Plasma secretin concentrations in fasting and postprandial states in dog.

1979 ◽  
Vol 236 (5) ◽  
pp. E539 ◽  
Author(s):  
M S Kim ◽  
K Y Lee ◽  
W Y Chey
Keyword(s):  
Pancreatic Secretion ◽  
Physiological Role ◽  
Fasting State ◽  
Meat Meal ◽  
Duodenal Ph ◽  
The Mean ◽  
Bicarbonate Output ◽  
Marked Suppression ◽  
Sustained Increase

In four dogs with a modified Herrara pancreatic fistula and gastric cannula and three dogs with two duodenal cannulas, ingestion of a meat meal resulted in a significant and sustained increase in the mean plasma immunoreactive secretin concentrations, from mean fasting levels of less than 10 pg/ml to 25--55 pg/ml. This increase in the plasma secretin concentration coincided with a marked increase in pancreatic bicarbonate output and frequent decreases in the mean proximal duodenal pH to less than 4.5 from the range of 6.5 in the fasting state. Intravenous administration of cimetidine, 150 mg, produced a marked suppression of postprandial increases in both pancreatic bicarbonate output and plasma secretin concentration. Moreover, the postprandial duodenal pH rarely reached below 5.0 after cimetidine administration. These studies indicate that plasma secretin concentration does increase significantly after a meal. The postprandial increase in plasma secretin concentration appears to depend on the gastric acid delivered in the proximal duodenum. A possible physiological role of secretin in the pancreatic secretion after a meal is indicated by these findings.

Gastrin is not a physiological regulator of pancreatic exocrine secretion in the dog

1987 ◽  
Vol 252 (1) ◽  
pp. G40-G44
Author(s):  
E. Kohler ◽  
C. Beglinger ◽  
V. Eysselein ◽  
U. Grotzinger ◽  
K. Gyr
Keyword(s):  
Pancreatic Secretion ◽  
Pancreatic Enzyme ◽  
Exocrine Secretion ◽  
Exocrine Pancreatic Secretion ◽  
Response Curves ◽  
Blood Concentrations ◽  
Pancreatic Enzyme Secretion ◽  
Pancreatic Exocrine ◽  
Bicarbonate Output

The role of gastrin as a regulator of exocrine pancreatic secretion has not been proven adequately. In the present study we therefore compared the relative molar potencies of sulfated and unsulfated gastrin 17 with structurally related CCK peptides (synthetic CCK-8 and natural porcine CCK-33) in stimulating exocrine pancreatic secretion in conscious dogs. Dose response curves were constructed for pancreatic and gastric acid secretion. Plasma gastrin levels after exogenous gastrin 17-I and -II were compared with postprandial gastrin concentrations (meal: ground beef 20 g/kg body wt). The molar potency estimates calculated with synthetic CCK8 as standard (potency = 1.00) for pancreatic protein secretion were natural porcine 50% pure CCK-33 1.60, gastrin 17-I 0.12, and gastrin 17-II 0.16. All four peptides induced a dose-dependent increase in pancreatic bicarbonate output. However, the blood concentrations needed to stimulate pancreatic secretion were above the postprandial gastrin levels. Our data indicate that both gastrin 17 peptides are not physiological regulators of pancreatic enzyme secretion in dogs.

Yohimbine increases sympathetic nerve activity and norepinephrine spillover in normal volunteers

1991 ◽  
Vol 260 (1) ◽  
pp. R142-R147 ◽  
Author(s):  
E. Grossman ◽  
R. F. Rea ◽  
A. Hoffman ◽  
D. S. Goldstein
Keyword(s):  
Sympathetic Nerve ◽  
Physiological Role ◽  
Normal Volunteers ◽  
Arterial Blood ◽  
The Mean ◽  
Arterial Plasma ◽  
Human Limb ◽  
Norepinephrine Spillover ◽  
Forearm Vascular Resistance

