Acute Superior Mesenteric Artery Occlusion Research Articles

Effect of prostaglandin and leukotriene antagonists in acute mesenteric artery occlusion.

Superior mesenteric artery occlusion leads to mesenteric ischemia, activation of arachidonic acid metabolism and release of endotoxins into the systemic circulation. The effect of leukotriene and prostaglandin antagonists on hemodynamic response and survival of rats after superior mesenteric artery (SMA) occlusion was investigated. The animals were divided into five groups: in group 1 (n = 105) the SMA was clamped for 2 h and mortality assessed after 24 h. Group 2 animals (n = 20) were pretreated with 5 mg/kg indomethacin and the SMA clamped similarly to group 1, group 3 animals (n = 15) were pretreated with 5 mg/kg Voltaren, group 4 animals (n = 20) received 20 mg/kg BW 755C before mesenteric artery occlusion, and group 5 animals (n = 50) were pretreated with 100 mg diethylcarbamazine. The blood pressure and pulse response as well as histologic appearance of the bowel 1 h after declamping was similar in all five groups. The mortality rate after 24 h was 34% in the control group, 36% with indomethacin treatment, 36% with voltaren, 47% with BW 755C and 40% with diethylcarbamazine. The mortality rate in all the treated groups was not significantly different from the control group. Plasma thromboxane B2 levels were inhibited significantly by indomethacin and Voltaren and to a lesser extent by BW 755C. There was a paradoxical rise in thromboxane B2 following diethylcarbamazine treatment. It is concluded that inhibition of the cyclooxygenase and/or the lipoxygenase pathways of arachidonic acid did not alter the hemodynamic response and mortality following 2 h of acute superior mesenteric artery occlusion.

Effect of intravenous glucagon on the survival of rats after acute occlusive mesenteric ischemia

The purpose of this study was to determine the optimal timing of intravenous glucagon infusion for the treatment of acute occlusive mesenteric ischemia. The superior mesenteric artery (SMA) was occluded for 85 min in 106 Sprague—Dawley anesthetized rats. The animals were divided into 12 treatment groups according to the timing of glucagon and saline administration, and survival was measured to 48 hr. Without treatment, all rats died within 24 hr. Intravenous saline (10 ml/kg/hr) for 2 hr did not significantly improve 48-hr survival (17–33%). Glucagon (1.6 μg/kg/min iv) plus saline (10 ml/kg/hr iv) for 2 hr after SMA occlusion significantly improved survival from 33% (saline control) to 83% ( P < 0.02). The same treatment begun 1 hr before SMA release (during ischemia) did not significantly improve survival (33% at 48 hr). Glucagon infusion during occlusive mesenteric ischemia was detrimental when added to effective postischemia treatment, reducing survival from 83 to 33% ( P < 0.02). Adequate saline infusion was required for glucagon efficacy after ischemia, as shown by an intermediate 48-hr survival of 50% when only maintenance saline (1.5 ml/kg/hr) was given. These data suggest that glucagon therapy should be delayed until after operative release of an acute SMA occlusion and should be accompanied by vigorous volume expansion.

Acute portal hypertension and reduced renal blood flow: An intestinal-renal neurogenic reflex

In a series of experiments in anesthetized dogs, the origin and mechanism of reduced renal blood flow (RBF) during acute portal hypertension was investigated. With acute superior mesenteric vein (SMV) occlusion and normalization of cardiac hemodynamics RBF remained reduced at 66 ± 14 ml/min compared to baseline of 160 ± 25 ml/min ( P < 0.01). Neither acute superior mesenteric artery occlusion, nor acute hepatic portal hypoperfusion with normal SMV pressures maintained by SMV-caval shunt, resulted in reduction of RBF. Cross-perfusion studies failed to produce alterations of RBF in recipient dogs from donor dogs with SMV occlusion, reduced RBF, and normal cardiac outputs. Finally, splanchnic ganglionectomy prevented RBF reduction during SMV occlusion after volume restoration. We conclude that reduced RBF during acute portal hypertension is a result of an intestinal-renal neurogenic reflex initiated by intestinal venous congestion.

Intestinal diamine oxidase and histamine release in rabbit mesenteric ischemia

It has been suggested that histamine contributes to lethal circulatory collapse after acute superior mesenteric artery occlusion. The activity of the histamine inactivating enzyme diamine oxidase, the release of the amine, and the effect of histamine receptor antagonists was therefore studied in rabbits. The main results were: (a) Diamine oxidase activity decreased by 60% after intestinal ischemia and reperfusion. A monoexponential dose-response relationship was found between the specific diamine oxidase inhibitor aminoguanidine and reduced survival time, (b) Plasma histamine levels in the right atrium rose only slightly after ischemia, but considerably during reperfusion of the gut, and remained high for at least 20 min. In sham-operated animals the plasma histamine concentration was unchanged throughout the experiment. The histamine content in the intestinal wall did not fall significantly at any time after mesenteric artery occlusion and reperfusion. (c) The aminoguanidine-induced reduction in survival time was completely reversed by pretreatment of the animals with the H1-receptor antagonist dimethylpyridine and the H2-receptor antagonist cimetidine. This study provides strong evidence for the protective role of intestinal diamine oxidase in intestinal ischemia.

THE EARLY DIAGNOSIS OF ACUTE OCCLUSIVE MESENTERIC ISCHAEMIA: EXPERIMENTAL RESULTS AND CLINICAL APPLICATIONS

The diagnosis of acute superior mesenteric artery occlusion in the dog has been achieved in every case by isotope scanning of the abdomen using technetium-labelled red cells or technetium-labelled human serum albumin. The white cell count is also significantly elevated, but the changes in the levels of the enzymes CPK, LDH, AST and serum amylase are not specific for actue mesenteric ischaemia. In the human the presence of a normal gut circulation can be demonstrated by isotope scanning provided that the patient is not severely shocked. The presence of a normal gut circulation as shown on the scintigram conclusively eliminates the possibility of acute main trunk occlusion of the superior mesenteric artery. This should be of help in differentiating acute occulusive mesenteric ischaemia from other causes of the acute abdomen. Abdominal scintiscanning is complementary to angiography, which still remains the most precise means of diagnosing acute mesenteric ischaemia. Although the abdominal scintigram is more limited in its application and is not as accurate as angiography, it is quicker to perform, non-invasive, and entirely safe. Abdominal scintiscanning is an excellent screening test to be used in patients suspected of suffering from acute occlusive mesenteric ischaemia.