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PubMedDate not supplied

Arteriovenous fistulas of the mesenteric vessels. Report of a case and review of the literature.

Arteriovenous fistulae of the mesenteric circulation are rare, only 30 cases having been reported in the English literature. These lesions may follow operations on the abdominal viscera or abdominal injuries, either blunt or penetrating. We report a case of an iatrogenic mesenteric arteriovenous fistula diagnosed 20 years after a small bowel resection for an ileocecal intussusception. A review of the English literature is presented and the diagnosis, treatment, and pathophysiology of mesenteric arteriovenous fistulas is discussed, with special emphasis on the possible sequelae of a hyperkinetic portal blood flow.

Abdominal Injuries↗
PubMed1980

[Change in the activity of the histamine and serotonin systems in acute obstruction of the mesenteric vessels].

It was shown in experiments on 24 dogs that acute occlusion of the cranial mesenteric artery results, depending on its duration, in biphasic changes in the activity of the histamine and serotonin systems. During intestinal ischemia there was an enhanced discharge of histamine and serotonin from mast cells with activation of their inhibitors (di- and monoamine oxidase). A remarkable inhibition of the histamine system enzymatic unit apart from a fall in serotonin activity because of progressing body poisoning by substances of microbial and metabolic origin were observed during intestinal infarction.

Acute Disease↗
PubMed1999

1-Ethyl-2-benzimidazolinone stimulates endothelial K(Ca) channels and nitric oxide formation in rat mesenteric vessels.

Hyperpolarization of most blood vessels occurs by the opening of K(Ca) channels. 1-Ethyl-2-benzimidazolinone (1-EBIO) is a direct activator of K(Ca) channels in epithelial cells and is potentially valuable for studying cellular hyperpolarization. This study reports the effects of 1-EBIO on isolated rat mesenteric beds perfused with normal (4.7 mM), or high (20 or 80 mM) K+ physiological salt solution (PSS) and constricted with an alpha1-adrenoceptor agonist, cirazoline (0.3-1 microM). Arterial perfusion pressures were decreased by 1-EBIO (0.1-30 nmol) in a dose- and endothelium-dependent manner. Infusion of penitrem A (100 nM), a maxi-K+ channel blocker, or apamin (0.5 microM), a small-conductance (SK(Ca)) K+ channel blocker, produced significant increases in cirazoline-mediated tone (mm Hg): 103.3 +/- 8.7 (control) vs. 156.3 +/- 14.3 (penitrem A); or 93.0 +/- 15.8 (control) vs. 114.0 +/- 15.4 (apamin). 1-EBIO relaxations were attenuated by penitrem A, while apamin, dendrotoxin (50 nM; a Kv channel antagonist), or ouabain (100 microM; a sodium pump blocker) failed to alter the responses. I-EBIO-mediated relaxations decreased significantly with increasing extracellular [K+]: relaxations to 30 nmol were 89.3% +/- 3.2% (4.7 mM K+, normal PSS) vs. 59.5% +/- 3.4% and 19.0% +/- 3.9% for 20 and 80 mM K+ PSS, respectively. Nomega-nitro-L-arginine-methyl ester (L-NAME; 100 microM), and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 10 microM), selective inhibitors of nitric oxide synthase, and nitric oxide-sensitive guanylate cyclase, respectively, abolished 1-EBIO relaxations in vessels perfused with 20 or 80 mM K+ PSS. We conclude that: (1) maxi-K+ and SK(Ca) channels are present in rat mesenteric arterial vessels and actively contribute to vascular tone, (2) vasodilator action of 1-EBIO involves the opening of endothelial maxi-K+ channels and nitric oxide synthesis.

Acetylcholine↗