It has been difficult to examine clinically the physiological role of central and peripheral alpha 2-adrenoceptors in humans. We simultaneously measured directly recorded peroneal skeletal muscle sympathoneural activity (MSNA) and the rate of appearance (spillover) of norepinephrine (NE) in forearm venous and arterial plasma before and at 15 min during intravenous administration of the alpha 2-blocker yohimbine (Yoh, 125 micrograms/kg bolus, 1 microgram.kg-1.min-1 infusion) in seven normal volunteers. Yoh administration increased mean arterial pressure by 16% (P less than 0.005), heart rate by 8% (P less than 0.05), and forearm vascular resistance by 67% (P less than 0.05). MSNA was increased by 73% (P less than 0.05), NE spillover into arterial blood by 125% (P less than 0.05), and forearm NE spillover (FSO) by 337% (P less than 0.005). Ganglion blockade by trimethaphan during Yoh infusion decreased MSNA to below detection limits and reversed Yoh-induced increases in arterial concentrations of NE and epinephrine. The results demonstrate that Yoh administration increases sympathoadrenal outflow. Because the mean increase of FSO was much larger than that of MSNA, the results suggest that alpha 2-adrenoceptors on sympathetic nerve endings modulate the neuronal release of NE for a given amount of sympathetic nerve traffic in humans; this effect seems prominent in the human limb.

scholarly journals Endotoxin Stimulates Leptin in the Human and Nonhuman Primate

2003 ◽  
Vol 88 (3) ◽  
pp. 1285-1291 ◽  
Author(s):  
Rita E. Landman ◽  
Jardena J. Puder ◽  
Ennian Xiao ◽  
Pamela U. Freda ◽  
Michel Ferin ◽  
...  
Keyword(s):  
Nonhuman Primate ◽  
Time Course ◽  
Energy Homeostasis ◽  
Human Subjects ◽  
Control Period ◽  
Initial Study ◽  
The Mean ◽  
Plasma Leptin ◽  
Sustained Increase

Leptin, which plays a key role in regulating energy homeostasis, may also modulate the inflammatory response. An inflammatory challenge with endotoxin has been shown to stimulate leptin release in the rodent. This finding has not been reproduced in humans or in nonhuman primates, although leptin levels have been reported to increase in septic patients. We have therefore examined the effects of endotoxin injection on plasma leptin levels in nine ovariectomized monkeys and four postmenopausal women. In an initial study in five monkeys, mean leptin levels did not increase during the first 5 h after endotoxin treatment, but did increase significantly from 6.4 ± 2.1 ng/ml at baseline to 12.3 ± 4.4 ng/ml at 24 h (P = 0.043). In a second study, a significant increase in leptin over time was noted after endotoxin treatment (P < 0.001); leptin release during the 16- to 24-h period after endotoxin injection was 48% higher than during the control period (P = 0.043). A similar stimulatory effect of endotoxin on leptin was observed when monkeys received estradiol replacement. In a third study, repeated injections of endotoxin over a 3-d period stimulated IL-6, ACTH, cortisol, and leptin release (P < 0.001). Leptin increased during the first day of treatment in all animals, but only monkeys with baseline plasma leptin levels greater than 10 ng/ml exhibited a sustained increase in leptin throughout the 3-d period. There was a significant correlation (r = 0.81; P = 0.008) between the mean baseline leptin level and the percent increase in leptin over baseline on the last day of treatment. In the human subjects, plasma leptin concentrations did not change significantly during the 7-h period after endotoxin injection. However, leptin increased in all four women from a mean baseline of 8.34 ± 3.1 to 13.1 ± 4.3 ng/ml 24 h after endotoxin (P = 0.038). In summary, endotoxin stimulates the release of leptin into peripheral blood in the human and nonhuman primate, but the time course is different from that reported in the rodent. These results are consistent with previous reports of increased blood leptin levels in patients with sepsis. The significance of these findings and the potential role of leptin in modulating the response to inflammation in the human require further study.

