Journal articles on the topic 'Pancreas; alcohol; blood flow'

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1

Weaver, Fr C. "Blood flow in the atrophied pancreas." Experimental Pathology 38, no. 2 (January 1990): 119–27. http://dx.doi.org/10.1016/s0232-1513(11)80246-x.

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2

Studley, J. G. N., R. T. Mathie, and L. H. Blumgart. "Blood flow measurement in the canine pancreas." Journal of Surgical Research 42, no. 1 (January 1987): 101–15. http://dx.doi.org/10.1016/0022-4804(87)90071-0.

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3

Knol, James A., William E. Strodel, and Frederic E. Eckhauser. "Blood flow and distribution in the canine pancreas." Journal of Surgical Research 43, no. 3 (September 1987): 278–85. http://dx.doi.org/10.1016/0022-4804(87)90082-5.

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4

Korsgren, Olle, Rolf Karlsten, Frank Sundler, and Leif Jansson. "BLOOD FLOW REGULATION IN THE TRANSPLANTED FETAL ENDOCRINE PANCREAS." Transplantation 61, no. 5 (March 1996): 772–77. http://dx.doi.org/10.1097/00007890-199603150-00017.

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5

Caspari, D., W. Trabert, N. Lion, H. Henkes, and G. Huber. "REGIONAL CEREBRAL BLOOD FLOW DURING ALCOHOL WITHDRAWAL." Clinical Neuropharmacology 15 (1992): 229B. http://dx.doi.org/10.1097/00002826-199202001-00441.

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6

Ulrich-Baker, M. G., M. E. Hollwarth, P. R. Kvietys, and D. N. Granger. "Blood flow responses to small bowel resection." American Journal of Physiology-Gastrointestinal and Liver Physiology 251, no. 6 (December 1, 1986): G815—G822. http://dx.doi.org/10.1152/ajpgi.1986.251.6.g815.

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The objective of this study was to determine whether the gastrointestinal blood flow response to small bowel resection is related to the compensatory hyperplasia resulting from resection. In one group of rats, a laparotomy was performed and 80% of the small bowel resected, reanastomosing proximal jejunum with distal ileum. In the second group (controls), a transection followed by reanastomosis was performed either in the jejunum or ileum. One, two, three, or five days later, the animals were anesthetized, and blood flows to the stomach, jejunum, ileum, cecum, colon, and pancreas were measured using the radioactive microsphere technique. Samples of these tissues were obtained for determination of thymidine incorporation and DNA content. Growth, as evidenced by increases in tissue weight, DNA content, and rate of DNA synthesis, occurred in all tissues. Blood flow was elevated in the pancreas and in bowel segments (ileum and cecum) distal to the site of resection. Gastric, jejunal and colonic blood flows were not affected by bowel resection, in spite of similar trophic changes. Paired-value analyses did not reveal any correlation between blood flow and rate of DNA synthesis. The results of these studies suggest that humoral, rather than metabolic, factors are responsible for the gastrointestinal and pancreatic hyperemia that occurs after small bowel resection.
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7

Boden, G. "Glucose metabolism and leg blood flow after pancreas/kidney transplantation." Journal of Clinical Endocrinology & Metabolism 76, no. 5 (May 1, 1993): 1229–33. http://dx.doi.org/10.1210/jc.76.5.1229.

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8

Boden, G., R. DeSantis, X. Chen, M. Morris, and F. Badoza. "Glucose metabolism and leg blood flow after pancreas/kidney transplantation." Journal of Clinical Endocrinology & Metabolism 76, no. 5 (May 1993): 1229–33. http://dx.doi.org/10.1210/jcem.76.5.8496315.

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9

Aharinejad, S., I. C. MacDonald, and A. Miksovsky. "Morphologic sites for regulating blood flow in the exocrine pancreas." Microscopy Research and Technique 37, no. 5-6 (June 1, 1997): 434–49. http://dx.doi.org/10.1002/(sici)1097-0029(19970601)37:5/6<434::aid-jemt7>3.0.co;2-d.

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10

von Ritter, C., R. A. Hinder, W. Womack, P. Bauerfeind, C. J. Fimmel, P. R. Kvietys, D. N. Granger, and A. L. Blum. "Microsphere estimates of blood flow: methodological considerations." American Journal of Physiology-Gastrointestinal and Liver Physiology 254, no. 2 (February 1, 1988): G275—G279. http://dx.doi.org/10.1152/ajpgi.1988.254.2.g275.

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The microsphere technique is a standard method for measuring blood flow in experimental animals. Sporadic reports have appeared outlining the limitations of this method. In this study we have systematically assessed the effect of blood withdrawals for reference sampling, microsphere numbers, and anesthesia on blood flow estimates using radioactive microspheres in dogs. Experiments were performed on 18 conscious and 12 anesthetized dogs. Four blood flow estimates were performed over 120 min using 1 X 10(6) microspheres (15 microns) each time. The effects of excessive numbers of microspheres (13 million), pentobarbital sodium anesthesia (30 mg/kg), and replacement of volume loss for reference samples with dextran 70 were assessed. In both conscious and anesthetized dogs a progressive decrease in gastric mucosal blood flow and cardiac output was observed over 120 min. This was also observed in the pancreas in conscious dogs. The major factor responsible for these changes was the volume loss due to reference sample withdrawals. Replacement of the withdrawn blood with dextran 70 led to stable blood flows to all organs. The injection of excessive numbers of microspheres did not modify hemodynamics to a greater extent than did the injection of 4 million microspheres. Anesthesia exerted no influence on blood flow other than raising coronary flow. We conclude that although blood flow to the gastric mucosa and the pancreas is sensitive to the minor hemodynamic changes associated with the microsphere technique, replacement of volume loss for reference samples ensures stable blood flow to all organs over a 120-min period.
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11

Jansson, L., and S. Sandler. "Altered blood flow regulation in autotransplanted pancreatic islets of rats." American Journal of Physiology-Endocrinology and Metabolism 259, no. 1 (July 1, 1990): E52—E56. http://dx.doi.org/10.1152/ajpendo.1990.259.1.e52.

