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Understanding gastrointestinal perfusion in critical care: so near, and yet so far.

Ackland G, Grocott MP, Mythen MG - Crit Care (2000)

Bottom Line: Much of the data to support this idea comes from studies using gastric tonometry.Furthermore, current understanding of the physiology of gastrointestinal perfusion in health and disease is incomplete.This review considers critically the striking clinical data and basic physiological investigations that support a key role for gastrointestinal hypoperfusion in initiating and/or perpetuating critical disease.

View Article: PubMed Central - PubMed

Affiliation: Centre for Anaesthesia, University College London, London, UK.

ABSTRACT
An association between abnormal gastrointestinal perfusion and critical illness has been suggested for a number of years. Much of the data to support this idea comes from studies using gastric tonometry. Although an attractive technology, the interpretation of tonometry data is complex. Furthermore, current understanding of the physiology of gastrointestinal perfusion in health and disease is incomplete. This review considers critically the striking clinical data and basic physiological investigations that support a key role for gastrointestinal hypoperfusion in initiating and/or perpetuating critical disease.

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A complex interplay of neural, hormonal and endothelial-derived factors regulates the balance of gastrointestinal perfusion between vasodilatation and vasoconstriction. Question marks indicate possible interactions; dashed lines indicate endothelium-derived production. ACh, acetylcholine; CCK, cholecystokinin; CGRP, calcitonin gene-related peptide; EDHF, endothelium-derived hyperpolarizing factor; 5-HT, 5-hydroxytryptamine; PG, prostaglandin; VIP, vasoactive intestinal peptide.
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Figure 4: A complex interplay of neural, hormonal and endothelial-derived factors regulates the balance of gastrointestinal perfusion between vasodilatation and vasoconstriction. Question marks indicate possible interactions; dashed lines indicate endothelium-derived production. ACh, acetylcholine; CCK, cholecystokinin; CGRP, calcitonin gene-related peptide; EDHF, endothelium-derived hyperpolarizing factor; 5-HT, 5-hydroxytryptamine; PG, prostaglandin; VIP, vasoactive intestinal peptide.

Mentions: The hepatosplanchnic circulation receives 30% of total cardiac output. With increasing age, splanchnic blood flow declines both absolutely and as a fraction of total cardiac output [30]. Splanchnic anatomy is described in detail elsewhere [31]. Briefly, the mesenteric circulation consists of the muscularis propria, submucosa and mucosa, which are arranged in parallel [32]. Resistance arterioles regulate blood flow to the splanchnic bed, so at constant hydrostatic pressure flow is inversely proportional to resistance. Although these arterioles partake in a markedly less impressive autoregulatory system than in the kidney or brain, they do enable a partial compensation for falls in blood flow [33]. The tone of these vessels depends on the complex balance between neurally mediated sympathetic vasoconstriction, the local action of vasoregulatory substances that are under the influence of the apparently paradoxically named 'sensory-motor' nerves, the parasympathetic cholinergic nerve supply, the enteric nervous system and endothelial-derived agents [34] (Fig. 4).


Understanding gastrointestinal perfusion in critical care: so near, and yet so far.

Ackland G, Grocott MP, Mythen MG - Crit Care (2000)

A complex interplay of neural, hormonal and endothelial-derived factors regulates the balance of gastrointestinal perfusion between vasodilatation and vasoconstriction. Question marks indicate possible interactions; dashed lines indicate endothelium-derived production. ACh, acetylcholine; CCK, cholecystokinin; CGRP, calcitonin gene-related peptide; EDHF, endothelium-derived hyperpolarizing factor; 5-HT, 5-hydroxytryptamine; PG, prostaglandin; VIP, vasoactive intestinal peptide.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC137256&req=5

Figure 4: A complex interplay of neural, hormonal and endothelial-derived factors regulates the balance of gastrointestinal perfusion between vasodilatation and vasoconstriction. Question marks indicate possible interactions; dashed lines indicate endothelium-derived production. ACh, acetylcholine; CCK, cholecystokinin; CGRP, calcitonin gene-related peptide; EDHF, endothelium-derived hyperpolarizing factor; 5-HT, 5-hydroxytryptamine; PG, prostaglandin; VIP, vasoactive intestinal peptide.
Mentions: The hepatosplanchnic circulation receives 30% of total cardiac output. With increasing age, splanchnic blood flow declines both absolutely and as a fraction of total cardiac output [30]. Splanchnic anatomy is described in detail elsewhere [31]. Briefly, the mesenteric circulation consists of the muscularis propria, submucosa and mucosa, which are arranged in parallel [32]. Resistance arterioles regulate blood flow to the splanchnic bed, so at constant hydrostatic pressure flow is inversely proportional to resistance. Although these arterioles partake in a markedly less impressive autoregulatory system than in the kidney or brain, they do enable a partial compensation for falls in blood flow [33]. The tone of these vessels depends on the complex balance between neurally mediated sympathetic vasoconstriction, the local action of vasoregulatory substances that are under the influence of the apparently paradoxically named 'sensory-motor' nerves, the parasympathetic cholinergic nerve supply, the enteric nervous system and endothelial-derived agents [34] (Fig. 4).

Bottom Line: Much of the data to support this idea comes from studies using gastric tonometry.Furthermore, current understanding of the physiology of gastrointestinal perfusion in health and disease is incomplete.This review considers critically the striking clinical data and basic physiological investigations that support a key role for gastrointestinal hypoperfusion in initiating and/or perpetuating critical disease.

View Article: PubMed Central - PubMed

Affiliation: Centre for Anaesthesia, University College London, London, UK.

ABSTRACT
An association between abnormal gastrointestinal perfusion and critical illness has been suggested for a number of years. Much of the data to support this idea comes from studies using gastric tonometry. Although an attractive technology, the interpretation of tonometry data is complex. Furthermore, current understanding of the physiology of gastrointestinal perfusion in health and disease is incomplete. This review considers critically the striking clinical data and basic physiological investigations that support a key role for gastrointestinal hypoperfusion in initiating and/or perpetuating critical disease.

Show MeSH
Related in: MedlinePlus