time: 9.75 patients vs. 0.48 controls during fasting, p less than 0.02; 7.21 patients vs. 0.18 controls postcibally, p less than 0.001), (b) impaired antral contractility (mean motility index, 12.8 patients vs. 14.2 controls, p less than 0.002), (c) delayed emptying of solids, (d) decreased postcibal blood levels of norepinephrine and neurotensin (levels of beta-endorphin, insulin, glucagon, gastric inhibitory polypeptide, gastrin, cholecystokinin, and human pancreatic polypeptide were normal), and (e) impaired autonomic function (resting diastolic blood pressure and skin conductance were decreased and the response to the cold pressor test was dampened). Differences between patient and control groups were statistically significant. We conclude that patients with anorexia nervosa present multiple gastrointestinal abnormalities involving control mechanisms as well as target organs.

Adolescent↗

PubMed1987

Effect of total sympathectomy and of decentralization on migrating complexes in dogs.

The effect of total sympathectomy and of decentralization on interdigestive myoelectric activity of the stomach and small intestine and on cycling levels of plasma motilin were studied in conscious dogs. In controls, 98.3% +/- 7.9% of the migrating myoelectric complexes (mean +/- SD) originated in the stomach. In sympathectomized dogs, 38.17% +/- 16.7% originated in the stomach, 35.8% +/- 12.3% in the duodenum, and 26.3% +/- 4.3% in the jejunum. In decentralized dogs, 5.3% +/- 1.4% of the migrating myoelectric complexes originated in the stomach, 71.0% +/- 16.5% in the duodenum, and 23.9% +/- 17.4% in the jejunum. Cycling of plasma motilin was not affected by long-term sympathectomy but coordination of peak levels of plasma motilin and initiation of gastric migrating myoelectric complexes was disrupted in decentralized dogs. These data suggest that central nervous input is required for initiation of migrating myoelectric complexes in the stomach and that central vagal but not central sympathectic input is essential for cycling of plasma motilin.

Animals↗

PubMed1987

The effect of unilateral dorsal root ganglionectomies or ventral rhizotomies on alpha 2-adrenoceptor binding to, and the substance P, enkephalin, and neurotensin content of, the cat lumbar spinal cord.

The density of alpha 2-adrenoceptor binding sites and the content of substance P, enkephalins, and neurotensin were determined in quadrants of the lumbar spinal enlargement of control cats and of cats upon which either unilateral dorsal root ganglionectomies or unilateral ventral rhizotomies had been performed. The performance of unilateral dorsal root ganglionectomies resulted in a significant decrease (45-55%) of substance P content in the ipsilateral dorsal horn 7 and 21 days postoperatively. The concentration of alpha 2-adrenoceptor binding sites ([3H]rauwolscine Bmax) in the ipsilateral dorsal horn was consistently and significantly decreased at these same postganglionectomy times (20% reduced relative to the contralateral dorsal horn). Enkephalin content 7 and 21 days after ganglionectomies was not significantly different from control, whereas the neurotensin content of the ipsilateral dorsal horn was significantly increased in the 21-day survival cats. The performance of unilateral ventral rhizotomies did not produce any statistically significant changes in the density of alpha 2-adrenoceptor binding sites or in the substance P or enkephalin content of any spinal quadrant. The neurotensin content of both the ipsilateral dorsal and ipsilateral ventral quadrants of the ventral rhizotomized cats was significantly increased. The significant decrease of alpha 2-adrenoceptor binding site concentration in the ipsilateral dorsal horn after unilateral dorsal root ganglionectomies suggests that approximately 20% of the alpha 2-adrenoceptors present within the cat lumbar spinal dorsal gray are located on the axons or terminals of primary sensory afferents. Consistent with this interpretation of the ganglionectomy results, we found significant levels of saturable [3H]rauwolscine binding to homogenates of the cat L4-Sl spinal dorsal root ganglia. Because alpha 2-adrenoceptor binding sites in the ipsilateral ventral lumbar spinal gray were not significantly reduced after unilateral ventral rhizotomies, our results provide no evidence for the location of alpha 2-adrenoceptor on lumbar spinal motoneurons.

