Mesenteric infarction as a vascular emergency the clinical problems

Mavor, G. E.; Lyall, Alexander; Chrystal, K. M. R.; Tsapogas, Makis J.

doi:10.1002/bjs.18005022020

Cited by 36 publications

(8 citation statements)

References 15 publications

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“…In the present study, VIP has been infused to achieve similar concentrations of the peptide to those seen during reperfusion and the cardiovascular effects measured. In fusion of VIP in the present experiments resulted in the rapid onset of widespread vasodilation with hypotension, suggesting that it has the potential to be the causative agent eliciting a vascular collapse after re leasing mesenteric arterial occlusion [1][2][3]. However, it should be noted that in addition to VIP there are a number of other vaso active agents released by intestinal isch aemia, such as histamine and myocardial depressant factor [5,21], which could con tribute to the cardiovascular responses.…”

Section: Discussionmentioning

confidence: 86%

“…A sustained vasodilation was detected in the coeliac artery and portal vein vascular beds during a 30-min VIP infusion. VIP is likely to be a contributory factor involved in the development of circulatory collapse during reperfusion after experimental mesenteric ischaemia.In man, re-establishment of blood flow to a previously ischaemic intestine leads to vas cular collapse which is characterized by gen eralized vasodilation, hypotension and shock [1][2][3]. Vaso-active agents liberated from the ischaemic splanchnic vascular bed are believed to be responsible for the circula tory changes [4][5][6].…”

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confidence: 99%

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Effect of Vaso-Active Intestinal Polypeptide on Systemic and Splanchnic Haemodynamics: Role in Vasodilation following Mesenteric Ischaemia

Somjen

Fletcher²,

Shulkes³

et al. 1988

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Vaso-active intestinal polypeptide (VIP) and the related peptide, peptide histidine isoleucine, were infused intravenously in anaesthetized sheep. The VIP doses were designed to reproduce plasma concentrations seen after mesenteric ischaemia. The vasodilator action of VIP varied between different segments of the circulation and these differences in sensitivity were observed for both the degree and duration of the vaso-active action. A sustained vasodilation was detected in the coeliac artery and portal vein vascular beds during a 30-min VIP infusion. VIP is likely to be a contributory factor involved in the development of circulatory collapse during reperfusion after experimental mesenteric ischaemia.

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Section: Discussionmentioning

confidence: 86%

mentioning

confidence: 99%

Effect of Vaso-Active Intestinal Polypeptide on Systemic and Splanchnic Haemodynamics: Role in Vasodilation following Mesenteric Ischaemia

Somjen

Fletcher²,

Shulkes³

et al. 1988

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“…Intestinal ischaemia may be due to both occlusive and non-occlusive mesenteric vascular insufficiency. Mortality in these conditions is high, ranging up to 93 per cent in reported series (6).…”

Section: Discussionmentioning

confidence: 95%

The recovery of intestine after ischaemic injury

Gorey

1980

British Journal of Surgery

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A reproducible model of reversible segmental ischaemia was used to evaluate methods of predicting intestinal viability after the release of strangulation. Visual assessment in the immediate period after reperfusion and at "second-look' 24 hours later was inaccurate in identifying recoverable bowel. A Doppler probe used to detect the return of pulsatile blood flow was overpredictive of necrosis. The pattern of surface fluorescence after injection of the supravital dye fluorescein increased the accuracy of predicting intestinal recovery. A series of silicone rubber injections was carried out to investigate whether the patency of the microvessels influenced the outcome. It was shown that as the ischaemic period increased there was progressive failure of the microcirculation. It was concluded that the fluorescein injection test correctly identifies recoverable bowel and that the outcome after ischaemic injury is related to microvascular patency.

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“…Acute mesenteric vascular occlusion continues to carry an unacceptably high mortality (Mavor et al, 1962;Aakhus and Brabrand, 1967;Marston, 1971;Wittenberg, et al, 1973;Boley et al, 1973;Singh et al, 1975), this being largely because of the diagnostic problem it presents (Recek et al, 1968;Mavor et al, 1972). Clinical diagnostic pointers are well known (Marston, 1971;Mavor, 1972) but are non-specific.…”

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confidence: 99%