Hepatosplanchnic blood flow control and oxygen extraction are modified by the underlying mechanism of impaired perfusion

Bracht, Hendrik; Takala, Jukka; Tenhunen, Jyrki; Brander, Lukas; Knuesel, Rafael; Merasto-Minkkinen, Minna; Jakob, Stephan M.

doi:10.1097/01.ccm.0000156445.59009.49

Cited by 19 publications

(6 citation statements)

References 35 publications

(40 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Since the splanchnic region receives almost one third of total body blood flow, it seemed reasonable that reduction of splanchnic blood flow should influence the systemic venous-arterial pCO 2 gradient [5,18,19]. However, we did not find a good correlation between systemic and regional pCO 2 changes, either in ischemia or in congestion of mesenteric territory (Fig.…”

Section: Discussionmentioning

confidence: 79%

Regional Blood Flow Distribution and Oxygen Metabolism During Mesenteric Ischemia and Congestion

Cruz

Garrido

Ribeiro

et al. 2010

Journal of Surgical Research

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 79%

Regional Blood Flow Distribution and Oxygen Metabolism During Mesenteric Ischemia and Congestion

Cruz

Garrido

Ribeiro

et al. 2010

Journal of Surgical Research

View full text Add to dashboard Cite

“…Data on regional blood flow distribution, pCO 2 gradients, and oxygen extraction of 5 animals at baseline before shunt activation and baseline before the interventions have been included in previously published studies (23,24).…”

Section: Resultsmentioning

confidence: 99%

Effects of Low Abdominal Blood Flow and Dobutamine on Blood Flow Distribution and on the Hepatic Arterial Buffer Response in Anaesthetized Pigs

Brander

Jakob

Knuesel

et al. 2006

Shock

Self Cite

View full text Add to dashboard Cite

Low cardiac output impairs the hepatic arterial buffer response (HABR). Whether this is due to low abdominal blood flow per se is not known. Dobutamine is commonly used to increase cardiac output, and it may further modify hepatosplanchnic and renal vasoregulation. We assessed the effects of isolated abdominal aortic blood flow changes and dobutamine on hepatosplanchnic and renal blood flow. Twenty-five anesthetized pigs with an abdominal aorto-aortic shunt were randomized to 2 control groups [zero (n = 6) and minimal (n = 6) shunt flow], and 2 groups with 50% reduction of abdominal blood flow and either subsequent increased abdominal blood flow by shunt reduction (n = 6) or dobutamine infusion at 5 and 10 microg kg(-1) min(-1) with constant shunt flow (n = 7). Regional (ultrasound) and local (laser Doppler) intra-abdominal blood flows were measured. The HABR was assessed during acute portal vein occlusion. Sustained low abdominal blood flow, by means of shunt activation, decreased liver, gut, and kidney blood flow similarly and reduced local microcirculatory blood flow in the jejunum. Shunt flow reduction partially restored regional blood flows but not jejunal microcirculatory blood flow. Low-but not high-dose dobutamine increased gut and celiac trunk flow whereas hepatic artery and renal blood flows remained unchanged. Neither intervention altered local blood flows. The HABR was not abolished during sustained low abdominal blood flow despite substantially reduced hepatic arterial blood flow and was not modified by dobutamine. Low-but not high-dose dobutamine redistributes blood flow toward the gut and celiac trunk. The jejunal microcirculatory flow, once impaired, is difficult to restore.

show abstract

“…An increase in hepatic arterial blood flow is able to buffer 25%‐60% of the decreased portal flow. Furthermore, hepatic oxygen extraction can be increased up to 90% in the case of reduced hepatic perfusion and venous congestion, due to the high permeability of hepatic sinusoids that promote diffusion of oxygen to hepatic cells . Liver sinusoidal endothelial cells respond to inflammatory signals like endotoxin by an iNOS‐dependent endothelial dysfunction contributing to a decreased vasodilatory response and decreased endothelial nitric oxide synthase phosphorylation .…”

Section: Hypoxic Liver Injurymentioning

confidence: 99%

Liver Injury and Failure in Critical Illness

et al. 2019

View full text Add to dashboard Cite

The frequency of acquired liver injury and failure in critical illness has been significantly increasing over recent decades. Currently, liver injury and failure are observed in up to 20% of patients in intensive care units and are associated with significantly increased morbidity and mortality. Secondary forms of liver injury in critical illness are divided primarily into cholestatic, hypoxic, or mixed forms. Therefore, sufficient knowledge of underlying alterations (e.g., hemodynamic, inflammatory, or drug induced) is key to a better understanding of clinical manifestations, prognostic implications, as well as diagnostic and therapeutic options of acquired liver injury and failure. This review provides a structured approach for the evaluation and treatment of acquired liver injury and failure in critically ill patients.

show abstract

Hepatosplanchnic blood flow control and oxygen extraction are modified by the underlying mechanism of impaired perfusion

Cited by 19 publications

References 35 publications

Regional Blood Flow Distribution and Oxygen Metabolism During Mesenteric Ischemia and Congestion

Regional Blood Flow Distribution and Oxygen Metabolism During Mesenteric Ischemia and Congestion

Effects of Low Abdominal Blood Flow and Dobutamine on Blood Flow Distribution and on the Hepatic Arterial Buffer Response in Anaesthetized Pigs

Liver Injury and Failure in Critical Illness

Contact Info

Product

Resources

About