Prostanoids in regulation of postprandial jejunal hyperemia and oxygen uptake

Chou, C. C.; Alemayehu, Adamu; Mangino, Martin J.

doi:10.1152/ajpgi.1989.257.5.g798

Cited by 11 publications

(8 citation statements)

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“…Following the observations that L-NAME produces a sustained increase in systemic arterial blood pressure and motility, we determined whether or not the jejunal motility is a consequence of the increase in systemic arterial blood pressure. Previously we have shown that a single intravenous injection of mefenamate (10 mg kg-') produces a sustained increase in blood pressure (Mangino & Chou, 1986;Chou et al, 1989). Therefore, utilizing the same jejunal preparation and the same protocol as in series II, jejunal lumen pressure add blood flow and systemic arterial pressure were recorded before and after a single intravenous injection of mefenamate (10 mg kg-') for 1 h.…”

Section: Methodsmentioning

confidence: 99%

l‐NAME, nitric oxide and jejunal motility, blood flow and oxygen uptake in dogs

Alemayehu

Lock

Coatney

et al. 1994

British J Pharmacology

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1The effects of the inhibitor of nitric oxide (NO) synthesis, N0-nitro-L-arginine methyl ester (L-NAME), on systemic arteriil blood pressure and jejunal motility, blood flow, and oxygen uptake have been investigated in anaesthetized dogs. 2 L-NAME (cumulative doses of 0.1-20 mg kg-', i.v.) dose-dependently increased blood pressure and jejunal motility and decreased heart rate. The maximal response of these three variables occurred at doses, 3, 10 and 10mgkg-l, respectively. L-NAME (cumulative doses of 0.5-5mgkg-') also dosedependently induced jejunal vasoconstriction. The jejunal vascular resistance returned to control values as the cumulative doses reached 10 and 20 mg kg-', which corresponded to the maximal increase in jejunal motility. 3 A single intravenous injection of L-NAME (10mgkg-') produced a prompt increase in blood pressure, which lasted for at least 50min. 4 L-NAME (10 mg kg-') produced a progressive rise in jejunal motility reaching its maximum (47 ± 6 mmHg) 15 min after the administration, and lasting for 40-50 min. Both the basal lumen pressure and the amplitude of rhythmic contractions increased during this period. 5 L-NAME (10 mg kg-') produced a triphasic change in jejunal vascular resistance and blood flow measured by timed collection of venous outflow. The blood flow decreased initially (-43% at 5 min), increased (+ 35%) and returned to control value between 15 and 35 min, then decreased (-35%) 40-50 min post-infusion. Jejunal vascular resistance reflected the blood flow response (+ 88% at both 5 and 50 min). The time during which the reversal of the vasoconstriction occurred (15-35 min) corresponded to the time of marked increase in motility, and was accompanied by a significant increase in jejunal oxygen uptake (+ 18%). 6 The L-NAME-induced increase in motility was prevented by L-arginine (1 g kg-', i.v.) but not by D-arginine pretreatment. The interim (15-35 min) changes in jejunal blood flow, vascular resistance and oxygen uptake were also prevented by L-arginine pretreatment. 7 L-Arginine pretreatment attenuated L-NAME-induced hypertension for 5 min. 8 The L-NAME-induced increases in jejunal vascular resistance and motility were inhibited by either local intra-arterial infusion of L-arginine (32 mM local arterial blood concentration) or topical application of 2 gM nitroglycerin. Infusion of D-arginine (32 mM local arterial blood concentration) had no such effect. 9 The L-NAME-induced increase in blood pressure was not the mechanism by which jejunal motility was increased, because similar increases in blood pressure by mefenamate (10 mg kg-', i.v.) had no such effect. 10 Thus, inhibition of nitric oxide synthesis by L-NAME increased jejunal motility and vascular resistance and the marked increase in motility can abolish or reverse the vasoconstriction. Endogenous nitric oxide may play a role in regulating motility and blood flow in the resting canine jejunum.

