AJP - Regulatory, Integrative and Comparative Physiology, Vol 269, Issue 4 869-R873, Copyright © 1995 by American Physiological Society
Impaired gut lipid absorptive capacity after trauma-hemorrhage and resuscitation
J. Kerner, P. Wang and I. H. Chaudry
Department of Surgery, Michigan State University, East Lansing 48824, USA.
Although the barrier function of the intestinal mucosa is impaired after
hemorrhage, it remains unclear whether this is associated with a deficit in
mucosal function. The aim of this study, therefore, was to determine
whether trauma-hemorrhage affects the in vivo lipid absorptive capacity of
the gut and, if so, to characterize the uptake process of free fatty acids
in isolated enterocytes. To study this, rats were anesthetized, a
laparotomy was performed (i.e., trauma was induced), and various blood
vessels were cannulated. For in vivo lipid absorption, the main intestinal
lymph vessel was cannulated and a jejunostomy feeding tube was inserted.
The animals were bled to and maintained at a mean arterial pressure of 40
mmHg until 40% of shed blood volume was returned in the form of Ringer
lactate. They were then resuscitated with four times the volume of maximal
bleed out with Ringer lactate. The in vivo and in vitro lipid absorptive
capacities were assessed by measuring lymph triglyceride output after a fat
load and by determining the linoleic acid uptake rates on isolated
enterocytes, respectively. The results show that the in vivo lipid
absorption capacity of the gut is severely depressed after
trauma-hemorrhage and resuscitation. Similarly, in enterocytes isolated
from hemorrhaged rats, fatty acid uptake capacity, as reflected by the
decreased maximal uptake rates, was significantly reduced: 1.2 +/- 0.2 and
2.6 +/- 0.6 nmol.min-1 x 10(6) cells-1 for hemorrhaged and sham,
respectively. Thus gut lipid absorptive function is depressed after
trauma-hemorrhage and resuscitation, which is at least partially due to the
depressed uptake mechanism of the enterocyte.
