Possible mechanisms for the initiation and maintenance of postprandial intestinal hyperemia

Gallavan, Robert H.; Chou, C. C.

doi:10.1152/ajpgi.1985.249.3.g301

Cited by 61 publications

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“…Digestion is accompanied by intestinal vasodilatation (postprandial hyperemia) (42), which is dependent on an intact vagus but not mediated by parasympathetic vasodilator activity (36). The mechanisms associated with postpran- dial hyperemia appear to be complex (16) and may include release of local factors such as nitric oxide, prostaglandins, and polypeptides such as secretin, neurotensin, and CCK. A potential mechanism that may play a permissive role in postprandial hyperemia is withdrawal of sympathetic vasomotor drive to the gastrointestinal vasculature.…”

Section: Discussionmentioning

confidence: 99%

Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

Sartor

Verberne

2002

American Journal of Physiology-Regulatory, Integrative and Comp

102

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To determine whether CCK influences sympathetic vasomotor function, we examined the effect of systemic CCK administration on mean arterial blood pressure (MAP), heart rate (HR), lumbar sympathetic nerve discharge (LSND), splanchnic sympathetic nerve discharge (SSND), and the discharge of presympathetic neurons of the rostral ventrolateral medulla (RVLM) in ␣-chloralose-anesthetized rats. CCK (1-8 g/kg iv) reduced MAP, HR, and SSND and transiently increased LSND. Vagotomy abolished the effects of CCK on MAP and SSND as did the CCK-A receptor antagonist devazepide (0.5 mg/kg iv). The bradycardic effect of CCK was unaltered by vagotomy but abolished by devazepide. CCK increased superior mesenteric arterial conductance but did not alter iliac conductance. CCK inhibited a subpopulation (ϳ49%) of RVLM presympathetic neurons whereas ϳ28% of neurons tested were activated by CCK. The effects of CCK on RVLM neuronal discharge were blocked by devazepide. RVLM neurons inhibited by exogenous CCK acting via CCK-A receptors on vagal afferents may control sympathetic vasomotor outflow to the gastrointestinal tract vasculature. blood pressure; splanchnic sympathetic nerve; lumbar sympathetic nerve; rat CHOLECYSTOKININ (CCK) is a gastrointestinal hormone with actions including gastrointestinal vasodilatation (18), reduced gut motility, gastric acid secretion, and pancreatic secretion (3, 28). In the central nervous system, it is one of the most abundant neuropeptides, probably playing a major role in satiety as well as anxiety-related behavior (6, 38). Of the two types of CCK receptors, the A-type (CCK-A receptor) is predominantly found in the periphery, although it is also present in discrete brain regions and has a higher affinity for the sulfated octapeptide form of CCK. In the brain, the B-type receptor (CCK-B receptor) predominates and has a high affinity for both the sulfated and nonsulfated forms of CCK (13).Peripherally, CCK has been implicated in postprandial intestinal hyperemia because systemic administration of the peptide produces intestinal vasodilatation (18). In contrast, its effects on the vascular resistance of forelimb, skin, or muscle have been found to be negligible (10), suggesting that the actions of CCK may target specific vascular beds.CCK receptors are located on vagal afferents (11, 35) and in the nucleus of solitary tract (NTS) (7, 35), a major site of termination of vagal afferents. Although peptides generally do not permeate the blood-brain barrier, CCK may potentially act on neurons of the area postrema, a circumventricular organ with neuronal cell bodies lying outside the blood brain barrier but with projections to several areas within the brain (6). There are also regions within the NTS and the dorsal nucleus of vagus nerve that have altered blood-brain barrier properties potentially facilitating the access of peptides such as CCK (6). Thus CCK may act either directly on the central nervous system to influence sympathetic vasomotor function and/or peripherally via vagal afferent fibers, conveying ...

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Section: Discussionmentioning

confidence: 99%

Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

Sartor

Verberne

2002

American Journal of Physiology-Regulatory, Integrative and Comp

102

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“…The significance of this observation is uncertain. We could not determine gastric oxygen transport directly because gastric venous oxygen content data were unavailable; however, we assume that nutrients in the lumen would further increase oxygen demand and consumption (23) and decrease the oxygen availability-to-demand ratio within the tissues. According to the metabolic theory of blood flow regulation, this should cause the generation of a metabolic feedback signal which leads to a dilatation of both resistance vessels which regulate blood flow and precapillary sphincters which modulate O2 extraction (27).…”

Section: Discussionmentioning

confidence: 99%

Postprandial Gastrointestinal Blood Flow and Oxygen Consumption: Effects of Hypoxemia in Neonatal Piglets