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Adult rats were partially depancreatized, and approximately 500 islets were isolated from each excised pancreas, maintained in tissue culture for 7 days, and subsequently transplanted back to the same animals beneath the renal capsule. Four weeks after transplantation the animals were anesthetized and given an intravenous injection of 1 ml of either saline, 30% (wt/vol) D-glucose, 30% (wt/vol) D-galactose, DL-propranolol (15 mg/kg body wt) dissolved in saline, or terbutaline (1 mg/kg body wt) dissolved in saline. Five minutes later blood perfusion of the islet grafts and the pancreatic remnant were measured with a microsphere technique. Islet blood flow was also measured in animals with pancreas intact and no islet grafts after administration of saline, glucose, or galactose. These animals demonstrated a significant and preferential increase in islet blood flow after glucose administration, whereas galactose caused a selective decrease in islet blood perfusion. Both whole pancreatic blood flow and islet blood flow in the pancreatic remnant were decreased by terbutaline administration, whereas the other substances had no effect. Blood flow to the transplanted islets was decreased by glucose and galactose, whereas propranolol and terbutaline had no effect compared with the saline-injected animals. These results suggest that blood flow regulation differs between transplanted pancreatic islets, islets in the normal pancreas, and islets in the pancreatic remnant after partial pancreatectomy. Whether this reflects lack of innervation or an altered reactivity of the newly formed blood vessels in islet grafts is presently unknown.
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12

Dybala, Michael P., Andrey Kuznetsov, Maki Motobu, Bryce K. Hendren-Santiago, Louis H. Philipson, Alexander V. Chervonsky, and Manami Hara. "Integrated Pancreatic Blood Flow: Bidirectional Microcirculation Between Endocrine and Exocrine Pancreas." Diabetes 69, no. 7 (March 20, 2020): 1439–50. http://dx.doi.org/10.2337/db19-1034.

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13

GDOVINOVA´, Z. "Cerebral Blood Flow Velocity, Erythrocyte Deformability and Alcohol Intake." Comparative Clinical Pathology 11, no. 2 (April 2002): 77–81. http://dx.doi.org/10.1007/s005800200002.

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14

Christie, Israel C., Julie Price, Louisa Edwards, Matthew Muldoon, Carolyn C. Meltzer, and J. Richard Jennings. "Alcohol consumption and cerebral blood flow among older adults." Alcohol 42, no. 4 (June 2008): 269–75. http://dx.doi.org/10.1016/j.alcohol.2008.03.132.

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15

Harringer, W., C. Fernandez-del Castillo, D. W. Rattner, J. L. Guerrero, A. L. Warshaw, and G. J. Vlahakes. "Evaluation and validation of microsphere technique for determination of pancreatic blood flow." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 3 (September 1, 1993): G587—G594. http://dx.doi.org/10.1152/ajpgi.1993.265.3.g587.

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The purpose of this study was to evaluate the radiolabeled microsphere technique for pancreatic blood flow measurements. Using a canine model with an isolated pancreatic circulation, we assessed the shunting of 11- and 15-microns-diam microspheres in the pancreas, correlated pancreatic blood flow measurements obtained with the microsphere technique with those made with an ultrasonic flow probe, and determined the effects of high doses of microspheres on pancreatic blood flow and its measurement. Microspheres of 11 microns demonstrate significant shunting through the pancreatic microcirculation with underestimation of pancreatic blood flow of approximately 10% compared with results obtained with 15-microns microspheres. There is a close linear relationship between flow results obtained with 15-microns microspheres and with an ultrasonic flow probe for both the resting (r = 0.85) and the secretin-stimulated pancreas (r = 0.97). Left atrial injections of very large doses of 15-microns microspheres (50 x 10(6)) caused an acute transient reduction of pancreatic blood flow (to 39% of baseline flow) with a return to baseline values within 2 min. The accuracy of flow results and absence of physiological changes after repeated injections support the use of 15-microns microspheres for pancreatic blood flow measurements.
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16

Jansson, Leif, Birgitta Bodin, Örjan Källskog, and Arne Andersson. "Duct ligation and pancreatic islet blood flow in rats: physiological growth of islets does not affect islet blood perfusion." European Journal of Endocrinology 153, no. 2 (August 2005): 345–51. http://dx.doi.org/10.1530/eje.1.01966.

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Objectives: The aim of this study was to evaluate islet blood-flow changes during stimulated growth of the islet organ without any associated functional impairment of islet function. Design: A duct ligation encompassing the distal two-thirds of the pancreas was performed in adult, male Sprague–Dawley rats. Methods: Pancreatic islet blood flow was measured in duct-ligated and sham-operated rats 1, 2 or 4 weeks after surgery. In some animals studied 4 weeks after surgery, islet blood flow was also measured also during hyperglycaemic conditions. Results: A marked atrophy of the exocrine pancreas was seen in all duct-ligated rats. Blood glucose and serum insulin concentrations were normal. An increased islet mass was only seen 4 weeks after surgery. No differences in islet blood perfusion were noted at any time point after duct ligation. In both sham-operated and duct-ligated rats islet blood flow was increased during hyperglycaemia; the response was, however, slightly more pronounced in the duct-ligated part of the gland. Conclusions: Normal, physiological islet growth does not cause any major changes in the islet blood perfusion or its regulation. This is in contrast to findings during increased functional demands on the islets or during deteriorated islet function, when increased islet blood flow is consistently seen.
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17

Kenney, Michael J., and Timothy I. Musch. "Senescence alters blood flow responses to acute heat stress." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 4 (April 2004): H1480—H1485. http://dx.doi.org/10.1152/ajpheart.00857.2003.

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Renal and splanchnic sympathetic nerve discharge (SND) responses to heating are significantly reduced in senescent compared with young Fischer-344 (F344) rats (Kenney MJ and Fels RJ. Am J Physiol Regul Integr Comp Physiol 283: R513–R520, 2002). However, the functional significance of this finding is not known. We tested the hypothesis that blood flow distribution profiles to heating are altered in senescent (24 mo old) compared with mature (12 mo old) and young (3 mo old) F344 rats. Visceral organ, skeletal muscle, and tail blood flows were determined with the radionuclide-tagged microsphere technique before (control, 38°C) and during heating that increased body temperature to 41°C in anesthetized F344 rats. Vascular conductance in the kidney, stomach, large intestine, pancreas, spleen, and tail was significantly reduced during control before heating in senescent compared with young F344 rats. Heating significantly decreased kidney, stomach, small and large intestine, and pancreas vascular conductance in young and mature but not senescent F344 rats. Vascular conductance at 41°C in the kidney and small intestine was significantly lower and in the stomach tended to be lower in young compared with senescent rats. Splenic conductance increased during heating in young and senescent rats but was highest in young rats. Tail conductance during heating was significantly increased in young rats but remained unchanged in mature and senescent rats. These results demonstrate a marked attenuation in heating-induced vascular conductance changes in senescent rats, suggesting an important functional consequence for the attenuated SND responses to heating in aged rats.
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18

Svensson, Annika M., Samy M. Abdel-Halim, Suad Efendic, Leif Jansson, and Claes-Göran Östenson. "Pancreatic and islet blood flow in F1-hybrids of the non-insulin-dependent diabetic GK-Wistar rat." European Journal of Endocrinology 130, no. 6 (June 1994): 612–16. http://dx.doi.org/10.1530/eje.0.1300612.

