Intensive Care Medicine

, Volume 22, Issue 12, pp 1453–1460

Prostacyclin counteracts the increase in capillary permeability induced by tumour necrosis factor-α

Authors

  • J. Jahr
    • Department of Physiology and NeuroscienceUniversity of Lund
    • Department of Anaesthesia and Intensive CareUniversity Hospital of Lund
  • P. -O. Grände
    • Department of Physiology and NeuroscienceUniversity of Lund
    • Department of Anaesthesia and Intensive CareUniversity Hospital of Lund
Experimental

DOI: 10.1007/BF01709568

Cite this article as:
Jahr, J. & Grände, P.-. Intensive Care Med (1996) 22: 1453. doi:10.1007/BF01709568

Abstract

Objective

To analyse how prostacyclin interferes with the short-term local circulatory effects of tumour necrosis factor-α (TNFα) in a skeletal muscle.

Design

An autoperfused sympathectomised cat gastrocnemius muscle enclosed in a plethysmograph.

Interventions

Arterial blood flow, total and segmental vascular resistances (large-bore arterial vessels, arterioles and veins), hydrostatic capillary pressure, tissue volume and capillary filtration coefficient were followed during local intraarterial infusion of TNFα at various rates (2.5, 5.0 and 7.5 μg/kg per min) and during intra-arterial infusion of prostacyclin simultaneously with the highest dose of TNFα. The capillary filtration coefficient reflects the capillary surface for fluid exchange.

Results

Arterial infusion of TNFα had no influence on vascular resistance up to 5.0 μg/kg per min but induced vasodilation at 7.5 μg/kg per min. No effects on the recorded hydrostatic capillary pressure were observed. The capillary filtration coefficient and the capillary filtration increased with the infusion rate of TNFα the former by 55%. Simultaneous arterial infusion of prostacyclin (350 ng/kg per min) caused further vasodilation and an increase in hydrostatic capillary pressure and completely restored the capillary filtration coefficient to control. The TNFα-induced filtration was partly restored.

Conclusions

The local circulatory effect of TNFα is small apart from a graded increase in the capillary filtration coefficient, most likely reflecting an increase in capillary permeability. The prostacyclininduced decrease in capillary filtration coefficient most likely reflects a restoration of capillary permeability. The TNFα-induced transcapillary filtration is not fully reduced by prostacyclin due to a simultaneous increase in hydrostatic capillary pressure.

Key words

Capillary permeabilityCapillary pressureCritical illnessHaemodynamicsProstacyclinSepsisTumour necrosis factorVascular resistance

Copyright information

© Springer-Verlag 1996