Interdigestive gastric blood flow: the relation to motor and secretory activities in conscious dogs

Naruse, Satoru; Takagi, Tohru; Kato, Masamitsu; Ozaki, Tsuyoshi

doi:10.1113/expphysiol.1992.sp003636

Cited by 13 publications

(9 citation statements)

References 14 publications

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“…In this study, systemic administration of OT transiently increased BP. This result was consistent with the report of Costa et al 15 Although the gut circulation influences the GI motility, 16 we believe that the transient decrease and subsequent increase of the gastric pressure were caused by the indirect and direct effect of OT not due to the change of gastric blood flow. First of all, devazepide, the specific CCK 1 receptor antagonist, abolished the early transient decrease of gastric motility but did not influence the increase of BP (data not shown) following OT administration.…”

Section: Discussionsupporting

confidence: 93%

Oxytocin receptor expressed on the smooth muscle mediates the excitatory effect of oxytocin on gastric motility in rats

Qin

Feng

Wang

et al. 2009

Neurogastroenterology Motil

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The aim of this study was to localize oxytocin receptor (OTR) in the stomach and to investigate the effect of OT on gastric motility in rats. Western blot and immunohistochemistry methods were used to localize OTR in stomach. The motility of stomach was recorded in vivo (recording of the intragastric pressure), in vitro (recording of the contraction of muscle strips) and on isolated smooth muscle cells. OTR was expressed on cells of both circular and longitudinal muscle of stomach. Systemic administration of OT induced an early transient decrease and a subsequent increase on intragastric pressure. Devazepide (1 mg kg(-1), i.v.), a cholecystokinin-1 (CCK(1)) receptor antagonist, completely abolished the transient response but did not influence the subsequent one. OT (10(-9)-10(-6) mol L(-1)) dose-dependently increased the contraction of the muscle strips of gastric body, antrum, and pyloric sphincter, and decreased the average cell length of isolated smooth muscle cells. Tetrodotoxin and atropine did not influence the effect of OT on muscle strips. Pretreatment with atosiban, an OTR antagonist, inhibited the spontaneous contraction of muscle strips and abolished the excitatory effect of OT on the muscle strips and the isolated cells. These results suggest that the OTR is expressed on the smooth muscle of the stomach and mediates excitatory effect of OT on gastric motility.

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Section: Discussionsupporting

confidence: 93%

Oxytocin receptor expressed on the smooth muscle mediates the excitatory effect of oxytocin on gastric motility in rats

Qin

Feng

Wang

et al. 2009

Neurogastroenterology Motil

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“…While the postprandial hyperemia in the intestine is well characterized, there is a relative paucity of studies on the gastric vascular response to meals. Typically, a transient gastric hyperemia is noted at 10 to 45 min after a meal in conscious dogs and cats (52,250,347,433). However, in one study only 50% of the animals responded with a gastric hyperemia after feeding (145) while a postprandial hyperemia was not detected in another study (12).…”

Section: Stomach Postprandial Hyperemiamentioning

confidence: 88%

“…In fasting conscious dogs, periodic gastric contractile activity is associated with biphasic changes in blood flow; reduced flow during the contraction phase and increased flow during muscle relaxation (347). The hyperemia noted during relaxation exceeds the nadir in blood flow during contraction, such that average blood flow is increased during periods of enhanced motility.…”

Section: Stomach Postprandial Hyperemiamentioning

confidence: 99%

The Gastrointestinal Circulation: Physiology and Pathophysiology

Granger

Holm

Kvietys

2015

Comprehensive Physiology

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The gastrointestinal (GI) circulation receives a large fraction of cardiac output and this increases following ingestion of a meal. While blood flow regulation is not the intense phenomenon noted in other vascular beds, the combined responses of blood flow, and capillary oxygen exchange help ensure a level of tissue oxygenation that is commensurate with organ metabolism and function. This is evidenced in the vascular responses of the stomach to increased acid production and in intestine during periods of enhanced nutrient absorption. Complimenting the metabolic vasoregulation is a strong myogenic response that contributes to basal vascular tone and to the responses elicited by changes in intravascular pressure. The GI circulation also contributes to a mucosal defense mechanism that protects against excessive damage to the epithelial lining following ingestion of toxins and/or noxious agents. Profound reductions in GI blood flow are evidenced in certain physiological (strenuous exercise) and pathological (hemorrhage) conditions, while some disease states (e.g., chronic portal hypertension) are associated with a hyperdynamic circulation. The sacrificial nature of GI blood flow is essential for ensuring adequate perfusion of vital organs during periods of whole body stress. The restoration of blood flow (reperfusion) to GI organs following ischemia elicits an exaggerated tissue injury response that reflects the potential of this organ system to generate reactive oxygen species and to mount an inflammatory response. Human and animal studies of inflammatory bowel disease have also revealed a contribution of the vasculature to the initiation and perpetuation of the tissue inflammation and associated injury response.