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Svensson AM, Abdel-Halim SM, Efendic S, Jansson L, Östenson C-G. Pancreatic and islet blood flow in F1 -hybrids of the non-insulin-dependent diabetic GK-Wistar rat. Eur J Endocrinol 1994:130:612–16. ISSN 0804–4643 Previous studies have indicated that various conditions under which an increased functional load is posed on the pancreatic islets, e.g. partial pancreatectomy and continuous glucose infusions, may influence the microcirculation of the pancreas. To investigate further the effects of elevated functional demand on the islets, the blood perfusion of the whole pancreas and the pancreatic islets was measured with a microsphere technique in an animal model presenting impaired glucose tolerance and mild hyperglycemia, namely F 1-hybrids of the spontaneously non-insulin-dependent diabetic GK-Wistar rat. Normal Wistar rats served as controls. All hybrids had a pathological intraperitoneal glucose tolerance test 1 week before the blood flow measurements, which were performed in 10–12-week-old rats. Both the whole pancreatic and the islet blood flows were increased in the hybrids compared to controls. The fractional islet blood flow, i.e. the fraction of whole pancreatic blood flow diverted through the islets, also was increased in the hybrid rats (12.6 ±0.6% vs 9.8 ±0.5% in controls, p <0.01). A bilateral abdominal vagotomy performed 30 min before the blood flow measurement markedly decreased the blood flow values of the islets and the whole pancreas in both groups of rats. After vagotomy, the islet blood flow in the hybrid rats was similar to that of the vagotomized control animals (8.2 ± 0.8 and 7.5 ± 1.4%, respectively). It is concluded that the increased pancreatic and islet blood perfusion observed in F 1-hybrids of the GK-Wistar rat depends on a mechanism mediated by the vagus nerve. Annika M Svensson, Department of Medical Cell Biology, Biomedical Centre, PO Box 571, S-75123 Uppsala, Sweden
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19

Jansson, Leif, Birgitta Bodin, and Per-Ola Carlsson. "Changes in Graft Blood Flow early after Syngeneic Rat Pancreas-Duodenum Transplantation." Upsala Journal of Medical Sciences 110, no. 1 (January 2005): 57–67. http://dx.doi.org/10.3109/2000-1967-082.

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20

Vollmar, Brigitte, Peter F. Conzen, Thomas Kerner, Helmut Habazettl, Martin Vierl, Helmut Waldner, and Klaus Peter. "Blood Flow and Tissue Oxygen Pressures of Liver and Pancreas in Rats." Anesthesia & Analgesia 75, no. 3 (September 1992): 421???430. http://dx.doi.org/10.1213/00000539-199209000-00019.

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21

Lifson, N., C. V. Lassa, and P. K. Dixit. "Relation between blood flow and morphology in islet organ of rat pancreas." American Journal of Physiology-Endocrinology and Metabolism 249, no. 1 (July 1, 1985): E43—E48. http://dx.doi.org/10.1152/ajpendo.1985.249.1.e43.

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By intra-arterial postmortem staining of the pancreas with hematoxylin after the administration of nonradioactive microspheres to anesthetized unfasted rats, the following values (+/-SE) were obtained: mean single islet volume, 1.00 +/- 0.12 nl (median 0.32 +/- 0.04 nl, n = 14); pancreatic intensity of perfusion, 1.18 +/- 0.14 ml X min-1 X g-1 (n = 10); percentage of pancreatic flow to islets, 6 +/- 1% (n = 10); single islet blood flow, 20 +/- 3 ml X min-1 (n = 10); and islet perfusion, 19 +/- 3 ml X min-1 X g-1 (n = 10). Perfusion of islet tissue was calculated to be above average for very small islets and to decrease with increasing islet size to become below average for very large ones. Details of the distribution of the total islet flow to subpopulations of islets grouped according to single islet size are shown pictorially.
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22

Charbon, G. A., and M. F. Anderson. "Hepatic haemodynamics as related to blood flow through gut, spleen, and pancreas." Gut 30, no. 2 (February 1, 1989): 265–78. http://dx.doi.org/10.1136/gut.30.2.265.

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23

Nyman, Lara R., Eric Ford, Alvin C. Powers, and David W. Piston. "Glucose-dependent blood flow dynamics in murine pancreatic islets in vivo." American Journal of Physiology-Endocrinology and Metabolism 298, no. 4 (April 2010): E807—E814. http://dx.doi.org/10.1152/ajpendo.00715.2009.

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Pancreatic islets are highly vascularized and arranged so that regions containing β-cells are distinct from those containing other cell types. Although islet blood flow has been studied extensively, little is known about the dynamics of islet blood flow during hypoglycemia or hyperglycemia. To investigate changes in islet blood flow as a function of blood glucose level, we clamped blood glucose sequentially at hyperglycemic (∼300 mg/dl or 16.8 mM) and hypoglycemic (∼50 mg/dl or 2.8 mM) levels while simultaneously imaging intraislet blood flow in mouse models that express green fluorescent protein in the β-cells or yellow fluorescent protein in the α-cells. Using line scanning confocal microscopy, in vivo blood flow was assayed after intravenous injection of fluorescent dextran or sulforhodamine-labeled red blood cells. Regardless of the sequence of hypoglycemia and hyperglycemia, islet blood flow is faster during hyperglycemia, and apparent blood volume is greater during hyperglycemia than during hypoglycemia. However, there is no change in the order of perfusion of different islet endocrine cell types in hypoglycemia compared with hyperglycemia, with the islet core of β-cells usually perfused first. In contrast to the results in islets, there was no significant difference in flow rate in the exocrine pancreas during hyperglycemia compared with hypoglycemia. These results indicate that glucose differentially regulates blood flow in the pancreatic islet vasculature independently of blood flow in the rest of the pancreas.
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24

Wang, P., Z. F. Ba, and I. H. Chaudry. "Increase in hepatic blood flow during early sepsis is due to increased portal blood flow." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 261, no. 6 (December 1, 1991): R1507—R1512. http://dx.doi.org/10.1152/ajpregu.1991.261.6.r1507.