Animals↗

PubMed1987

Effect of a purified amylase inhibitor on carbohydrate metabolism after a mixed meal in healthy humans.

In previous studies we found that in healthy subjects, 5 and 10 g of a partially purified amylase inhibitor delayed and decreased starch digestion and reduced postprandial plasma glucose after a starch meal but produced diarrhea in two of six and four of six subjects, respectively. Thus, we wondered whether lower doses of the inhibitor, when given with a meal that contained protein and fat as well as carbohydrate, would have the same effect on carbohydrate tolerance without causing diarrhea. Eight healthy subjects were randomized to receive 2.0 or 2.9 g of the inhibitor with a 650-calorie meal that contained carbohydrate, fat, and protein. In comparison with a placebo, ingestion of 2.9 g, but not 2.0 g, of the inhibitor significantly reduced postprandial increases in plasma glucose (P less than 0.05), C peptide (P less than 0.03), and gastric inhibitory polypeptide (P less than 0.008). Similarly, 2.9 g of the inhibitor in comparison with 2.0 g was associated with more carbohydrate malabsorption and more breath hydrogen excretion. Because the carbohydrate malabsorption observed with the 2.9-g dose was similar to that with the previously tested 5- and 10-g doses of the inhibitor but diarrhea was less frequent, impurities in the partially purified preparation may, in part, have been responsible for these adverse effects. We conclude that 2.9 g of the amylase inhibitor given with a meal that contains a mixture of nutrients is effective in increasing carbohydrate tolerance without causing diarrhea. Therefore, this dose is appropriate for use in studies to determine whether the inhibitor has a beneficial effect in patients with diabetes mellitus or obesity.

Adult↗

PubMed1987

Cortical vasodilatation produced by vasoactive intestinal polypeptide (VIP) and by physiological stimuli in the cat.

In chloralose-urethanized cats, vasoactive intestinal peptide (VIP), applied by superfusion in steady-state concentration (10(-10)-10(-6) M) onto cortical vessels in situ resulted in a rapid concentration-dependent vasodilatation in vessels that were mildly constricted by prostaglandin F2 alpha (PGF2 alpha) (5 X 10(-5) M) or hypocarbia (PaCO2 = 26). The maximum dilatation produced by VIP (10(-6) M) was about 60% over baseline in pial arteries and 40% in pial veins. Blockade of local neuronal activity with tetrodotoxin (TTX) (10(-5) M) had no effect on the VIP-evoked dilation of pial vessels. Activation of the cortex by either direct electrical stimulation or indirectly by stimulation of the mesencephalic reticular formation (MRF) resulted in a rapid dilatation of pial arterioles and venules. The vasodilatory effects of VIP and of cortical activation via direct cortical stimulation were not blocked by phentolamine (10(-4) M), propranolol (10(-4) M), atropine (10(-4) M), or naloxone (10(-4) M), indicating that the stimulated vasodilatation was not mediated by adrenergic, cholinergic, or opiate receptors. The dilatory effects of MRF, but not direct cortical stimulation, were not blocked by TTX. VIP antiserum (1:25) preincubated in cortical cups had no effect on resting vessel diameter, but resulted in a significant, though subtotal, reduction in the vasodilatation elicited by direct cortical and MRF stimulation. Normal rabbit sera or VIP antiserum preincubated with saturating amounts of VIP were ineffective. In similar experiments, pial arteriolar and venular dilation evoked by hypercarbia was not attenuated by cortically applied VIP antisera. These observations suggest that pial dilation evoked by local increases in neuronal activity may be mediated in part by the local release of VIP from intrinsic neurons. Such a substrate would define a close obligatory coupling between local neuronal activation and local perfusion, such that nutritive flow could be enhanced prior to the onset of any metabolic deficit.

