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Reperfusionsschock nach okklusion der A. mesenterica superior und akkumulation von leukozyten innerhalb der dünndarmwand

The reperfusion shock after occlusion of the superior mesenteric artery and the accumulation of the leucocytes within the intestinal wall

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Abstract

The epithelial damage and the accumulation of the leucocytes within intestinal wall layers after ischemia and reperfusion was investigated in a pig model. Superior mesenteric artery (SMA) was occluded for 1 h (group 2, n = 9), 2 h (group 3, n = 6) and 3 h (group 4, n = 7) with a consecutive 2 h reperfusion period. The histological evaluation was performed on hematoxylin-eosine and Naphtol AS-D chloracetate stained preparations.

The intensity of reperfusion shock depended on the duration of the intestinal ischemia. After 1 h SMA occlusion systolic blood pressure stabilized at a lower level with a normalization of the serum lactate level and the intestinal intramural pHi within the reperfusion period. After 2 h SMA occlusion the decrease of the systolic blood pressure was intensified (54–69 mm Hg) with a persistent elevated serum lactate concentration and a delayed increase of the ischemic pHi values. Reperfusion after 3 h SMA occlusion caused an irreversible shock.

The epithelial damage also depended on the duration of the SMA occlusion. There were no significant changes of the leucocytic accumulation within the submucosa. But a significant increase of the number of the leucocytes was seen within the inner and the outer layer of the muscularis after 1 h SMA occlusion (106±5/mm2 resp. 280/mm2; p<0.05). This increase was less pronounced after 2 h (92±5/mm2 *resp. 189±4/mm2; *p<0.05) and 3 h of SMA occlusion (84±5/mm2 resp. 185±23/mm2).

Intestinal ischemia and reperfusion caused no changes of the leucocytic accumulation within the submucosa but a significantly increased accumulation within the muscularis after 1 h SMA occlusion, which was not seen after a more elongated occlusion period. A reperfusion shock without normalization of the serum lactate level and the intramural pHi suggesting intestinal perfusion disturbances may also lead to a depression of the leucocytic accumulation within the muscularis.

Zusammenfassung

Der Epithelschaden und die Leukozytenakkumulation in der Wand des Ileums nach Ischämie und Reperfusion wurden experimentell am Schwein untersucht. Die A. mesenterica superior wurde für 1 h (Gruppe 2; n=9), 2 h (Gruppe 3; n=6) und 3 h (Gruppe 4; n=7) abgeklemmt und 2 h reperfundiert. Die histologische Beurteilung erfolgte an Hämatoxylin-Eosin- und NaphtolAS-D-Chlorazetatesterase-gefärbten Präparaten. Es entwickelte sich ein Reperfusionsschock in Abhängigkeit von der Ischämiedauer. Nach lstündiger Ischämie stabilisierte sich der Blutdruck mit erniedrigten Werten sowie einer Normalisierung des Serumlaktatspiegels und des intramuralen pHi des Dünndarms. Eine Verlängerung der Ischämie auf 2 h (Gruppe 3) führte zu einem Blutdruckabfall (54–69 mmHg), einem bleibend erhöhten Serumlaktatspiegel (5,2–6,0 mmol/1) und einem verzögerten Anstieg des pHi. Die Reperfusion nach 3stündiger Ischämie verursachte einen irreversiblen Schock. Der Epithelschaden des Dünndarms war abhängig von der Ischämiedauer. Es fand sich, kein Unterschied der Leukozytenakkumulation innerhalb der Submukosa im Vergleich zur Kontrollgruppe. Ein signifikanter Anstieg der Leukozytenzahl war jedoch in der Lamina interna und externa der Muskularis nach lstündiger Ischämie zu verzeichnen (106±5/mm2 bzw. 280/mm2; p<0,05), der nach 2stündiger [92±5/mm2 (p<0,05) bzw. 189±4/mm2 und 3stündiger Ischämiedauer (84±5/mm2 bzw. 185±23/mm2) nur geringgradig erhöht war. Während die intestinale Ischämie und der anschließende reperfusionsbedingte Schock nicht zu einer Beeinflussung der Leukozytenakkumulation innerhalb der Submukosa, aber zu einer signifikanten Akkumulation innerhalb der Muskularis nach einer lstündigen Ischämie führten, scheint bei ausbleibender Normalisierung des Serumlaktatspiegels und einem verzögerten oder fehlenden Anstieg der ischämischen intramuralen pHi-Werte als Hinweis auf eine intestinale Perfusionsstörung als Folge einer längeren Ischeämiedauer die Akkumulation der Leukozyten innerhalb der Muscularis mucosae abgescwächt zu sein.

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Jonas, J., Heimann, A., Alebrahim-Dehkordy, A. et al. Reperfusionsschock nach okklusion der A. mesenterica superior und akkumulation von leukozyten innerhalb der dünndarmwand. Langenbecks Arch Chir 381, 95–101 (1996). https://doi.org/10.1007/BF00183939

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  • DOI: https://doi.org/10.1007/BF00183939

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