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Although hepatic blood flow increases significantly during early sepsis [as produced by cecal ligation and puncture (CLP)], it is not known whether this is due to the increase in portal or hepatic arterial blood flows. To study this, rats were subjected to CLP, after which they and sham-operated rats received either 3 or 6 ml normal saline/100 g body wt subcutaneously (i.e., all rats received crystalloid therapy). Blood flow in various organs was determined by using a radioactive microsphere technique at 5 and 20 h after CLP or sham operation. Portal blood flow was calculated as the sum of blood flows to the spleen, pancreas, gastrointestinal tract, and mesentery. Total hepatic blood flow was the sum of portal blood flow and hepatic arterial blood flow. A significant increase in portal blood flow and in total hepatic blood flow was observed at 5 h after CLP (i.e., early sepsis), and this was not altered by doubling the volume of crystalloid resuscitation after the induction of sepsis. In contrast, hepatic arterial blood flow during early sepsis was found to be similar to control; however, it was significantly reduced in late sepsis (i.e., 20 h after CLP). Cardiac output was significantly higher than the control in early sepsis. However, even in late sepsis, cardiac output and total hepatic blood flow were not significantly different from controls. These results indicate that the increased total hepatic blood flow during early hyperdynamic sepsis is solely due to the increased portal blood flow.
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25

Carlsson, P. O., A. Andersson, and L. Jansson. "Pancreatic islet blood flow in normal and obese-hyperglycemic (ob/ob) mice." American Journal of Physiology-Endocrinology and Metabolism 271, no. 6 (December 1, 1996): E990—E995. http://dx.doi.org/10.1152/ajpendo.1996.271.6.e990.

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The present study evaluated whether a microsphere technique could be used for islet blood flow measurements in anesthetized mice. When this was confirmed, we applied the technique in different strains of mice. Approximately 9 x 10(4) microspheres could be given without interfering with mean arterial blood pressure. Mixing of the microspheres with arterial blood was adequate, and the extraction of microspheres in capillary beds was nearly 100%. In NMRI mice whole pancreatic blood flow was estimated to be 0.54 +/- 0.11 ml.min-1.g pancreatic tissue-1 and islet blood flow to be 18 +/- 4 microliters.min-1.g pancreas-1 (n = 12 animals per experiment), whereas corresponding values in lean C57Bl/6 mice were twice as high. In C57Bl/6 mice glucose (3 g/kg iv) doubled islet blood flow without affecting whole pancreatic blood flow, whereas no effect was seen after an equimolar dose of 3-O-methylglucose. In obese-hyperglycemic C57Bl/6 mice, islet blood flow was more than five times higher than in the lean C57Bl/6 mice when expressed as blood flow per gram pancreas. However, when islet blood perfusion was corrected for islet weight, it was lower in the obese than in the lean mice, suggesting an impaired ability in obese mice to increase blood flow in concert with the increased islet mass. This may contribute to the insufficient insulin secretion and resulting hyperglycemia seen in these animals.
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26

Kadyrov, R. K., and D. E. Tsyplakov. "Morphology of the pancreas at early terms after disruption of organ blood flow." Kazan medical journal 82, no. 5 (October 15, 2001): 382. http://dx.doi.org/10.17816/kazmj84094.

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The aim of the present work was an experimental morphological study of the pancreas at early stages of ischemia. Particular attention was paid to the condition of blood microcirculatory channel. The study was carried out on cats.
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27

Hultström, Michael, Leif Jansson, Birgitta Bodin, and Örjan Källskog. "Moderate hypothermia induces a preferential increase in pancreatic islet blood flow in anesthetized rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 3 (September 2007): R1438—R1443. http://dx.doi.org/10.1152/ajpregu.00259.2007.

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The aim of the study was to characterize the effects of induced moderate hypothermia on splanchnic blood flow, with particular reference to that of the pancreas and the islets of Langerhans. We also investigated how interference with the autonomic nervous system at different levels influenced the blood perfusion during hypothermia. For this purpose, hypothermia (body temperature of 28°C) was induced by external cooling, whereas normothermic (37.5°C) anesthetized Sprague-Dawley rats were used as controls. Some rats were pretreated with either propranolol, yohimbine, atropine, hexamethonium, or a bilateral abdominal vagotomy. Our findings suggest that moderate hypothermia elicits complex, organ-specific circulatory changes, with increased perfusion noted in the pylorus, as well as the whole pancreas and the pancreatic islets. The pancreatic islets maintain their high blood perfusion through mechanisms involving both sympathetic and parasympathetic mediators, whereas the increased pyloric blood flow is mediated through parasympathetic mechanisms. Renal blood flow was decreased, and this can be prevented by ganglionic blockade and is also influenced by β-adrenoceptors.
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28

Lai, Enyin, Ulrika Pettersson, Alberto Delgado Verdugo, Per-Ola Carlsson, Birgitta Bodin, Örjan Källskog, A. Erik G. Persson, Monica Sandberg, and Leif Jansson. "Blood lipids affect rat islet blood flow regulation through β3-adrenoceptors." American Journal of Physiology-Endocrinology and Metabolism 307, no. 8 (October 15, 2014): E653—E663. http://dx.doi.org/10.1152/ajpendo.00680.2013.

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Pancreatic islet blood perfusion varies according to the needs for insulin secretion. We examined the effects of blood lipids on pancreatic islet blood flow in anesthetized rats. Acute administration of Intralipid to anesthetized rats increased both triglycerides and free fatty acids, associated with a simultaneous increase in total pancreatic and islet blood flow. A preceding abdominal vagotomy markedly potentiated this and led acutely to a 10-fold increase in islet blood flow associated with a similar increase in serum insulin concentrations. The islet blood flow and serum insulin response could be largely prevented by pretreatment with propranolol and the selective β3-adrenergic inhibitor SR-59230A. The nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester prevented the blood flow increase but was less effective in reducing serum insulin. Increased islet blood flow after Intralipid administration was also seen in islet and whole pancreas transplanted rats, i.e., models with different degrees of chronic islet denervation, but the effect was not as pronounced. In isolated vascularly perfused single islets Intralipid dilated islet arterioles, but this was not affected by SR-59230A. Both the sympathetic and parasympathetic nervous system are important for the coordination of islet blood flow and insulin release during hyperlipidemia, with a previously unknown role for β3-adrenoceptors.
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29

Kuwahira, I., N. C. Gonzalez, N. Heisler, and J. Piiper. "Changes in regional blood flow distribution and oxygen supply during hypoxia in conscious rats." Journal of Applied Physiology 74, no. 1 (January 1, 1993): 211–14. http://dx.doi.org/10.1152/jappl.1993.74.1.211.

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The effects of acute hypoxia on central hemodynamics, regional blood flow, and regional oxygen supply (blood flow x arterial O2 concentration) were studied in conscious resting rats. Regional blood flow was determined by the radiolabeled microsphere technique. Blood pressure, heart rate; and aortic blood flow increased and total peripheral resistance decreased significantly during hypoxia. Blood flow to brain, respiratory muscles, and liver increased both in absolute value and as a fraction of the aortic blood flow. Fractional blood flow to the gastrointestinal tract, spleen, pancreas, skin, fat, and hindlimb bones decreased during hypoxia; blood flow decreased in absolute values only in stomach and fat. Oxygen supply to brain, respiratory muscles, and liver increased during hypoxia, whereas it decreased in the remaining organs investigated.
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30

Harper, S. L., V. H. Pitts, D. N. Granger, and P. R. Kvietys. "Pancreatic tissue oxygenation during secretory stimulation." American Journal of Physiology-Gastrointestinal and Liver Physiology 250, no. 3 (March 1, 1986): G316—G322. http://dx.doi.org/10.1152/ajpgi.1986.250.3.g316.

