Defense mechanisms to increasing back pressure for hepatic oxygen transport and venous return in porcine fecal peritonitis.

Liu, Shengchen; do Amaral Campos, Pedro Paulo Zanella; Casoni, Daniela; Berger, David; Kohler, Andreas; Bloch, Andreas; Bervini, David; Setzer, Florian; Cameron, David R.; Z'Graggen, Werner; Hana, Anisa; Langer, Rupert; Corrêa, Thiago D.; Beldi, Guido; Takala, Jukka; Jakob, Stephan M. (2020). Defense mechanisms to increasing back pressure for hepatic oxygen transport and venous return in porcine fecal peritonitis. American journal of physiology - gastrointestinal and liver physiology, 319(3), G289-G302. American Physiological Society 10.1152/ajpgi.00216.2020

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High central venous pressure (CVP) acutely decreases venous return. How this affects hepatic oxygen transport in sepsis remains unclear. The aim of this study was to evaluate the effects of repeated increases in CVP via standard nursing procedures (NPs) on hepato-splanchnic and renal oxygen transport in a prolonged porcine sepsis model. Twenty anesthetized and mechanically ventilated pigs with regional hemodynamics monitored were randomized to fecal peritonitis or controls (n = 10 pigs/group). Resuscitation was started after 8 h of observation and continued for 3 days. NPs were performed at baseline and 8 h, 32 h, 56 h, and 72 h after resuscitation started. NPs increased CVP by 4-7 mmHg in both groups. In controls, this was associated with less decrease in hepatic arterial (Qha; 62 ± 70 mL/min) than portal venous flow (Qpv; 364 ± 151 mL/min). Portal venous oxygen content and hepatic O2 delivery (Do2) and consumption (V̇o2) decreased by 11 ± 6 mL/dL and 0.9 ± 0.3 and 0.4 ± 0.3 mL·min-1·kg-1, respectively. In septic animals, hepatic Do2 decreased more in response to increasing CVP (1.5 ± 0.9 mL·min-1·kg-1), which was attributable to a larger fall in both Qha (88 ± 66 ml/min) and portal O2 content (14 ± 10 mL/dL, all P < 0.05). This resulted in numerically lower hepatic V̇o2 since O2 extraction did not increase significantly. In control conditions, a smaller decrease in Qha compared with Qpv helped to limit the reduction in hepatic V̇o2 in response to acute CVP increase. In sepsis, the contribution of Qha to maintain hepatic Do2 was reduced, which jeopardized hepatic V̇o2 further. Renal arterial flow was similarly affected by CVP increase as Qha.NEW & NOTEWORTHY Sepsis impairs intrinsic mechanisms to attenuate effects of increasing back pressure on hepatic oxygen transport.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Intensive Care, Emergency Medicine and Anaesthesiology (DINA) > Clinic of Intensive Care
04 Faculty of Medicine > Pre-clinic Human Medicine > BioMedical Research (DBMR)
04 Faculty of Medicine > Service Sector > Institute of Pathology
04 Faculty of Medicine > Department of Head Organs and Neurology (DKNS) > Clinic of Neurosurgery
04 Faculty of Medicine > Department of Gastro-intestinal, Liver and Lung Disorders (DMLL) > Clinic of Visceral Surgery and Medicine > Visceral Surgery

Graduate School:

Graduate School for Cellular and Biomedical Sciences (GCB)

UniBE Contributor:

Liu, Shengchen; Casoni, Daniela; Berger, David; Kohler, Andreas; Bloch, Andreas; Bervini, David; Setzer, Florian; Cameron, David Robert; Z'Graggen, Werner Josef; Hana, Anisa; Langer, Rupert; Beldi, Guido; Takala, Jukka and Jakob, Stephan

Subjects:

500 Science > 570 Life sciences; biology
600 Technology > 610 Medicine & health

ISSN:

0193-1857

Publisher:

American Physiological Society

Language:

English

Submitter:

Nicole Söll

Date Deposited:

09 Oct 2020 15:01

Last Modified:

09 Oct 2020 15:09

Publisher DOI:

10.1152/ajpgi.00216.2020

PubMed ID:

32658622

Uncontrolled Keywords:

hepatic oxygen transport nursing procedures resuscitation sepsis venous return

BORIS DOI:

10.7892/boris.146898

URI:

https://boris.unibe.ch/id/eprint/146898

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