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“…The blood flow in the gastroduodenal artery (just above the branch of the superior pancreaticoduodenal artery), measured by Doppler flow probe, is approximately 10 ml min-' in anaesthetized 8-10 kg piglets (S. G. Pierzynowski & P. Kiela, unpublished observation). The blood flow opposing the infusion reaching tlhe superior pancreaticoduodenal artery is likely to be even greater in conscious pigs since halothane anaesthesia reduces mesenteric blood flow and cardiac output in pigs by about 50% (Loick, Tokyay, Abdi, Traber, Nichols & Herndon, 1991) and, indeed, flows of some 30-60 ml min-' have been recorded in the left gastric artery in conscious, fasted dogs of (Naruse, Takagi, Kato & Ozaki, 1992). Therefore, our observations that the infusion of Evans Blue into anaesthetized pigs, via the same route and at the same rate (1 ml min-') as for peptide infusions in the conscious pig, stained the pylorus and proximal duodenum only, and not the pancreas, strongly suggests that the stimulatory effect of these two peptides arose from an action in the duodenum and was not due to the infusions reaching the pancreas.…”

Section: Discussionmentioning

confidence: 99%

Cholecystokinin‐8 and vasoactive intestinal polypeptide stimulate exocrine pancreatic secretion via duodenally mediated mechanisms in the conscious pig

Kiela¹,

Zabielski²,

Podgurniak³

et al. 1996

Experimental Physiology

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SUMMARYThe effects of local and peripheral administration of cholecystokinin-8 (CCK-8) and vasoactive intestinal polypeptide (VIP) on basal pancreatic secretion were investigated in conscious pigs. Five pigs (20 + 2 kg, mean + S.E.M.) were chronically fitted with a T-shaped cannula in the duodenum, and catheters in the pancreatic duct, jugular vein, and right gastroepiploic artery. The arterial catheter was inserted against the bloodstream with its tip opposite the duodenal branch(es) of the right gastroepiploic artery, so that all injected peptides would reach the duodenal arterial circulation excluding the pancreas. Pancreatic secretion during basal conditions (i.e. after an overnight fast) exhibited a characteristic cyclic pattern (cycle duration, 70 + 4.2 min). Secretion volume oscillated between 0.2 + 0-04 and 4 0 + 0 9 ml kg-' h-' (P < 0.001), trypsin output between 9 6 + 1.9 and 29-1 + 4-1 U kg-' h-1 (P < 0.001) and protein output between 0-36 + 0 08 and 9-2 + 1 7 mg kg-1 h-' (P < 0.001). Infusion into the jugular vein for 1 min, during the trough of pancreatic secretion, of either CCK-8 (15 pmol kg-' min-') or VIP (7 pmol kg-' min-') did not stimulate pancreatic secretion. However, local infusion of an identical dose of CCK-8 or VIP into the duodenal arterial circulation increased the volume, protein output and trypsin output of the pancreatic juice (P < 0.05 to < 0.001). These results indicate that CCK-8 and VIP can stimulate the exocrine pancreas by a duodenally mediated mechanism.

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Interdigestive gastric blood flow: the relation to motor and secretory activities in conscious dogs

Cited by 13 publications

References 14 publications

Oxytocin receptor expressed on the smooth muscle mediates the excitatory effect of oxytocin on gastric motility in rats

Oxytocin receptor expressed on the smooth muscle mediates the excitatory effect of oxytocin on gastric motility in rats

The Gastrointestinal Circulation: Physiology and Pathophysiology

Cholecystokinin‐8 and vasoactive intestinal polypeptide stimulate exocrine pancreatic secretion via duodenally mediated mechanisms in the conscious pig

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