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Pancreatic acinar tissue O2 tension (PO2) was measured in anesthetized rats using recessed-tip microelectrodes (tip diam 1-2 micron). Pancreatic blood flow was measured using radioactive microspheres. Volume rate of pancreatic secretion, as well as protein concentration, was also measured. Average resting PO2 was 24.8 +/- 1.6 mmHg, with relatively little variation evident within a given pancreas. Bolus intravenous infusion of cholecystokinin octapeptide (CCK-OP, 4 micrograms X kg body wt-1) induced a reduction in tissue PO2 and profoundly increased protein output, while not directly affecting pancreatic blood flow. By contrast, secretin infusion (1.0 CU X kg body wt-1 iv bolus) affected neither tissue PO2 nor blood flow, although secretory rate increased by nearly sevenfold. This difference in PO2 response to the two compounds is interpreted in light of the fact that CCK-OP primarily stimulates acinar cell function, while secretin preferentially activates secretory epithelium. Pancreatic PO2 was found to be linearly related to resting blood flow at flows above 44 ml X min-1 X 100 g-1. No regional differences in blood flow were found in the head, body, and tail of the pancreas.
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31

Gundersen, Hilde, Heidi van Wageningen, and Renate Grüner. "Alcohol-Induced Changes in Cerebral Blood Flow and Cerebral Blood Volume in Social Drinkers." Alcohol and Alcoholism 48, no. 2 (November 21, 2012): 160–65. http://dx.doi.org/10.1093/alcalc/ags121.

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32

Ulrich-Baker, M. G., W. R. Smidt, T. S. Gaginella, and D. N. Granger. "Splanchnic blood flow during stimulation of gastrointestinal growth." American Journal of Physiology-Gastrointestinal and Liver Physiology 252, no. 5 (May 1, 1987): G692—G698. http://dx.doi.org/10.1152/ajpgi.1987.252.5.g692.

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The primary objective of this study is to determine whether a relationship exists between the rate of blood flow and the gastrointestinal response to a trophic stimulus. A new prostaglandin E2 (PGE2) derivative, Ro 22-1327, was employed as a growth stimulus. Rats were treated by gavage for 14 days with Ro 22-1327 (0.5 and 5 mg/kg). The vascular and trophic effects of Ro 22-1327 were studied in the gastric antrum and oxyntic gland area, duodenum, jejunum, ileum, colon, liver, and pancreas. Generally, the trophic effects were 1) similar to those reported with other PGE2 analogues, 2) more pronounced in the antrum than in the oxyntic gland area, 3) greatest in the stomach, diminishing toward the colon, and 4) dose dependent. Organ blood flows were largely unaffected by the low-dose treatment, while the high-dose treatment tended to increase blood flow. The changes in blood flow were most pronounced proximally where the trophic responses were maximal. We speculate that the greater trophic response to the high dose of Ro 22-1327 may reduce the vasoconstriction produced by this agent.
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33

Tolentino, Neil J., Christina E. Wierenga, Shana Hall, Susan F. Tapert, Martin P. Paulus, Thomas T. Liu, Tom L. Smith, and Marc A. Schuckit. "Alcohol Effects on Cerebral Blood Flow in Subjects With Low and High Responses to Alcohol." Alcoholism: Clinical and Experimental Research 35, no. 6 (February 17, 2011): 1034–40. http://dx.doi.org/10.1111/j.1530-0277.2011.01435.x.

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34

Girgis, Mark D., Tove Olafsen, Vania Kenanova, Katelyn E. McCabe, Anna M. Wu, and James S. Tomlinson. "CA19-9 as a Potential Target for Radiolabeled Antibody-Based Positron Emission Tomography of Pancreas Cancer." International Journal of Molecular Imaging 2011 (September 6, 2011): 1–9. http://dx.doi.org/10.1155/2011/834515.

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Introduction. Sensitive and specific imaging of pancreas cancer are necessary for accurate diagnosis, staging, and treatment. The vast majority of pancreas cancers express the carbohydrate tumor antigen CA19-9. The goal of this study was to determine the potential to target CA19-9 with a radiolabeled anti-CA19-9 antibody for imaging pancreas cancer. Methods. CA19-9 was quantified using flow cytometry on human pancreas cancer cell lines. An intact murine anti-CA19-9 monoclonal antibody was labeled with a positron emitting radionuclide (Iodine-124) and injected into mice harboring antigen positive and negative xenografts. MicroPET/CT were performed at successive time intervals (72 hours, 96 hours, 120 hours) after injection. Radioactivity was measured in blood and tumor to provide objective confirmation of the images. Results. Antigen expression by flow cytometry revealed approximately 1.3×106 CA19-9 antigens for the positive cell line and no expression in the negative cell line. Pancreas xenograft imaging with Iodine-124-labeled anti-CA19-9 mAb demonstrated an average tumor to blood ratio of 5 and positive to negative tumor ratio of 20. Conclusion. We show in vivo targeting of our antigen positive xenograft with a radiolabeled anti-CA19-9 antibody. These data demonstrate the potential to achieve anti-CA19-9 antibody based positron emission tomography of pancreas cancer.
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35

Liard, Jean-Francois. "Effects of intra-arterial arginine-vasopressin infusions on peripheral blood flows in conscious dogs." Clinical Science 71, no. 6 (December 1, 1986): 713–21. http://dx.doi.org/10.1042/cs0710713.