An important role of endogenous insulin on exocrine pancreatic secretion in rats

1990 ◽  
Vol 258 (2) ◽  
pp. G268-G274 ◽  
Author(s):  
K. Y. Lee ◽  
L. Zhou ◽  
X. S. Ren ◽  
T. M. Chang ◽  
W. Y. Chey
Keyword(s):  
Pancreatic Secretion ◽  
Physiological Role ◽  
Rabbit Serum ◽  
Normal Rabbit Serum ◽  
Dependent Manner ◽  
Exocrine Pancreatic Secretion ◽  
Liquid Meal ◽  
Amylase Output ◽  
Endogenous Insulin

We have investigated a physiological role of endogenous insulin on exocrine pancreatic secretion stimulated by a liquid meal as well as exogenous secretin and cholecystokinin octapeptide (CCK-8) in conscious rats. Each rat was prepared with a chronic pancreatic fistula and an indwelling catheter in a jugular vein. Oral ingestion of a liquid meal (5 ml) resulted in significant increases in pancreatic secretion, including volume, bicarbonate, and amylase output, in these rats. A rabbit anti-insulin serum (1.0 ml) given intravenously completely blocked the postprandial exocrine pancreatic secretion, whereas a normal rabbit serum did not influence the pancreatic secretion in the same rats. When pancreatic secretion was stimulated by intravenous administration of both secretin and CCK-8 in three different doses, including 0.015, 0.03, and 0.06 clinical unit and microgram.kg-1.h-1, respectively, volume, bicarbonate, and amylase output increased significantly in a dose-dependent manner. This increase in pancreatic secretion was also completely blocked by a rabbit anti-insulin serum, whereas it was not influenced by a normal rabbit serum. The amount of the antiserum employed abolished the postprandial increases in plasma insulin concentration. We conclude that endogenous insulin plays an important role on the regulation of postprandial pancreatic secretion in rats. Furthermore, for the stimulatory action of the two intestinal hormones secretin and CCK-8 on the pancreatic exocrine secretion, endogenous insulin is need.

Biphasic secretory response of exocrine pancreas to feeding

1980 ◽  
Vol 238 (4) ◽  
pp. G332-G337 ◽  
Author(s):  
Z. Itoh ◽  
R. Honda ◽  
K. Hiwatashi
Keyword(s):  
Pancreatic Secretion ◽  
Exocrine Pancreas ◽  
Physiological Role ◽  
Secretory Response ◽  
Conscious Dogs ◽  
Bicarbonate Secretion ◽  
Secretory Pattern ◽  
Second Peak

By means of a newly developed device, secretory response of the exocrine pancreas to feeding was continuously recorded for 24 h in conscious dogs. It was then found that the postprandial secretory pattern of the pancreas was biphasic. The first peak of secretion, rich in enzymes, occurred 2.3 +/- 0.11 h after feeding and its secretory volume was 25.3 +/- 3.10 ml/h. After the first peak, pancreatic secretion decreased slightly, but started to increase again. At 10.8 +/- 0.31 h after feeding, the second peak of secretion occurred and this was 40.5 +/- 2.93 ml/h, significantly higher than the first peak secretion and the greatest in 1 day. The second peak secretion did not contain a higher concentration of enzymes, but was rich in bicarbonate. Approximately 16 h after feeding, pancreatic secretion returned to the basal level, which continued until the next meal. That water and bicarbonate secretion of the pancreas is the greatest at about the 11th postprandial h had never been reported before. The physiological role of the pancreatic secretion at that time is more likely to be related to the neutralization of acid entering from the stomach than to the digestion of food.

scholarly journals CD33 as a Leukocyte-Associated Marker Expressed on Human Spermatozoa

