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Adenosine as putative regulator of hepatic arterial flow (the buffer response)
The American Journal of Physiology
|March 1, 1985
Summary
Adenosine accumulation causes hepatic arterial (HA) dilation when portal flow decreases, as shown in cats. This adenosine washout into portal blood regulates the HA buffer response.
Area of Science:
- Physiology
- Hepatology
- Cardiovascular Research
Background:
- The hepatic arterial (HA) system plays a crucial role in liver blood supply.
- Understanding the regulation of HA flow is vital for liver health and disease.
- Previous studies suggest a compensatory increase in HA flow upon portal flow reduction.
Purpose of the Study:
- To investigate the role of adenosine in the hepatic arterial buffer response.
- To test the hypothesis that adenosine concentration near HA resistance vessels is regulated by washout into portal vessels.
Main Methods:
- Anesthetized cats underwent superior mesenteric artery occlusion to reduce portal flow.
- Hepatic arterial flow was monitored.
- Adenosine's effects were studied using infusions and dipyridamole and 1-methyl-3-isobutylxanthine (MIX) administration.
Main Results:
- Reduced portal flow led to a significant increase in HA flow, buffering 25.5% of the decrease.
- Adenosine was identified as a potent HA dilator.
- Dipyridamole enhanced the HA buffer response, while MIX antagonized adenosine and reduced the buffer response.
Conclusions:
- The hepatic arterial buffer response is mediated by local adenosine concentrations.
- Adenosine levels are controlled by its washout rate into the portal blood.
- This mechanism is crucial for maintaining liver blood flow homeostasis.