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1. We reported in an earlier study that intravenous infusions of arginine-vasopressin (AVP), 220 pg min−1 kg−1 for 1 h, substantially reduced blood flow to the skin, skeletal muscle, pancreas, colon, small intestine, abdominal fat and myocardium [1] in conscious dogs. In the present study, we infused AVP directly into the artery supplying these organs and tissues in order to determine the relative contribution of local versus systemic mechanisms in the vascular resistance changes previously observed. 2. Regional blood flows were measured with radioactive microspheres in conscious, chronically instrumented dogs before and during intra-arterial infusions of AVP administered into the left axillary artery (n = 6), the left coronary artery (n = 6), and the cranial mesenteric artery (n = 6). The infusion rates were calculated to increase local, target organ plasma concentrations of AVP to the levels reached in our previous study while minimizing systemic changes. 3. Left axillary AVP artery infusion significantly reduced skin and compact bone blood flow, but had no effect on skeletal muscle blood flow. Intra-coronary AVP infusion had no effect on myocardial blood flow nor on cardiac output. Intramesenteric AVP infusion had no effect on blood flow to the colon, small intestine and abdominal fat, but significantly reduced blood flow to those areas of the pancreas which received blood from the cannulated artery. 4. Measurements in a limited number of dogs indicated that the local axillary and mesenteric venous levels of AVP were similar when the hormone was infused systemically at a rate of 220 pg min−1 kg−1 or intra-arterially at a lower rate. 5. These findings suggest that the increase in resistance measured in the skeletal muscle, small intestine, colon and abdominal fat after systemic administration of small amounts of AVP results in large part from indirect mechanisms. Direct vasoconstrictor effects of AVP at these plasma concentrations appear limited to the skin, the pancreas and the compact bones.
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36

Choudhry, Mashkoor A., Zheng F. Ba, Shadab N. Rana, Kirby I. Bland, and Irshad H. Chaudry. "Alcohol ingestion before burn injury decreases splanchnic blood flow and oxygen delivery." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 2 (February 2005): H716—H721. http://dx.doi.org/10.1152/ajpheart.00797.2004.

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Recent studies from our laboratory have shown that alcohol and burn injury impair intestinal barrier and immune functions. Although multiple factors can contribute to impaired intestinal barrier function, such an alteration could result from a decrease in intestinal blood flow (BF) and oxygen delivery (Do2). Therefore, in this study, we tested the hypothesis that alcohol ingestion before burn injury reduces splanchnic blood flow and oxygen delivery. Rats (250 g) were gavaged with alcohol to achieve a blood ethanol level in the range of 100 mg/dl before burn or sham injury (25% total body surface area). Day 1 after injury, animals were anesthetized with methoxyflurane. Blood pressure, cardiac output (CO), ±dP/d t, organ BF (in ml·min−1·100 g−1), and Do2 (in mg·ml−1·100 g−1) were determined. CO and organ BF were determined using a radioactive microsphere technique. Our results indicate that blood pressure, CO, and +dP/d t were decreased in rats receiving a combined insult of alcohol and burn injury compared with rats receiving either burn injury or alcohol alone. This is accompanied by a decrease in BF and Do2 to the liver and intestine. No significant change in BF to the coronary arteries (heart), brain, lung, skin, and muscles was observed after alcohol and burn injury. In conclusion, the results presented here suggest that alcohol ingestion before burn injury reduces splanchnic BF and Do2. Such decreases in BF and Do2 may cause hypoxic insult to the intestine and liver. Although a hypoxic insult to the liver would result in a release of proinflammatory mediators, a similar insult to the intestine will likely perturb both intestinal immune cell and barrier functions, as observed in our previous study.
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37

Kusterer, K., M. Enghofer, S. Zendler, C. Blochle, and K. H. Usadel. "Microcirculatory changes in sodium taurocholate-induced pancreatitis in rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 260, no. 2 (February 1, 1991): G346—G351. http://dx.doi.org/10.1152/ajpgi.1991.260.2.g346.

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Using an in vivo microscopy technique, we studied the microcirculatory changes in sodium taurocholate-induced pancreatitis in rats. With a computerized image analyzer system, blood flow, vascular permeability changes, and capillary densities were measured. Intraductal infusion of 0.4 ml saline had only minor effects on the microcirculation. Various concentrations and volumes of sodium taurocholate solutions were infused into the pancreatic duct. Sodium taurocholate (0.4 ml, 4%) led to increased vascular permeability preceding stasis within 232 +/- 47 s, followed by hemorrhagic necrosis in the head of the pancreas. In the corpus close to the tail of the pancreas capillary blood flow was maintained. In conclusion, this study shows that the microcirculation of the pancreas can be excellently investigated with in vivo microscopy. With this method, tremendous distribution disturbances of the microcirculation in the pancreas can be seen in the course of acute pancreatitis. Vascular permeability changes and stasis of the microcirculation represent the primary microcirculatory events in acute pancreatitis induced by sodium taurocholate in the areas where hemorrhagic necrosis occurs.
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38

Iwatsuki, K., T. Homma, and K. U. Malik. "Contribution of prostaglandins to dopamine actions in the pancreas of anesthetized dogs." American Journal of Physiology-Gastrointestinal and Liver Physiology 248, no. 1 (January 1, 1985): G110—G117. http://dx.doi.org/10.1152/ajpgi.1985.248.1.g110.

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We investigated the effect of dopamine and arachidonic acid on pancreatic blood flow and exocrine secretion in the isolated blood-perfused pancreas of pentobarbital sodium-anesthetized dogs without or with pretreatment with indomethacin or sodium meclofenamate in the absence and during infusion of prostaglandins I2 or E2 (PGI2 or PGE2). Intra-arterial administration of dopamine (50-500 ng/kg) produced an initial vasoconstriction followed by vasodilation and enhanced flow rate of pancreatic exocrine secretion. Arachidonic acid (0.5-5 micrograms/kg) produced vasodilation without altering the flow rate of pancreatic exocrine secretion. In animals pretreated with indomethacin or sodium meclofenamate (10 mg/kg iv), the magnitude and the duration of the biphasic vascular response but not the increase in flow rate of pancreatic exocrine secretion elicited by dopamine were reduced. Arachidonic acid-induced vasodilation was abolished by the cyclooxygenase inhibitors. During infusion of PGI2 or PGE2 (10 ng X kg-1 X min-1 ia), the inhibitory effect of indomethacin or sodium meclofenamate on the vasodilator phase of the response to dopamine was diminished. These data suggest that prostaglandins, presumably PGI2 and PGE2, contribute to the effect of dopamine to increase pancreatic blood flow but not to increase pancreatic exocrine secretion in anesthetized dogs.
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39

Ullah Wazir, Noman, Jehanzeb Khan, Zilli Huma, Farooq Khan, Nighat Ara, and Ambereen Humayun. "Counter effects of Vitamin E against Outcomes of Alcohol Toxicity in Pancreatic Acini: Histomorphometric Study." Pakistan Journal of Medical and Health Sciences 15, no. 11 (November 30, 2021): 2974–78. http://dx.doi.org/10.53350/pjmhs2115112974.

