title: Small intestinal mucosal pH and lactate production during experimental ischemia-reperfusion and fecal peritonitis in pigs.
abstract: The aim of this study was to investigate mucosal pH and lactate production in a porcine model of ischemia/reperfusion and sepsis using both tonometry and a technique for segmental intestinal perfusion. Eighteen pigs (17-23 kg) were anesthetized and mechanically ventilated. They were divided into three groups and followed for 4 h. Group C (n = 6) served as controls. In the ischemia/reperfusion group (I/R; n = 6), the superior mesenteric artery was totally occluded for 60 min. In group P (n = 6), sepsis was induced by fecal peritonitis. Cardiac index (CI) was determined by thermodilution and blood flow in the superior mesenteric artery (QSMA), using a Transonic flow probe. Intramucosal pH (pHi) was calculated using tonometry. A special balloon tube for segmental perfusion was introduced in the midileum for lactate measurement. Lactate and oxygen saturation were measured in arterial blood and in the superior mesenteric vein. CI, QSMA, pHi, and lactate in blood and perfusate remained unchanged in controls. Occlusion of intestinal blood flow induced a fall in pHi from 7.28 +/- .02 to 6.76 +/- .04, a marked rise in lactate in the perfusate, and an increased arteriovenous lactate difference. During reperfusion, pHi tended to return to baseline values. Lactate in the perfusate and the arteriovenous lactate difference decreased. In sepsis there was a continuous reduction in CI and QSMA to 45 +/- 13% and 40 +/- 20% of baseline, respectively. pHi decreased moderately from 7.22 +/- .09 to 6.98 +/- .25. Lactate remained unchanged in blood and perfusate. Microscopic mucosal injury was observed in all animals subjected to ischemia/reperfusion and in three of six pigs in group P. A good association between pHi and lactate production was seen in ischemia/reperfusion. However, in sepsis, lactate in superior mesenteric venous blood or in intestinal perfusate did not increase, despite the fall in pHi. The mechanism causing ischemic mucosal injury has different characteristics in sepsis and in ischemia caused by arterial occlusion.
authors.affiliation: Department of Surgery, University Hospital, Uppsala, Sweden.
authors.forename: M
authors.initials: M
authors.lastname: Ljungdahl
authors.forename: I
authors.initials: I
authors.lastname: Rasmussen
authors.forename: Y
authors.initials: Y
authors.lastname: Raab
authors.forename: L
authors.initials: L
authors.lastname: Hillered
authors.forename: U
authors.initials: U
authors.lastname: Haglund
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D005243:Feces; D005260:Female; D006454:Hemoglobins / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D007413:Intestinal Mucosa / Q000378:metabolism*; D007421:Intestine, Small / Q000098:blood supply* / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism*; D019344:Lactic Acid / Q000378:metabolism*; D008297:Male; D010101:Oxygen Consumption; D010538:Peritonitis / Q000150:complications / Q000378:metabolism*; D015424:Reperfusion; D018805:Sepsis / Q000150:complications / Q000378:metabolism; D012709:Serum Albumin / Q000378:metabolism; D013552:Swine; D014065:Tonometry, Ocular
chemical_list: D006454:Hemoglobins; D012709:Serum Albumin; D019344:Lactic Acid