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Severe haemorrhage partially reverses moderate haemorrhage-induced decrease in intestinal vascular capacitance

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Abstract:

The purpose of the present study was to compare the effect of severe haemorrhage with moderate haemorrhage on intestinal vascular capacitance. In 12 chloralose-anaesthetized pigs, moderate and subsequent severe haemorrhage was induced by removal of 15 and 25% of blood volume, respectively. Six of the animals were vagotomized prior to induction of haemorrhage. The portal vein pressure/intestinal blood volume (PV) relationship was measured by using blood pool scintigraphy and varying portal vein pressure. Moderate haemorrhage resulted in a leftward shift of the PV relationship towards the pressure axis with decreases in cardiac output, portal blood flow and arterial pressure, and an increase in heart rate. Severe haemorrhage shifted the P–V relationship back towards the volume axis compared with moderate haemorrhage, with further decreases in cardiac output, portal blood flow and arterial pressure. While moderate haemorrhage reduced intestinal blood volume at a portal vein pressure of 7 mmHg (Vp7) to 81 ± 3% of the control value (P < 0.01), severe haemorrhage increased Vp7 to 88 ± 1% of the control value (P < 0.05 compared with moderate haemorrhage). After vagotomy, moderate haemorrhage decreased Vp7 to 84 ± 4% of the control value (P < 0.01), whereas Vp7 did not change significantly after severe haemorrhage (Vp7 increased to 86 ± 1% of the control value). Thus, severe haemorrhage is associated with an increase in intestinal vascular capacity compared with moderate haemorrhage. This increase is mediated in part via the cardiac vagal reflex. The attenuation of intestinal venoconstriction during severe haemorrhage probably contributes to further decreases in cardiac output and arterial pressure by redistribution of blood to the peripheral circulation.

Keywords: cardiac vagal reflex; pressure–volume relationship; splanchnic circulation; vascular capacitance; vasovagal syncope

Document Type: Original Article

DOI: http://dx.doi.org/10.1046/j.1365-201X.1998.0268f.x

Affiliations: 1: Department of Anesthesia, Brigham and Women's Hospital, Boston, MA, USA 2: Department of Medicine, Brigham and Women's Hospital, Boston, MA, USA 3: Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA

Publication date: January 1, 1998

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