Animals↗

PubMed1987

Release of substance P from the cat spinal cord.

1. The present experiments examine the physiology and pharmacology of the release of substance P-like immunoreactivity (SP-l.i.), from the spinal cord in the halothane-anaesthetized, artificially ventilated cat. 2. Resting release of SP-l.i. was 36 +/- 4 fmol/30 min (mean +/- S.E.; n = 106). Bilateral stimulation of the sciatic nerves at intensities which evoked activity in fibres conducting at A beta conduction velocities (greater than 40 m/s), resulted in no change in blood pressure, pupil diameter or release of SP-l.i. Stimulation intensities which activate fibres conducting at velocities less than 2 m/s resulted in increased blood pressure, miosis and elevated release of SP-l.i. (278 +/- 16% of control). 3. The relationship between nerve-stimulation frequency and release was monotonic up to approximately 20 Hz. Higher stimulation frequencies did not increase the amounts of SP-l.i. released. At 200 Hz there was a reduction. 4. Capsaicin (0.1 mM) increased the release of SP-l.i. from the spinal cord and resulted in an acute desensitization to subsequent nerve stimulation. This acute effect was not accompanied by a reduction in spinal levels of SP-l.i. measured 2 h after stimulation. 5. Cold block of the cervical spinal cord resulted in an increase in the amounts of SP-l.i. released by nerve stimulation. 6. Pre-treatment with intrathecal 5,6-dihydroxytryptamine (300 micrograms) 7 days prior to the experiment caused a reduction in the dorsal and ventral horn stores of SP-l.i., but had no effect on the release of SP-l.i. evoked by nerve stimulation. Similar pre-treatment with intrathecal capsaicin (300 micrograms) resulted in depletion of SP-l.i. in the dorsal but not in the ventral horn of the spinal cord and diminished the release of SP-l.i. evoked by nerve stimulation. 7. Intense thermal stimulation of the flank resulted in small (20-35%), but reliable increases in the release of SP-l.i. above control. 8. Putative agonists for the opioid mu-receptor (morphine, 10-100 microM; sufentanil, 1 microM), and for the delta-receptor (D-Ala2-D-Leu5-enkephalin, 1-10 microM; D-Pen2-D-Pen5-enkephalin, 10 microM), but not the kappa-receptor (U50488H, 100-1000 microM), produced a dose-dependent, naloxone-reversible reduction of the evoked, but not of the resting release of SP-l.i. (-)-Naloxone, but not (+)-naloxone, resulted in a significant increase in evoked but not resting SP-l.i. release.(ABSTRACT TRUNCATED AT 400 WORDS)

5,6-Dihydroxytryptamine↗

PubMed1987

Effect of central administration of motilin on migrating complexes in the dog.

The effects of intravenous, intrathecal, and intracerebroventricular injection of motilin on the interdigestive myoelectric (MMC) activity of the stomach and small intestine were examined in conscious dogs. To monitor electrical activity, electrodes were implanted on the stomach and small bowel. To inject motilin into the central nervous system, catheters were chronically positioned in the intrathecal space at the lumbar level and in one of the lateral cerebral ventricles. In all dogs, intravenous injection of motilin caused a transient increase in the plasma concentration of motilin and initiated gastric MMCs, which propagated aborally to the ileum. Intrathecal and intracerebroventricular injections of motilin did not affect plasma motilin levels and did not induce MMCs. These data suggest that initiation of MMCs after intravenous injections of motilin occurs through receptors for motilin possibly located outside the central nervous system. These data also suggest the hypothesis that initiation of naturally occurring MMCs in the dog may not be dependent on endogenous release of motilin from the central nervous system.

Animals↗

PubMed1987

The significance of impaired pancreatic polypeptide and epinephrine responses to hypoglycemia in patients with insulin-dependent diabetes mellitus.

