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Effect of intra-abdominal pressure on hepatic microcirculation: implications of the endothelin-1 receptor. | LitMetric

AI Article Synopsis

  • The study aimed to examine how blocking endothelin receptors A and B affects liver blood flow and oxygen levels when intra-abdominal pressure (IAP) is increased.
  • Fifteen anesthetized pigs were divided into two groups: one received a blocker for endothelin-1 (TG) and the other received a saline solution (CG) while IAP was gradually increased from 0 to 25 mmHg.
  • Results showed that the blocker helped maintain liver microcirculation and oxygenation better than the saline solution during high pressure, suggesting a protective effect against stress from increased IAP.

Article Abstract

Objective: To investigate the effect of endothelin receptor A (ET(A)) and endothelin receptor B (ET(B)) blockade on liver microcirculation and oxygenation during intra-abdominal pressure (IAP) increase.

Methods: Fifteen anesthetized pigs were randomized to receive either nonselective endothelin-1 (ET-1) blocker tezosentan (TG, n = 7) or saline (CG, n = 8). Helium was insufflated to increase IAP from 0 to 25 mmHg. Stroke volume variability was maintained ≤ 12% with colloid infusion. Total liver blood flow (TLBF), hepatic microcirculatory blood flow (MBF), hepatic tissue oxygenation (HpO(2)), hyaluronic acid and plasma disappearance rate (PDR) of indocyanine green (ICG) were recorded.

Results: TLBF remained mostly unaltered in both groups at low IAP and decreased only in CG at the IAP of 25 mmHg. As IAP increased, a significant decline in MBF was observed without correlation with cardiac output or TLBF. In CG, HpO(2) decreased as early as IAP of 10 mmHg to high levels of pressure. However, in TG the decrease was significant only at the IAP of 25 mmHg. PDR of ICG decreased in both groups at IAP of 25 mmHg (P = 0.046 and P = 0.009 in TG and CG, respectively). These changes correlated with MBF (r = 0.793).

Conclusion: Blocking ET(A) and ET(B) receptors partially protects sinusoidal circulation and tissue oxygenation against stress induced by high IAP.

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Source
http://dx.doi.org/10.1111/j.1751-2980.2012.00613.xDOI Listing

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