Szabo

Mayfield

et al. 1987

Pediatr Res

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ABSTRACT'. The effects of feeding on gastrointestinal (GI) perfusion and oxygen transport in hypoxemic neonates is unknown. We evaluated these effects in unanesthetized, spontaneously breathing newborn piglets by comparing three experimental groups: nine hypoxemic piglets (mean P a 0 2 26 torr) which were fed with formula, six hypoxemic piglets (mean PaOz 27 torr) which were not fed, and four normoxemic piglets (mean P a 0 2 79 torr) which were fed and served as controls. The control-fed group exhibited an increase in stomach and small intestinal mucosal-submucosal blood flow within 30 min following feeding which was significantly greater than that observed in the hypoxemic fed piglets. GI O2 delivery and 0, uptake rose significantly (p c 0.05) following a meal secondary to increases in total GI blood flow. Oxygen extraction was unchanged postprandially in the control group. In the hypoxemic nonfed piglets, total and regional GI blood flow was unaltered during hypoxemia. Reductions in arterial Oz content led to significant decreases in GI 0, delivery. Gastrointestinal oxygen uptake remained stable with a compensatory increase in GI O2 extraction. In the hypoxemic-fed piglets, hypoxia significantly decreased stomach blood flow and led to unchanged blood flow in the remainder of the GI tract. Significant reductions in arterial Oz content and GI O2 delivery were observed, accompanied by significant increases in O2 extraction. Hypoxemic fed animals did not exhibit the expected increase in OZ uptake to meet postprandial metabolic demands. When the hypoxemic insult was terminated, fed piglets demonstrated significant total and regional GI hyperemia leading to increased GI Oz uptake when compared with hypoxemic nonfed piglets. We conclude that in the presence of hypoxemia, the newborn piglet's GI tract is subject to decreased oxygen availability. In contrast to the fasted GI tract, the fed GI tract exhibits a significant hyperemia following a limited period of severe hypoxemia and an ability to increase oxygen uptake in an attempt to meet the demands of nutrient absorption. Oxygen uptake is not increased to the same extent as in normoxemic fed animals, thus the efficiency of these mechanisms in satisfying the postprandial O2 demand remains to be determined. (Pediatr Res 21: 93-98, 1987 Controversy exists as to the advisability of feeding infants soon after a hypoxic insult. Feeding is generally withheld in neonates during and for variable periods following hypoxemia because of the increased metabolic demand it places on a compromised gastrointestinal tract and an association with the development of necrotizing enterocolitis (1). However, a recent clinical study in preterm infants with oxygen and ventilator requirements has shown that early enteral feedings may prove beneficial and do not increase the incidence of necrotizing enterocolitis (2).The awake newborn animal meets the postprandial oxidative demands associated with nutrient absorption through enhanced GI oxygen extraction and selective GI hyperemia (3,4). Studi...

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“…It is well known that the presence of digested or hydrolyzed food components in the intestine is the principal determinant of the postprandial hyperemia in mammals Chou et al, 1985;Fara, 1984;Gallavan and Chou, 1985;Kvietys et al, 1980;Siregar and Chou, 1982;Sit et al, 1980) and in fish ). The information concerning what controls this hyperemia is much more limited, especially the neural contribution.…”

Section: Regulation Of Nutrient-induced Intestinal Hyperemiamentioning

confidence: 99%

Sympathetic, parasympathetic and enteric regulation of the gastrointestinal vasculature in rainbow trout (Oncorhynchus mykiss) under normal and postprandial conditions

Seth

Axelsson

2010

Journal of Experimental Biology

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It is probable that the postprandial gastrointestinal hyperemia is influenced by, or depends on, neural components, either extrinsic (sympathetic and/or parasympathetic) or intrinsic (enteric) to the gastrointestinal tract. A few studies have revealed an extrinsic neural component that directly influences the postprandial hyperemia in rats (Rozsa and Jacobson, 1989) Accepted 20 May 2010 SUMMARY The control of the gastrointestinal hyperemia that occurs after feeding in most animals is of fundamental importance for the subsequent absorption, metabolism and redistribution of nutrients. Yet, in fish, it has received little attention and the nature of it is far from clear. We sought to investigate the importance of extrinsic and intrinsic innervation of the gastrointestinal tract in the regulation of gastrointestinal blood flow in rainbow trout (Oncorhynchus mykiss). The contribution of the extrinsic innervation, i.e. by the sympathetic and the parasympathetic nervous system, was examined by comparing the response to the injection of a predigested nutrient diet into the proximal intestine of untreated fish with the response in fish in which the splanchnic and vagal innervation of the gut had been removed. We also injected the predigested nutrient diet into anaesthetized fish treated with tetrodotoxin that would block the intrinsic innervation of the gut (i.e. enteric nervous system). Our results confirm the notion that the sympathetic portion of the extrinsic innervation maintains the basal vascular tone, but neither the splanchnic nor the vagal innervation is fundamental to the postprandial hyperemia. However, the tetrodotoxin treatment completely abolished the postprandial hyperemia, indicating the importance of the enteric nervous system. In conclusion, it seems as though the enteric nervous system is essential to the regulation of the postprandial hyperemia, and that the extrinsic innervation is involved mainly in the regulation of gastrointestinal blood flow under normal conditions and in response to central coordination with other organs.

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Possible mechanisms for the initiation and maintenance of postprandial intestinal hyperemia

Cited by 61 publications

References 0 publications

Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

Postprandial Gastrointestinal Blood Flow and Oxygen Consumption: Effects of Hypoxemia in Neonatal Piglets

Sympathetic, parasympathetic and enteric regulation of the gastrointestinal vasculature in rainbow trout (Oncorhynchus mykiss) under normal and postprandial conditions

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