The impaired epinephrine and glucagon responses to hypoglycemia often found in patients with insulin-dependent diabetes mellitus (IDDM) may be due to autonomic neuropathy. Since the pancreatic polypeptide response to hypoglycemia is mediated by cholinergic mechanisms, we used this response as an indicator of autonomic neuropathy to determine whether deficient epinephrine and glucagon responses in IDDM could be ascribed to an autonomic defect. The relationships between pancreatic polypeptide, epinephrine, and glucagon responses during insulin-induced hypoglycemia were assessed in 18 patients with IDDM who had no overt evidence of autonomic neuropathy, including normal standard cardiovascular reflex tests, and 11 age-matched nondiabetic subjects. All of the diabetic patients had impaired glucagon responses [19 +/- 3 (SEM) vs. 96 +/- 11 pg/ml, peak increment, P less than 0.001]. Ten of the 18 diabetic patients had either impairment of plasma epinephrine or plasma pancreatic polypeptide responses or both to hypoglycemia. Moreover, pancreatic polypeptide responses were significantly correlated with epinephrine responses (r = 0.53, P less than 0.003). There was no association between the plasma glucagon response and the epinephrine (r = 0.02, NS), norepinephrine (r = 0.03, NS), or pancreatic polypeptide (r = 0.35, NS) response. Last, there was no correlation between the plasma hormone responses and the cardiovascular reflex test results. Therefore, the association of impaired plasma pancreatic polypeptide responses with impaired plasma epinephrine responses suggests that the impaired epinephrine responses are due to autonomic neuropathy, whereas the dissociation of plasma glucagon responses with both plasma pancreatic polypeptide and epinephrine responses suggests that the impaired pancreatic alpha-cell response to hypoglycemia is not due to autonomic neuropathy. In addition, the plasma pancreatic polypeptide and epinephrine responses to hypoglycemia appear to be an earlier indicator of underlying autonomic dysfunction than standard cardiovascular reflex tests. Thus, the responses of plasma pancreatic polypeptide and epinephrine to insulin-induced hypoglycemia may be a useful test for the identification of early autonomic neuropathy in IDDM.

Adolescent↗

PubMed1987

Analysis of the immunomodulatory properties of the secretin-glucagon family of peptides on mouse lymphoid cell functions and the demonstration of specific receptors on T cells.

The ability of members of the secretin-glucagon family of peptides to modulate the responses of mouse lymphoid cells stimulated with Concanavalin A (Con A), Lipopolysaccharide (LPS) and alloantigens was determined. It was observed that vasoactive intestinal peptide (VIP) and peptide having NH2-terminal histidine and COOH-terminal Isoleucine (PHI) inhibited the incorporation of 3H-methyl-thymidine by cells stimulated with Con A (55% inhibition) or alloantigen-bearing cells (40% inhibition). Secretin was approximately 10,000 less effective as an immunomodulator. Other members of the neuropeptide family, including glucagon and gastric inhibitory peptide, were ineffective in affecting mitogenesis elicited by Con A (20% inhibition). Lipopolysaccharide stimulated spleen cells were refractory to modulation by all members of the secretin-glucagon family of peptides (less than 5% modulation). The inhibition measured was concentration dependent over the range of 10(-6) to 10(-16) M. A peptide fragment of VIP encompassing amino acid residues 10-28, although capable of modulating in vitro responses, was 30-50% less effective than intact VIP. In addition, a VIP specific binding assay for mouse lymphoid cells was described. The binding of 125I-VIP to lymph node cells was rapid, saturable and reversible. Apparent equilibrium was reached within 15 minutes and nonspecific binding, measured as 125I-VIP binding in the presence of an excess (2 x 10(-7) M) of native VIP, did not exceed 25% of the total binding. In competitive experiments using VIP related peptides, PHI but not gastric inhibitory peptide, glucagon or secretin was able to significantly inhibit 125I-VIP binding. PHI had only one-eighth of the competitive capacity of native VIP. Scatchard analyses indicated the existence of a single class of high affinity receptors on lymph node cells (KD = 3.46 nM; 26,000 sites/cell). 125I-VIP specific binding to purified T cells (14%) was markedly higher than to B cells (3% binding). Thymocytes bound less than 2% of the label and had relatively few VIP binding sites (8,000) as compared with purified T cells (45,000 sites/cell). There was variability in the ability of various T cells tumors and functional T cell clones to bind 125I-VIP. The role of VIP as a physiological modulator of T cell activation is discussed.

