Gastrointestinal Blood Flow

Author(s):  
Thorsten Vowinkel ◽  
D. Neil Granger
1983 ◽  
Vol 245 (5) ◽  
pp. G697-G702 ◽  
Author(s):  
P. T. Nowicki ◽  
B. S. Stonestreet ◽  
N. B. Hansen ◽  
A. C. Yao ◽  
W. Oh

Regional and total gastrointestinal (GI) blood flow, O2 delivery, and whole-gut O2 extraction and O2 consumption were measured before and 30, 60, and 120 min after feeding in nonanesthetized, awake 2-day-old piglets. Cardiac output and blood flow to kidneys, heart, brain, and liver were also determined. Blood flow was measured using the radiolabeled microsphere technique. In the preprandial condition, total GI blood flow was 106 +/- 9 ml X min-1 X 100 g-1, while O2 extraction was 17.2 +/- 0.9% and O2 consumption was 1.99 +/- 0.19 ml O2 X min-1 X 100 g-1. Thirty minutes after slow gavage feeding with 30 ml/kg artificial pig milk, O2 delivery to the GI tract and O2 extraction rose significantly (P less than 0.05) by 35 +/- 2 and 33 +/- 2%, respectively. The increase in O2 delivery was effected by a significant increase in GI blood flow, which was localized to the mucosal-submucosal layer of the small intestine. O2 uptake by the GI tract increased 72 +/- 4% 30 min after feeding. Cardiac output and blood flow to non-GI organs did not change significantly with feeding, whereas arterial hepatic blood flow decreased significantly 60 and 120 min after feeding. The piglet GI tract thus meets the oxidative demands of digestion and absorption by increasing local blood flow and tissue O2 extraction.


1989 ◽  
Vol 256 (2) ◽  
pp. G364-G368
Author(s):  
S. R. Mayfield ◽  
W. Oh ◽  
D. L. Piva ◽  
B. S. Stonestreet

We studied the independent and combined effects of feeding and environmental cold stress by measuring pre- and postprandial gastrointestinal blood flow (QGI), oxygen consumption (GIVO2), and oxygen extraction (GIO2ex) in seven awake 3- to 4-day-old piglets while in a thermoneutral environment (control phase, 31 degrees C) and during environmental cold stress (experimental phase, 20.5 degrees C). Each animal consecutively completed both the control and experimental phases. In the control phase, measurements were made before and 30 min after feeding. In the experimental phase, measurements were made before and 30 min after induction of cold stress. A feeding was then given and measurements repeated 30 min later during continued cold stress. QGI (ml.100 g-1.min-1) increased postprandially while in a thermoneutral environment (130 +/- 11 to 152 +/- 12) but not while in a cold environment (126 +/- 15 to 121 +/- 8). Postprandial GIVO2 (ml O2.100 g-1.min-1) increased from 2.1 +/- 0.2 to 3.7 +/- 0.5 while in a warm environment. During preprandial cold stress, an unexpected increase in GIVO2 was observed (1.7 +/- 0.2 to 3.1 +/- 0.5). Feeding while in a cold environment provoked a further significant increase in GIVO2 (3.1 +/- 0.5 to 4.2 +/- 0.4). All increases in GIVO2 were associated with increased GIO2ex. This study has demonstrated that 1) postprandial GIVO2 is appropriately increased during cold stress as a function of GIO2ex and 2) that fasting GIVO2 is increased during cold stress, demonstrating an intestinal metabolic contribution to cold-induced systemic thermogenesis.


1978 ◽  
Vol 74 (5) ◽  
pp. 1031
Author(s):  
R.W. Emery ◽  
J.J. Leonard ◽  
S. Einzig ◽  
D.M. Nicoloff ◽  
D. Fletcher ◽  
...  

2010 ◽  
Vol 298 (5) ◽  
pp. R1240-R1248 ◽  
Author(s):  
Henrik Seth ◽  
Albin Gräns ◽  
Michael Axelsson

We have studied the potential role of CCK as a regulator/modulator of the postprandial increase in gastrointestinal blood flow. Rainbow trout ( Oncorhynchus mykiss ) were instrumented with pulsed Doppler flow probes to measure the effects of CCK on cardiac output and gastrointestinal blood flow. Furthermore, vascular preparations were used to study the direct effects of CCK on the vessels. In addition, we used in situ perfused hearts to further study the effects of CCK on the cardiovascular system. When the sulfated form of CCK-8 was injected at a physiological concentration (0.19 pmol/kg) in vivo, there was a significant increase in the gastrointestinal blood flow (18 ± 4%). This increase in gastrointestinal blood flow was followed by a subsequent increase in cardiac output (30 ± 6%). When the dose was increased to 0.76 pmol/kg, there was only a 14 ± 6% increase in gastrointestinal blood flow; possibly due to a dose-dependent increase in the gill vascular resistance as previously reported or a direct effect on the heart. Nevertheless, CCK did not affect the isolated vessel preparations, and thus, it seems unlikely that CCK has a direct effect on the blood vessels of the second or third order. CCK did, however, have profound effects on the dynamics of the heart, and without a change in cardiac output, there was a significant increase in the amplitude (59 ± 4%) and rate (dQ/d t: 55 ± 4%; -dQ/d t: 208 ± 49%) of the phasic flow profile. If and how this might be coupled to a postprandial gastrointestinal hyperemia remains to be determined. We conclude that CCK has the potential as a regulator of the postprandial gastrointestinal blood flow in fish and most likely has its effect by inducing a gastrointestinal hyperemia. The mechanism by which CCK acts is at present unknown.


1991 ◽  
Vol 30 (6) ◽  
pp. 633-633
Author(s):  
Mathias Nelle ◽  
Martina Kraus ◽  
Eugen P Zilow ◽  
Otwin Linderkamp

Sign in / Sign up

Export Citation Format

Share Document