Abstract
BackgroundEvidence suggests that early adaptive responses of hepatic mitochondria occur in experimentally induced sepsis. Little is known about both colonic mitochondrial function during abdominal infection and long-term changes in mitochondrial function under inflammatory conditions. We hypothesize that hepatic and colonic mitochondrial oxygen consumption changes time-dependently after sterile laparotomy and in the course of abdominal infection. The aim of the present study was to investigate the hepatic and colonic mitochondrial respiration after sterile laparotomy and abdominal infection over up to 96 h.MethodsAfter approval of the local Animal Care and Use Committee, 95 Wistar rats were randomized into 8 groups (n = 11–12): 1–4 sham (laparotomy only) and 5–8 colon ascendens stent peritonitis (CASP). Healthy, unoperated animals served as controls (n = 9). The mitochondrial respiration in colon and liver homogenates was assessed 24, 48, 72, and 96 h after surgery. Mitochondrial oxygen consumption was determined using a Clark-type electrode. State 2 (oxygen consumption in the presence of the substrates for complexes I and II) and state 3 respiration (ADP dependent) were assessed. The respiratory control ratio (RCR state 3/state 2) and ADP/O ratio (ADP added/oxygen consumed) were calculated for both complexes. Data are presented as means ± SD, two-way ANOVA followed by Tukey’s post hoc test.ResultsHepatic RCR was initially (after 24 h) elevated in both operated groups; after 48 h only, the septic group was elevated compared to controls. In CASP groups, the hepatic ADP/O ratio for complex I was elevated after 24 h (vs. controls) and after 48 h (vs. sham) but declined after 72 h (vs. controls). The ADP/O ratio for complex II stayed unchanged over the time period until 96 h.The colonic RCR and ADP/O did not change over time after sham or CASP operation.ConclusionHepatic, but not colonic, mitochondrial respiration is increased in the initial phase (until 48 h) and normalizes in the longer course of time (until 96 h) of abdominal infection.
Highlights
Evidence suggests that early adaptive responses of hepatic mitochondria occur in experimentally induced sepsis
In colon ascendens stent peritonitis (CASP) groups, the ADP/O ratio for complex I was elevated after 24 h and after 48 h and declined after 72 h (Fig. 3c)
We focused on time-dependent and organ-specific effects and investigated mitochondrial respiration in the liver and colon over 96 h after laparotomy or CASP surgery
Summary
Evidence suggests that early adaptive responses of hepatic mitochondria occur in experimentally induced sepsis. We hypothesize that hepatic and colonic mitochondrial oxygen consumption changes time-dependently after sterile laparotomy and in the course of abdominal infection. The aim of the present study was to investigate the hepatic and colonic mitochondrial respiration after sterile laparotomy and abdominal infection over up to 96 h. The mortality rate in sepsis, septic shock, and the consecutive multiorgan dysfunction syndrome (MODS) in humans remains very high (30–40%); various attempts to modulate the inflammatory response and prevent organ damage failed to improve survival [1, 2]. The role of mitochondria in the manifestation of sepsis pathophysiology remains controversial. It is still debatable whether mitochondria are the initiators, amplifiers, targets, or only bystanders in sepsis-induced organ dysfunction [7]. Whereas studies on hepatic mitochondria are numerous, studies on mitochondrial function of other organs are lacking
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