Animals↗

PubMed1987

Abnormalities of fasting serum concentrations of peptide YY in the idiopathic inflammatory bowel diseases.

Peptide YY has been localized within human ileocolonic endocrine cells and may contribute to the regulation of gastric secretion and gastric emptying in man. Since our previous studies had shown decreased colonic concentrations of peptide YY in the idiopathic inflammatory bowel diseases, a specific radioimmunoassay was used to measure fasting serum concentrations of peptide YY in healthy controls and in patients with adenocarcinoma of the rectum, idiopathic chronic active liver disease and hepatic cirrhosis, ulcerative colitis, and Crohn's disease. In healthy controls and in patients with adenocarcinoma of the rectum, serum concentrations of peptide YY ranged from 50 to 260 pg/ml. Serum concentrations of peptide YY in patients with hepatic cirrhosis ranged from 59 to 717 pg/ml. Serum concentrations of peptide YY in patients with ulcerative colitis were similar to healthy controls. In patients with Crohn's disease, serum concentrations of peptide YY were less than 50 pg/ml in three patients who had had a previous proctocolectomy, and were more than 260 pg/ml in 14 patients who had had previous resection of more than 48 cm of ileum or presently had symptomatic Crohn's disease subsequently requiring surgical resection of a total of more than 75 cm of ileum. These results suggest that most circulating peptide YY is released from the colorectal region. Hepatic cirrhosis, previous ileal resection, and symptomatic Crohn's disease were associated with elevation of fasting serum peptide YY. The mechanism of increased fasting serum peptide YY in patients with Crohn's disease could be the loss of an ileal inhibitory factor or possibly an increased release of colonic peptide YY in response to fat malabsorption. The effect of alteration of serum peptide YY concentrations on the pathophysiology of Crohn's disease is yet unknown.

Adenocarcinoma↗

PubMed1987

Proximal gastric vagotomy and mucosal antrectomy: effect on gastric acid secretion, plasma gastrin, and experimental ulcerogenesis in the dog.

The aim of this study was to determine whether mucosal antrectomy, which preserves antropyloric motility, would enhance the antiulcer properties of proximal gastric vagotomy (PGV). Hydrochloric acid and gastrin secretion were studied in five dogs before and after PGV and mucosal antrectomy, while the response to the Mann-Williamson operation (an ulcer-producing operation) was evaluated in four control dogs with intact stomachs, five dogs with PGV alone, and six dogs with PGV plus mucosal antrectomy. Proximal gastric vagotomy and mucosal antrectomy decreased mean +/- SEM basal and pentagastrin-stimulated acid secretion from 4.3 +/- 1.3 to 0.4 +/- 0.3 mEq/hr and from 21 +/- 0.7 to 7.4 +/- 1.8 mEq/hr, respectively (p less than 0.05). Basal plasma gastrin was altered little by the operation (68 +/- 9.7 pg/ml before, 58 +/- 11 pg/ml after; p greater than 0.05) but the 4-hour integrated plasma gastrin response to a 200 gm meat meal decreased from 13 +/- 1.8 to 3.3 +/- 0.7 ng X min/ml (p less than 0.05). Only one of six dogs with mucosal antrectomy and PGV developed peptic ulcer after the Mann-Williamson operation, whereas four of five with PGV alone and three of four controls developed ulcers (p less than 0.05, PGV alone versus PGV and mucosal antrectomy). In conclusion, PGV and mucosal antrectomy decreased acid secretion and postcibal gastrin response and provided greater protection against peptic ulcer than PGV alone.

