Intestinal phase of superior mesenteric artery blood flow in man.

Sieber, Cornel; Beglinger, Christoph; Jäger, K; Stalder, G

doi:10.1136/gut.33.4.497

Cited by 68 publications

(34 citation statements)

References 16 publications

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“…In addition to having these regulatory actions, CCK also acts on gastrointestinal blood flow (18,39). 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.…”

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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“…15,33 The reason to do so was twofold: first, the upper small intestine is the major site for the stimulation of the postprandial hyperemia in humans. Second, different peptides including somatostatins are known to interfere with the physiological gastric emptying rate.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic effects of the somatostatin analog lanreotide in humans: Placebo-controlled, cross-over dose-ranging echo-doppler study

Mottet¹,

Sieber²,

Nauer³

et al. 1998

Hepatology

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Because of their vasoactive effects, somatostatin and its analogs are increasingly used in the management of complications of chronic liver diseases such as variceal bleeding. Postprandial hyperemia augments splanchnic blood flow, subsequently increasing portal pressure. The aim of this study was to explore effects of the somatostatin analog, lanreotide, on food-stimulated hemodynamic parameters in healthy human subjects. A dose-response curve was constructed in eight healthy male subjects in a placebo-controlled cross-over study. On 4 different days, either 0 (placebo), 50, 100, or 200 g/h of lanreotide was infused intravenously in random order, starting at 45 minutes for 7 hours. On each day, a liquid test meal (Ensure plus, 1.5 kcal/mL) was perfused intraduodenally at a rate of 3 mL/min over 7 hours after a 45-minute basal period. Diastolic arterial pressure (dBP), heart rate (HR), superior mesenteric arterial (SMA) average flow velocity (SMA-V), SMA pulsatility index (SMA-PI), portal venous volume flow (PV-F), and renal artery (RA) resistance index (RA-RI) were measured on regular intervals (flows using Echo-Doppler technology). Lanreotide at all doses abolished food-stimulated splanchnic hyperemia both in the SMA and PV over 7 hours. The fall in dBP and increase in HR after food perfusion were blunted under lanreotide. Food as well as lanreotide did not modify RA-RI. In summary: 1) lanreotide inhibits food-induced splanchnic hyperemia in normal subjects; 2) in parallel, systemic hemodynamic alterations to food stimulation are abolished with lanreotide; and 3) renal vascular resistance is unchanged. Because of its persistent splanchnic vasoconstrictive effect, lanreotide should be tested in patients with portal hypertension. (HEPATOLOGY 1998;27: 920-925.) Natural somatostatin, and especially its analog, octreotide, are increasingly used in the treatment of esophageal variceal bleeding. [1][2][3][4] In patients with cirrhosis and portal hypertension, it reduces splanchnic and azygos blood flow, 5,6 whereas the action with regard to portal pressure is modest. [5][6][7] Conversely, the effect(s) of natural somatostatin and its analog, octreotide, upon renal hemodynamics and function are unclear and have been a reason for debate. [8][9][10][11] Hemodynamic effects, at least for octreotide, have recently been shown to be only short-lasting, even when the drug is infused constantly. 12 In addition, no clear dose-response with regard to splanchnic hemodynamics has been performed, making a dose justification for the use of this compound difficult.Food is a very potent hyperemic stimulus in the splanchnic vascular area, both in normal subjects, 13-15 as well as in patients with portal hypertension. 16,17 It has been hypothesized that postprandial hyperemia may acutely augment portal pressure, and by this mechanism may probably increase the risk of bleeding from gastroesophageal varices. 18,19 It has also been shown that octreotide blunts this postprandial increase both in normal subjects 20,21 and cirrhotic patients....

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“…Postprandial intestinal hyperemia is a seemingly universal physiological phenomenon that has been documented for fishes, reptiles and mammals (Fioramonti and Bueno, 1984;Sieber et al, 1992;Starck and Wimmer, 2005;Altimiras et al, 2008). Among these organisms, blood flow to the gut generally increases by 50-150%, with the Gastrointestinal blood flow was measured from the *combined celiac and mesenteric (i.e.…”

Section: Cardiac Output and Regional Blood Flow During Rest Locomotimentioning

confidence: 99%

Prioritizing blood flow: cardiovascular performance in response to the competing demands of locomotion and digestion for the Burmese python,Python molurus

Secor

White

2010

Journal of Experimental Biology

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SUMMARYIndividually, the metabolic demands of digestion or movement can be fully supported by elevations in cardiovascular performance, but when occurring simultaneously, vascular perfusion may have to be prioritized to either the gut or skeletal muscles. Burmese pythons (Python molurus) experience similar increases in metabolic rate during the digestion of a meal as they do while crawling, hence each would have an equal demand for vascular supply when these two actions are combined. To determine, for the Burmese python, whether blood flow is prioritized when snakes are digesting and moving, we examined changes in cardiac performance and blood flow in response to digestion, movement, and the combination of digestion and movement. We used perivascular blood flow probes to measure blood flow through the left carotid artery, dorsal aorta, superior mesenteric artery and hepatic portal vein, and to calculate cardiac output, heart rate and stroke volume. Fasted pythons while crawling experienced a 2.7-and 3.3-fold increase, respectively, in heart rate and cardiac output, and a 66% decrease in superior mesenteric flow. During the digestion of a rodent meal equaling in mass to 24.7% of the snake's body mass, heart rate and cardiac output increased by 3.3-and 4.4-fold, respectively. Digestion also resulted in respective 11.6-and 14.1-fold increases in superior mesenteric and hepatic portal flow. When crawling while digesting, cardiac output and dorsal aorta flow increased by only 21% and 9%, respectively, a modest increase compared with that when they start to crawl on an empty stomach. Crawling did triggered a significant reduction in blood flow to the digesting gut, decreasing superior mesenteric and hepatic portal flow by 81% and 47%, respectively. When faced with the dual demands of digestion and crawling, Burmese pythons prioritize blood flow, apparently diverting visceral supply to the axial muscles.

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Intestinal phase of superior mesenteric artery blood flow in man.

Cited by 68 publications

References 16 publications

Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

Cholecystokinin selectively affects presympathetic vasomotor neurons and sympathetic vasomotor outflow

Hemodynamic effects of the somatostatin analog lanreotide in humans: Placebo-controlled, cross-over dose-ranging echo-doppler study

Prioritizing blood flow: cardiovascular performance in response to the competing demands of locomotion and digestion for the Burmese python,Python molurus

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