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Aim: To evaluate the effects of alcohol on the microscopic morphology of the exocrine pancreas and blood serum amylase and to explored that if vitamin E has a protective role against alcohol-induced damage in the pancreas of rabbits. Study design: Analytical experimental study Place and duration of study: Departments of Anatomy, Pathology and Pharmacology in Peshawar Medical College Pakistan from 1st January 2019 to 30th June 2019. Methodology: Eighteen healthy adult male domestic rabbits weighing 1-1.5 kg were chosen (oryctolaguscuniculus). The control group A received proper food and normal saline as drinking water, experimental group B received proper diet and 30 percent ethanol solution (30ml/kg/day) orally daily with normal saline, and experimental group C received proper diet, 30 percent ethanol solution (30ml/kg/day), vitamin E (50mg/kg/day) orally daily with normal saline. Each rabbit's blood was taken for serum amylase. Morphology of acinar cells included: 1) number of cells, (10 acini/field, 2) size of acini, 3) size of acinar cells, and 4) size of acinar nuclei. Results: Normal value of serum amylase in rabbits was found. The difference in serum amylase levels between the control and experimental groups for both E4 and E8 animals was not statistically significant. There was no significant difference in the number of pancreatic acinar cells, size of pancreatic acini, the pancreatic acinar cell size, and pancreatic acinar cells nuclear size in the control and experimental groups for both E4 and E8 animals. Conclusion: Alcohol consumption had no influence on the histomorphology of the rabbits' pancreatic acini in a short period (4-8 weeks). No significant variation was noted in the pancreatic acinar cells count & size, pancreatic acinar cells nuclear count and size, and pancreatic acini size. Therefore, protective role of vitamin E was not usefully identified. Keywords: Alcohol, Pancreas, Histomorphology, Vitamin E, Serum amylase
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40

Maule, S., K. Ray Chaudhuri, T. Thomaides, D. Pavitt, J. McCleery, and C. J. Mathias. "Effects of Oral Alcohol on Superior Mesenteric Artery Blood Flow in Normal Man, Horizontal and Tilted." Clinical Science 84, no. 4 (April 1, 1993): 419–25. http://dx.doi.org/10.1042/cs0840419.

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1. The cardiovascular effects of oral alcohol (0.5 g/kg body weight diluted to 300 ml in sugar-free orange juice) were compared with those of placebo in 10 normal subjects. Measurements were made while the subjects were supine and horizontal for 45 min and after 10 min of 45° head-up tilt. 2. After alcohol, plasma alcohol levels rose from 1.9 ± 1.3 to 61.6 ± 6.5 mg/100 ml. After placebo, plasma alcohol levels did not increase. After alcohol and placebo, supine blood pressure was unchanged; heart rate, both supine and during tilt, rose after alcohol only. 3. After alcohol, superior mesenteric artery and digital skin blood flow increased and calculated vascular resistances fell. There was no change after placebo. 4. Forearm blood flow, forearm vascular resistance and cardiac index did not change in either phase, except for a fall in cardiac index during tilt but only after alcohol. 5. In conclusion, the acute ingestion of 0.5 g of alcohol/kg body weight in normal subjects raised heart rate and actively dilated the superior mesenteric artery and digital skin vessels. There was no effect on blood pressure, cardiac output and skeletal muscle vascular tone. During head-up tilt after alcohol, there was a tendency for blood pressure to fall with a compensatory rise in heart rate.
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41

Kulenović, Amela, and Aida Sarač-Hadžihalilović. "Investigation of Vascularization of Human Pancreas Using Method of Selective Arteriography with Insight Into Significance to a Surgical Approach for this Organ." Bosnian Journal of Basic Medical Sciences 10, no. 1 (February 20, 2010): 15–18. http://dx.doi.org/10.17305/bjbms.2010.2727.

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This study explored arterial vascularisation of celiac trunk and superior mesenteric artery using method of selective arteriography in series of arteriogram which were done in 39 patients of Institute for Radiology. There were no pathological findings in a single case at pancreas or duodenum. Arteries which arise for vascularization of pancreas had a common spot of arising, flow and ramification. Pancreatic duodenal arteries arcade, which supply blood to the duodenum and the body of the pancreas, were shown in arteriogram. The branches which provide blood supply to the body and the tail of the pancreas were found. There was one case where lower pancreatic artery arose from gastroduodenal artery and in one case a direct anastomosis for celiac trunk and superior mesenteric arteries, better known as Tandler’s anastomosis.
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42

Orrego, H., F. J. Carmichael, and Y. Israel. "New insights on the mechanism of the alcohol-induced increase in portal blood flow." Canadian Journal of Physiology and Pharmacology 66, no. 1 (January 1, 1988): 1–9. http://dx.doi.org/10.1139/y88-001.

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Acute administration of ethanol increases portal blood flow by 40–60%. This increase in blood flow compensates for the increase in O2 consumption that follows alcohol intake and may play a protective role against hypoxic hepatocellular necrosis. We have investigated the mechanism of this hemodynamic effect of ethanol in the rat using the labeled microsphere technique. We ruled out a direct role of systemic glucagon and of acetaldehyde in mediating the increase in portal flow. However, the increase in flow is maximal at a blood ethanol concentration of 3.5 mM, corresponding to that required to achieve the Vmax of alcohol dehydrogenase, and is suppressed by 4-methylpyrazole, an inhibitor of alcohol dehydrogenase. Alcohol ingestion results in zonal liver hypoxia and in increases in acetate, both of which have been shown to increase the levels of adenosine, a potent vasodilator, in blood and tissues. Ethanol produces a 400% increase in arterial adenosine. Adenosine infusion leads to a dose-dependent increase in portal blood flow of up to 100%, an effect that is suppressed by administration of 8-phenyltheophylline, an antagonist of adenosine at A1 and A2 receptors. Similarly, the ethanol-induced increase in portal blood flow is fully suppressed by 8-phenyltheophylline. In conclusion, adenosine appears to play an important role in the mechanism by which ethanol increases portal blood flow.
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43

DALLY, S., A. LUFT, J. C. PONSIN, C. GIRRE, H. MAMO, and E. FOURNIER. "Abnormal Pattern of Cerebral Blood Flow Distribution in Young Alcohol Addicts." Addiction 83, no. 1 (January 1988): 105–9. http://dx.doi.org/10.1111/j.1360-0443.1988.tb00458.x.

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44

Amen, Daniel G. "Regional Cerebral Blood Flow in Alcohol-Induced Violence: A Case Study." Journal of Psychoactive Drugs 31, no. 4 (October 1999): 389–93. http://dx.doi.org/10.1080/02791072.1999.10471768.

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45

Sano, M., P. E. Wendt, A. Wirsén, G. Stenberg, J. Risberg, and D. H. Ingvar. "Acute effects of alcohol on regional cerebral blood flow in man." Journal of Studies on Alcohol 54, no. 3 (May 1993): 369–76. http://dx.doi.org/10.15288/jsa.1993.54.369.

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46

Lee, Samuel S. "Alcohol infusion to measure hepatic blood flow: Vanquishing the běte noire?" Hepatology 10, no. 6 (December 1989): 1021–22. http://dx.doi.org/10.1002/hep.1840100625.