Animals↗

PubMed1986

Renal hyperemia in portal hypertension is not mediated by gastrointestinal peptides.

The objectives of this study were to characterize the time course of development of the renal hyperemia induced by chronic portal vein stenosis (PVS) in the rat, and to assess the possibility that vasoactive blood-borne gastrointestinal peptides mediate the renal hyperemia in established portal hypertension. Blood flow to the kidneys was measured with radioactive microspheres over a ten day time course. On day 2, no difference in renal blood flow (RBF) was observed in PVS rats as compared with controls. However, by day 4, RBF significantly increased by 35% in PVS vs. control animals. On day 6, the renal hyperemia in PVS rats reached a maximal value that was 42% higher than controls. A steady state hyperemia (approximately 40%) was maintained thereafter. Radioimmunoassay of plasma from control and established portal hypertensive rats (10 days samples) revealed that vasoactive intestinal polypeptide, substance P, cholecystokinin, gastrin, neurotensin, pancreatic polypeptide, beta-endorphin and peptide histidine-isoleucine amide are not elevated in arterial plasma of portal hypertensive rats. These data suggest that the renal hyperemia induced by chronic portal vein stenosis is apparent within 4 days of the onset of a hypertensive state and attains a steady state by day 8. Furthermore, at least eight blood-borne gastrointestinal peptides are not directly involved in the renal hyperemia associated with chronic portal hypertension.

Animals↗

PubMed1986

The preoperative carcinoembryonic antigen test in the diagnosis, staging, and prognosis of colorectal cancer.

A study of preoperative carcinoembryonic antigen (CEA) levels was conducted in 319 patients with surgically treated colorectal cancer, 272 of whom had disease resectable with curative intent. Only three patients could not be completely followed. All of the remaining 316 patients have been followed for a minimum of 5 years or until death. From the standpoint of diagnosis, the CEA test was more frequently positive (greater than 5 ng/ml) in patients with advanced stage disease, with larger primary tumors, and with more differentiated histopathologic characteristics. It was grossly insensitive in diagnosis of resectable cancer (26%) and was only reasonably reliable (72%) in patients with unresectable and metastatic disease. In relationship to surgical pathology of colorectal cancer, CEA levels were significantly correlated with stage of disease and with size of the primary tumor in Dukes' B lesions, but not with extent of nodal metastasis in Dukes' C lesions. In advanced stage lesions, CEA was inversely correlated with degree of anaplasia. In the overall patient group, and also among resectable patients, the preoperative CEA level was strongly associated with survival after adjustment for the effects of a number of other prognostic factors. Within stages of resectable disease, however, CEA was not significantly associated with survival among patients with Dukes' A and B lesions or Dukes' C lesions with one to three nodes involved. CEA was found to be a significant and independent prognostic determinant only in patients with Dukes' C lesions who had four or more metastatically involved lymph nodes. Under these circumstances, a preoperative CEA level could perhaps be of some value for stratification of Dukes' C patients in randomized colorectal cancer surgical adjuvant trials. The value of this test as a prognostic guide in clinical practice, however, would seem to be limited because of a lack of sensitivity in identifying individual poor prognosis patients.

Adult↗

PubMed1986

Extraction of cholecystokinin peptides from biological fluids using octadecylsilane-packed cartridges.

Cholecystokinin is an important peptide hormone, which occurs naturally in molecular forms ranging in length from 4 to 58 amino acid residues and varying in charge from acidic to basic. In order to quantify the individual molecular forms of this hormone present in plasma or tissues, it is first necessary to efficiently extract all of the diverse forms. In this paper, we establish and validate a simple method to do this using octadecylsilane-packed cartridges. Peptide adsorption to the cartridge and subsequent elution from it is not significantly affected by the pH (3-7) or salt concentration (0-2 g per 100 ml) needed for extraction, or the protein concentration (0-10 g per 100 ml) in the applied sample. Peptides are extracted in a form which can be separated using reversed-phase high-performance liquid chromatography and subsequently quantified by a commonly available radioimmunoassay which recognizes both cholecystokinin and gastrin.