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Section: Methodsmentioning

confidence: 99%

l‐NAME, nitric oxide and jejunal motility, blood flow and oxygen uptake in dogs

Alemayehu

Lock

Coatney

et al. 1994

British J Pharmacology

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“…The importance of intrinsic and extrinsic nerves in gut has been investigated to some extent and has been ascribed a very limited role in the postprandial hyperemic response (39 -41), although nervous components cannot be completely ruled out (56). Some studies have addressed the importance of endocrine (21) and paracrine factors, such as histamines (22), prostaglandins (17), and adenosine (45,46) but with apparently varying results. The most likely explanation seems to be that metabolic factors such as O 2 , H ϩ , and CO 2, as well as adenosine and lactate mediate the postprandial hyperemia (43,49), and glucose has been found to stimulate adenosinemediated NO production (36).…”

Section: Cardiovascular Parametersmentioning

confidence: 99%

Nutrient-induced gastrointestinal hyperemia and specific dynamic action in rainbow trout (Oncorhynchus mykiss)—importance of proteins and lipids

Seth¹,

Sandblom²,

Axelsson³

2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Mechanical gastric distension induces a dorsal aortic pressor response in rainbow trout (Oncorhynchus mykiss) with no change in gastrointestinal blood flow. To elucidate what role chemical stimuli from the digested food has on the postprandial cardiovascular response, a new method was developed to investigate the contribution of individual nutrient components. Three predigested experimental diets were injected directly into the proximal intestine of rainbow trout and cardiac output (CO), gut blood flow (Qcma), heart rate (HR), and stroke volume (SV) were recorded. Specific dynamic action (SDA) was estimated by measuring oxygen consumption. When a balanced diet (50% protein, 25% fat, 15% carbohydrate) was injected, Qcma and CO increased within 1 h by 45 and 27%, respectively. The response to a high-protein diet (70% protein, 5% fat, 15% carbohydrate) was quantitatively similar but delayed, with a maximal blood flow response after 2 h. With a high-lipid diet (60% fat, 15% protein, 15% carbohydrate), the peak increase in Qcma by 22% occurred after 30 min and thereafter declined rapidly. The SDA response (19%) to the balanced diet was temporally matched with the hyperemia. With a high-protein diet, the response is delayed and enlarged (34%) compared with the balanced diet. The high-lipid diet gave no significant SDA response. We conclude that the chemical composition of the food influences the postprandial hyperemia and the SDA, such that the components appear to work in a synergistic fashion. The present results also demonstrate that both redistribution of blood flow and an overall increase in CO contribute to the postprandial increase in gut blood flow in this species.

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“…The chemical stimulus is dependent on the composition of the feed and it has been noted that different nutrients are not equally essential in inducing the postprandial hyperemia (Chou et al, 1972;Kvietys et al, 1981;Siregar and Chou, 1982). The exact mechanism controlling the hyperemia in mammals is under debate but may involve direct effects from the absorbed nutrients on the vasculature , endocrine factors (Biber, 1973;Chou et al, 1977;Chou et al, 1984;Fara et al, 1972), non-metabolic vasoactive factors (Chou et al, 1989;Chou and Siregar, 1982;Sawmiller and Chou, 1988;Sawmiller and Chou, 1990), metabolic vasoactive factors (Bohlen, 1980a;Bohlen, 1980b;Bohlen, 1998a;Pawlik et al, 1980) and neural mechanisms (Biber, 1973;Kato et al, 1989;Takagi et al, 1988). There are, however, large variations in mammals reported in the literature, which, to some extent, can be explained by large interspecies differences.…”

Section: Introductionmentioning

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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Prostanoids in regulation of postprandial jejunal hyperemia and oxygen uptake

Cited by 11 publications

References 0 publications

l‐NAME, nitric oxide and jejunal motility, blood flow and oxygen uptake in dogs

l‐NAME, nitric oxide and jejunal motility, blood flow and oxygen uptake in dogs

Nutrient-induced gastrointestinal hyperemia and specific dynamic action in rainbow trout (Oncorhynchus mykiss)—importance of proteins and lipids

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

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