Arteriovenous intestinal communications in shock. Experimental study using tagged microspheres

Area of Science:

• Gastrointestinal physiology
• Vascular biology
• Radiotracer methodology

Background:

• Arteriovenous anastomoses (AVAs) are crucial for regulating blood flow and pressure in tissues.
• The role of AVAs in the small intestine during physiological stress, such as oligemic shock, remains incompletely understood.
• Previous research has not definitively characterized the presence and function of larger AVAs in the intestinal mucosa.

Purpose of the Study:

• To investigate the influence of oligemic shock on the patency of arteriovenous anastomoses (AVAs) in the small intestine mucosa.
• To determine the size distribution of AVAs in the canine and rabbit small intestine under normal and oligemic shock conditions.
• To assess whether larger AVAs contribute to blood flow regulation during hypoperfusion.

Main Methods:

• Microspheres labeled with Cerium-141 (Ce141) and Strontium-85 (Sr85) were utilized as tracers.
• Microspheres with a diameter of 25 ± 5 microns were administered to assess vascular patency.
• Oligemic shock was induced in canine and rabbit models to simulate conditions of reduced blood flow.
• Vascular casting or histological analysis was performed to identify and measure AVAs in the small intestine mucosa.

Main Results:

• No arteriovenous anastomoses (AVAs) larger than 20 microns in diameter were detected in the small intestine mucosa.
• This finding held true both in the baseline state and during the induced oligemic shock.
• The labeled microspheres, although larger than 20 microns, did not reveal the presence of open AVAs of significant size.

Conclusions:

• The small intestine mucosa in dogs and rabbits does not appear to possess open arteriovenous anastomoses (AVAs) exceeding 20 microns in diameter.
• Oligemic shock does not lead to the opening or recruitment of larger AVAs in this specific tissue.
• These findings suggest that blood flow regulation in the small intestinal mucosa during hypoperfusion may rely on mechanisms other than large arteriovenous shunts.