Body Fluids↗

PubMed1986

An intragastric meal releases the putative satiety factor cholecystokinin from hypothalamic neurons in cats.

The release of cholecystokinin-like immunoreactivity (CCK-LI) from feline hypothalamus was studied in relation to a meal by use of the push-pull perfusion technique. While levels of CCK-LI in the perfusate of overnight-fasted anesthetized cats were below assay sensitivity (less than 7 pg/30 min), intragastric administration of a carbohydrate-amino acid meal elicited a 3-fold increase in CCK-LI, identified by high-performance liquid chromatography as the C-terminal octapeptide of CCK (CCK-8). Examination of an extrahypothalamic site showed no comparable release in CCK-LI. Intravenous infusions of CCK-8 at doses imitating physiological blood levels up to 400 times higher than those seen after physiological stimulation demonstrated the existence of a CCK blood-brain barrier in the lateral hypothalamus. These observations provide support that CCK may play a physiological role in termination of feeding behavior.

Animals↗

PubMed1986

Altered responsiveness to substance P and 5-hydroxytryptamine in cat dorsal horn neurons after 5-HT depletion with p-chlorophenylalanine.

The responsiveness of functionally identified cat spinal dorsal horn neurons to iontophoretically applied substance P (SP) and 5-hydroxytryptamine (5-HT) has been investigated by means of extracellular recording after 5-HT depletion with p-chlorophenylalanine (p-CPA). In addition, the spinal levels of 5-HT, SP, cholecystokinin octapeptide, neurotensin, and vasoactive intestinal polypeptide have been measured in intact and p-CPA-pretreated cats. In the present study we have demonstrated an altered responsiveness of dorsal horn neurons to locally applied SP and 5-HT. We found in p-CPA-pretreated cats that the proportion of neurons responding with excitation to SP and 5-HT was significantly increased. At the same time, depression induced by 5-HT in the dorsal horn cells was virtually absent in p-CPA-pretreated animals. Our finding that spinal level of 5-HT was significantly decreased in p-CPA-treated animals is consistent with previous studies. No convincing alteration in the spinal levels of 4 analyzed peptides was found in p-CPA-treated animals. The present study has shown that pharmacological depletion of 5-HT has two major effects: (1) it increases significantly the proportion of dorsal horn neurons excited by SP and 5-HT; and (2) it is ineffective in inducing 5-HT supersensitivity. Further work is needed to explain mechanisms involved in these effects.

Animals↗

PubMed1986

Canine mucosal antrectomy.

Our primary aim was to determine whether mucosal antrectomy decreases postcibal serum gastrin and gastric acid secretion. In four dogs with proximal gastric vagotomy and a Heidenhain pouch, mucosal antrectomy decreased the integrated postcibal serum gastrin response from a mean +/- SEM of 2.0 +/- 0.2 ng X h/mL before antrectomy to 0.8 +/- 0.1 ng X h/mL after antrectomy, while it decreased postcibal output of hydrochloric acid from the pouch from 9.5 +/- 3.3 mEq/7 h (9.5 +/- 3.3 mmol/7 h) to 4.3 +/- 2.2 mEq/7 h (4.3 +/- 2.2 mmol/7 h). However, these decreases were temporary in two of the four dogs. In five additional dogs without vagotomy, the distal, antral, mucosal gastrin level increased from 1 +/- 1 micrograms/g of tissue before mucosal antrectomy to 5 +/- 1 micrograms/g of tissue after the antrectomy. Moreover, gastrin and G cells were present in corporal mucosa transferred to the antrum in three of five dogs after the antrectomy, where none had been present in the corporal mucosa before the antrectomy. The conclusion was that mucosal antrectomy decreased serum gastrin and hydrochloric acid output from the stomach, but that these changes were counteracted in part by hyperplasia of residual G cells and G-cell neogenesis after the operation.

Animals↗