Increased IAP often coexists with sepsis in severely ill patients in the ICU, under mechanical ventilation and pharmaceutical support of the circulation with inotropes and vasoactive drugs. Both conditions have an unfavorable effect on the cardiovascular system. The purpose of this experimental study was to record the effect of increased intra-abdominal pressure on the cardiovascular system of pigs, with or without additional sepsis. Sixteen male pigs were randomly assigned in two groups A and B. In both groups, after induction to anesthesia and mechanical ventilation, the intra-abdominal pressure was increased to 25mmHg by helium insufflation in the peritoneal cavity, and that level of IAP was preserved until the end of the experiment. In Group A no other intervention apart from the increase in IAP was made, whereas in Group B, 60 minutes after the increase in IAP, 100μg/kg LPS were administered. Data were recorded after induction of anesthesia and initiation of mechanical ventilation (baseline measurement/measurement 0) and thereafter every 20 min after intra-abdominal pressure increase. The last measurement (measurement 9) was obtained immediately before release of pneumoperitoneum. Parameters measured or calculated included HR, BP(s,d,m), RVPs, PAP(s,d,m), PΑWP, CO, SV, SVR, PVR, SvO2, ETCO2. HR increased statistically significantly only in Group B, 60 minutes after the administration of LPS. BP (s, d, m) presented a significant change only in Group B, an initial increase immediately after LPS administration, followed by a decrease. CVP, RVPs and PAP (s, d, m) increased in both groups after IAP increase, whereas they presented an additional increase in Group B, after LPS administration. PΑWP changed only in Group B, after LPS administration. CO and SV were dramatically reduced in Group B, immediately after LPS administration, but gradually recovered their initial values until the end of the experiment. SVR changed only in Group B. They increased after LPS administration and then they gradually decreased. PVR increased dramatically after LPS administration and, despite gradual decrease they remained at high values until the end of the experiment. SvO2 decreased in Group B after LPS administration but gradually recovered its initial values. At the conditions of this particular experiment, the increase in intra-abdominal pressure was well tolerated by the laboratory animals. On the contrary, sepsis induction by LPS administration had an unfavorable effect on the cardiovascular system.

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Το γαλακτικό οξύ παράγεται στο κυτταρόπλασμα από γλυκόλυση και μεταβολίζεται κυρίως από το ήπαρ (60%) (γλυκογονογένεση και νεογλυκογένεση) και από τα νεφρά (30%), τόσο στο φλοιό (τόπος μεταβολισμού)μέσω της νεογλυκογένεσης όσο και στο μυελό (τόπος παραγωγής). Η σχέση μεταξύ πυρουβικού και γαλακτικού οξέος είναι αμφίδρομη και το παραγόμενο γαλακτικό οξύ μπορεί να μετατραπεί είτε έμμεσα από το πυρουβικό σε οξαλικό οξύ και αλανίνη είτε άμεσα σε γλυκογόνο και γλυκόζη από τα περιπυλαία ηπατικά κύτταρα με τον κύκλο του Cori. Κατά συνέπεια, η αυξημένη γλυκόλυση οδηγεί σε αυξημένη παραγωγή γαλακτικού οξέος.

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Pulmonary capillary pressure (Pcp) is the primary driving force determining the fluid flux across pulmonary capillary wall. Alterations of Pcp have been described in systemic inflammation, sepsis, ARDS, hypoxaemia and acute heart failure. The purpose of this study was to examine the Pcp alterations after lipopolysaccharide (LPS) intravenous administration in pigs. LPS has been administered (150μg/Kg BW) in the right atrium of 8 anesthetized and mechanical ventilated pigs (Group A) and the Pcp was calculated from pulmonary artery pressure tracings using the Gaar equation before, after LPS infusion and in 20min intervals for two hours.

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