AIMS: The aim of this study was to investigate mesenteric ischaemia by determining intragastric PCO(2) (iPCO(2)) with gastric tonometry during rest and exercise stress testing in patients with chronic heart failure (CHF). In CHF inflammatory immune activation is hypothesized to result from a chronic endotoxin challenge due to bacterial translocation of hypoperfused intestinal mucosa. METHODS AND RESULTS: In 10 patients with CHF and ten healthy controls a tonometry catheter was inserted into the stomach. IPCO(2) was measured at rest and during bicycle exercise every 5 min. At rest arterial pCO(2) (aPCO(2)), intragastric pCO(2) (iPCO(2)) and the intragastric/arterial gap did not differ between patients and controls. During low level exercise (25 W), patients showed an increase in iPCO(2) compared to resting iPCO(2), whereas controls did not show an increase in iPCO(2) (change in iPCO(2): 12+/-2% vs. 1+/-0.4%, P<0.001). In CHF, iPCO(2) during peak exercise was 25+/-3% higher than at rest, compared to controls (increase 2+/-1, P<0.0001). CONCLUSIONS: Patients with CHF already at low level exercise develop an increase in iPCO(2). This is likely to reflect hypoperfusion of the intestinal mucosa, which may contribute to the development of bacterial translocation.
AIMS: The aim of this study was to investigate mesenteric ischaemia by determining intragastric PCO(2) (iPCO(2)) with gastric tonometry during rest and exercise stress testing in patients with chronic heart failure (CHF). In CHF inflammatory immune activation is hypothesized to result from a chronic endotoxin challenge due to bacterial translocation of hypoperfused intestinal mucosa. METHODS AND RESULTS: In 10 patients with CHF and ten healthy controls a tonometry catheter was inserted into the stomach. IPCO(2) was measured at rest and during bicycle exercise every 5 min. At rest arterial pCO(2) (aPCO(2)), intragastric pCO(2) (iPCO(2)) and the intragastric/arterial gap did not differ between patients and controls. During low level exercise (25 W), patients showed an increase in iPCO(2) compared to resting iPCO(2), whereas controls did not show an increase in iPCO(2) (change in iPCO(2): 12+/-2% vs. 1+/-0.4%, P<0.001). In CHF, iPCO(2) during peak exercise was 25+/-3% higher than at rest, compared to controls (increase 2+/-1, P<0.0001). CONCLUSIONS:Patients with CHF already at low level exercise develop an increase in iPCO(2). This is likely to reflect hypoperfusion of the intestinal mucosa, which may contribute to the development of bacterial translocation.
Authors: Kim van Wijck; Kaatje Lenaerts; Luc J C van Loon; Wilbert H M Peters; Wim A Buurman; Cornelis H C Dejong Journal: PLoS One Date: 2011-07-21 Impact factor: 3.240
Authors: Hafid Narayan; Noor Mohammed; Paulene A Quinn; Iain B Squire; Joan E Davies; Leong L Ng Journal: Clin Sci (Lond) Date: 2010-03 Impact factor: 6.124