2021 ◽  
Author(s):  
Nasrin Sereshki ◽  
Mitra Rafiee ◽  
Razieh Alipour ◽  
Sasan Navkhasi ◽  
Vahid Ahmadipanah ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Immune Cells ◽  
Mean Fluorescence Intensity ◽  
Physiological Role ◽  
Human Spermatozoa ◽  
Healthy Men ◽  
Sialic Acid Binding ◽  
The Mean ◽  
Mediate Cell

Abstract Background Sialic acid-binding immunoglobulin-type lectins (Siglecs) are commonly present on immune cells and often mediate cell-to-cell interactions and signaling. Studies have shown the presence of Siglecs 1, 2, 5, 6, 10 and 14 on human spermatozoa. To the best of our knowledge, the expression of CD33 on spermatozoa has not yet been studied. Methods Semen samples were collected from 25 healthy men with normal semen status. CD33 expression on purified spermatozoa was evaluated by flow cytometry methods. Results The results demonstrate the expression of CD33 on the surface of purified spermatozoa. The mean (± SD) of MFI (mean fluorescence intensity) was 12.85 (± 1.33) and the mean percentage of spermatozoa that express CD33 was 73.75 (± 3.75). Conclusion Results were obtained showing that spermatozoa express CD33 (or Siglec-3) on their surface. The physiological role of these molecules on spermatozoa remains to be determined. It is recommended that further research should be undertaken regarding the role of Siglecs (such as CD33) on spermatozoa apoptosis.

A physiological role of peptide YY on exocrine pancreatic secretion in rats

1993 ◽  
Vol 105 (1) ◽  
pp. 208-215 ◽  
Author(s):  
Haiou Jin ◽  
Lixing Cai ◽  
Kaeyol Lee ◽  
Ta-Ming Chang ◽  
Ping Li ◽  
...  
Keyword(s):  
Pancreatic Secretion ◽  
Peptide Yy ◽  
Physiological Role ◽  
Exocrine Pancreatic Secretion

Role of cholecystokinin in intestinal phase and meal-induced pancreatic secretion

1989 ◽  
Vol 257 (5) ◽  
pp. G782-G790 ◽  
Author(s):  
W. E. Dale ◽  
C. M. Turkelson ◽  
T. E. Solomon
Keyword(s):  
Sodium Oleate ◽  
Pancreatic Secretion ◽  
Plasma Concentrations ◽  
Amylase Secretion ◽  
Bicarbonate Secretion ◽  
Lower Plasma ◽  
Intestinal Phase ◽  
Meat Meal ◽  
Plasma Cholecystokinin

Amylase secretion and plasma cholecystokinin (CCK) were measured in dogs in the interdigestive state and after exogenous CCK-8 and CCK-39 (12.5 to 400 pmol.kg-1.h-1), intestinal sodium oleate, tryptophan plus phenylalanine, HCl (0.74, 2.2, 6.7, 20 mmol/h), and a meat meal (20 g/kg). Interdigestive plasma CCK did not vary, although amylase output showed periodic 15-fold increases. Plasma CCK increased linearly after doubling doses of CCK-8 and CCK-39; the slope of plasma CCK-39 vs. dose was 2.8 times steeper than that of CCK-8, suggesting a longer circulating half-life. At similar plasma concentrations, CCK-8 and CCK-39 were equipotent for stimulating pancreatic secretion. Sodium oleate and tryptophan plus phenylalanine significantly increased plasma CCK and amylase secretion in a load-dependent pattern and were equipotent for both effects. HCl stimulated bicarbonate secretion but not plasma CCK or amylase secretion. Food significantly increased plasma CCK and amylase secretion. Amylase responses to intestinal stimulants and food were significantly greater than to exogenous CCK at low plasma CCK levels. Maximal amylase responses to intestinal stimulants were similar to that after CCK-39 but occurred at 10-fold lower plasma CCK levels. These results indicate that CCK and other factors interact to regulate pancreatic responses to food and intestinal stimulants in dogs.

Sign in / Sign up

Export Citation Format

Share Document