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47

Svensson, AM, B. Bodin, A. Andersson, and L. Jansson. "Pancreatic islet blood flow during pregnancy in the rat: an increased islet mass is associated with decreased islet blood flow." Journal of Endocrinology 180, no. 3 (March 1, 2004): 409–15. http://dx.doi.org/10.1677/joe.0.1800409.

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Increased blood perfusion of pancreatic islets is seen during various conditions of increased demand for insulin secretion. Pregnancy confers an increased need for insulin secretion, met by increased islet mass and volume as well as a decreased threshold for glucose-induced insulin secretion. In the present study, whole pancreatic and islet blood flow were studied with a microsphere technique in Wistar rats on days 15, 18 and 20 of pregnancy and days 2 and 7 post-partum. There were no changes in total pancreatic blood flow during pregnancy and the first post-partum week. Total blood perfusion through islet tissue expressed as flow per weight of whole pancreas was higher at day 15 of pregnancy. When islet blood flow was expressed per gram of islet tissue there was a decrease at day 18 of pregnancy. This decrease of islet blood flow was concomitant to a short-lived increase of the islet mass at the end of pregnancy. We conclude that upregulation of insulin output during late pregnancy does not specifically include increased net blood perfusion through the islets. One possible reason for this might be lack of synchronization between the proliferation of endocrine cells and angiogenesis, resulting in a relative decrease in islet vascular density in the islets.
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48

Musch, Timothy I., Kevin E. Eklund, K. Sue Hageman, and David C. Poole. "Altered regional blood flow responses to submaximal exercise in older rats." Journal of Applied Physiology 96, no. 1 (January 2004): 81–88. http://dx.doi.org/10.1152/japplphysiol.00729.2003.

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Maximal aerobic capacity and the ability to sustain submaximal exercise (Ex) declines with advancing age. Whether altered muscle blood flow (BF) plays a mechanistic role in these effects remains to be resolved. The present investigation determined the effects of aging on the hemodynamic and regional BF response to submaximal Ex in rats. Heart rate (HR), mean arterial pressure (MAP), and BF to different organs (kidneys, splanchnic organs, and 28 hindlimb muscles) were determined at rest and during submaximal treadmill Ex (20 m/min, 5% grade) with radiolabeled microspheres in young (Y; 6-8 mo old, 339 ± 8 g, n = 9) and old (O; 27-29 mo old, 504 ± 18 g, n = 7) Fischer 344 × Brown Norway rats. Results demonstrated that HR, MAP, and BF to the pancreas, small and large intestine, and total hindlimb musculature were similar between Y and O rats at rest. BF to the kidneys, spleen, and stomach were 33, 60, and 43% lower, respectively, in O compared with Y rats. BF to the total hindlimb musculature increased ( P < 0.05) during Ex and was similar for both Y and O rats (Y: 16 ± 3 to 124 ± 7 vs. O: 20 ± 3 to 137 ± 12 ml·min-1·100 g-1). However, in O vs. Y rats, BF was reduced in 6 (highly oxidative) and elevated in 8 (highly glycolytic) of the 28 individual hindquarter muscles or muscle parts examined ( P < 0.05). During Ex, BF to the spleen and stomach decreased ( P < 0.05) from rest in Y rats, whereas BF decreased in the kidneys, pancreas, spleen, stomach, as well as the small and large intestines of O rats. In conclusion, these data demonstrate that, despite similar increases in total hindlimb BF in Y and O rats during submaximal Ex, there is a profound BF redistribution from highly oxidative to highly glycolytic muscles.
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49

Mayock, Dennis E., Dana Ness, Robin L. Mondares, and Christine A. Gleason. "Binge alcohol exposure in the second trimester attenuates fetal cerebral blood flow response to hypoxia." Journal of Applied Physiology 102, no. 3 (March 2007): 972–77. http://dx.doi.org/10.1152/japplphysiol.00956.2006.

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Alcohol is detrimental to the developing brain and remains the leading cause of mental retardation in developed countries. The mechanism of alcohol brain damage remains elusive. Studies of neurological problems in adults have focused on alcohol's cerebrovascular effects, because alcoholism is a major risk factor for stroke and cerebrovascular injuries. However, few studies have examined similar cerebrovascular effects of fetal alcohol exposure. We examined the effect of chronic binge alcohol exposure during the second trimester on fetal cerebrovascular and metabolic responses to hypoxia in near-term sheep and tested the hypothesis that fetal alcohol exposure would attenuate cerebrovascular dilation to hypoxia. Pregnant ewes were infused with alcohol (1.5 g/kg) or saline intravenously at 60–90 days of gestation (full term = 150 days). At 125 days of gestation, we measured fetal cerebral blood flow (CBF) and oxygen metabolism at baseline and during hypoxia. Maternal blood alcohol averaged 214 ± 5.9 mg/dl immediately after the 1.5-h infusion, with similar values throughout the month of infusion. Hypoxia resulted in a robust increase in CBF in saline-infused fetuses. However, the CBF response to hypoxia in fetuses chronically exposed to alcohol was significantly attenuated. Cerebral oxygen delivery decreased in both groups of fetuses during hypoxia but to a greater degree in the alcohol-exposed fetuses. Prenatal alcohol exposure during the second trimester attenuates cerebrovascular responses to hypoxia in the third trimester. Altered cerebrovascular reactivity might be one mechanism for alcohol-related brain damage and might set the stage for further brain injury if a hypoxic insult occurs.
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50

Rooth, P., and I. B. Taljedal. "Vital microscopy of islet blood flow: catecholamine effects in normal and ob/ob mice." American Journal of Physiology-Endocrinology and Metabolism 252, no. 1 (January 1, 1987): E130—E135. http://dx.doi.org/10.1152/ajpendo.1987.252.1.e130.

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The pancreatic microcirculation in noninbred ob/ob mice and normal controls was visualized in a fluorescence microscope and examined for responses to intravenous infusions of epinephrine or norepinephrine. Evaluations of coded video recordings revealed a smooth dose-response relationship and validated a semiquantitative method of analysis. In ob/ob mice the islet microcirculation was markedly and reversibly inhibited by 0.14–4 micrograms of epinephrine X min-1 X kg body wt-1; the flow was almost totally stopped at the highest infusion rates. Capillary flow in the exocrine pancreas appeared unaffected, except for some inhibition at 4.0 micrograms X min-1 X kg-1. Norepinephrine was less potent an inhibitor of islet blood flow. Normal lean mice exhibited minor responses to 1–11.3 micrograms of epinephrine X min-1 X kg-1; in most cases there was no visible effect. It is concluded that there is a selective regulation of blood flow through the endocrine portion of the pancreas and that the islet microcirculation is hypersensitive to catecholamines in noninbred ob/ob mice. A defective inhibitory influence from the brain may play a role in the development of excessive hyperinsulinemia in ob/ob mice.
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