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The role of ATP and adenosine in the control of hepatic blood flow in the rabbit liver in vivo.

Browse DJ, Mathie RT, Benjamin IS, Alexander B - Comp Hepatol (2003)

Bottom Line: RESULTS: Hepatic arterial (HA) blood flow increased in response to reduced portal venous (PV) blood flow, the "buffer response", from 19.4 (3.3) ml min-1 100 g-1 to 25.6 (4.3) ml min-1 100 g-1 (mean (SE), p < 0.05, Student's paired t-test).Intra-portal injections of ATP or adenosine (1 micrograms kg-1-0.5 mg kg-1) elicited immediate increases in HA blood flow to give -log ED50 values of 2.0 and 1.7 mg kg-1 for ATP and adenosine respectively.Injection of ATP and adenosine had no measurable effect on PV flow.

View Article: PubMed Central - HTML - PubMed

Affiliation: Liver Sciences Unit, Academic Department of Surgery, GKT School of Medicine and Dentistry, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH, UK. barry.alexander@kcl.ac.uk

ABSTRACT
BACKGROUND: The role of adenosine and ATP in the regulation of hepatic arterial blood flow in the "buffer response" was studied in vitro and in a new in vivo model in the rabbit. The model achieves portal-systemic diversion by insertion of a silicone rubber prosthesis between the portal vein and inferior vena cava and avoids alterations in systemic haemodynamics. RESULTS: Hepatic arterial (HA) blood flow increased in response to reduced portal venous (PV) blood flow, the "buffer response", from 19.4 (3.3) ml min-1 100 g-1 to 25.6 (4.3) ml min-1 100 g-1 (mean (SE), p < 0.05, Student's paired t-test). This represented a buffering capacity of 18.7 (5.2) %. Intra-portal injections of ATP or adenosine (1 micrograms kg-1-0.5 mg kg-1) elicited immediate increases in HA blood flow to give -log ED50 values of 2.0 and 1.7 mg kg-1 for ATP and adenosine respectively. Injection of ATP and adenosine had no measurable effect on PV flow. In vitro, using an isolated dual-perfused rabbit liver preparation, the addition of 8-phenyltheophylline (10 MicroMolar) to the HA and PV perfusate significantly inhibited the HA response to intra-arterial adenosine and to mid-range doses of intra-portal or intra-arterial ATP (p < 0.001). CONCLUSIONS: It is suggested that HA vasodilatation elicited by ATP may be partially mediated through activation of P1-purinoceptors following catabolism of ATP to adenosine.

No MeSH data available.


Related in: MedlinePlus

Diagram of silastic H-shaped prosthesis inserted into the portal vein and the inferior vena cava of the in vivo rabbit model. During control conditions, the prosthesis is clamped across the horizontal limb at "a". Portal-systemic diversion is achieved by removal of the clamp from "a" and cross-clamping at point "b", distal to the point of entry of the splenic vein into the portal vein.
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Figure 1: Diagram of silastic H-shaped prosthesis inserted into the portal vein and the inferior vena cava of the in vivo rabbit model. During control conditions, the prosthesis is clamped across the horizontal limb at "a". Portal-systemic diversion is achieved by removal of the clamp from "a" and cross-clamping at point "b", distal to the point of entry of the splenic vein into the portal vein.

Mentions: The experimental preparation was based upon a model we have previously established in the dog [21,30]. After cannulation of the carotid artery for blood pressure monitoring, a midline laparotomy was performed and the inflow vessels to the liver dissected. The gastroduodenal artery and vein were ligated and divided. A prosthetic (H-shaped) mesocaval shunt, constructed from 3.0 mm internal diameter silicone rubber tubing, was inserted proximal to the splenic vein after heparinisation (300 iu. kg-1 i.v.). This allowed diversion of mesenteric blood flow to the systemic circulation as required. A clamp was placed on the cross limb of the "H" to restore portal flow. Pre-calibrated electromagnetic flow probes (Statham) were applied to the common hepatic artery and portal vein (1 and 3 mm diameter respectively) (Figure 1).


The role of ATP and adenosine in the control of hepatic blood flow in the rabbit liver in vivo.

Browse DJ, Mathie RT, Benjamin IS, Alexander B - Comp Hepatol (2003)

Diagram of silastic H-shaped prosthesis inserted into the portal vein and the inferior vena cava of the in vivo rabbit model. During control conditions, the prosthesis is clamped across the horizontal limb at "a". Portal-systemic diversion is achieved by removal of the clamp from "a" and cross-clamping at point "b", distal to the point of entry of the splenic vein into the portal vein.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC305370&req=5

Figure 1: Diagram of silastic H-shaped prosthesis inserted into the portal vein and the inferior vena cava of the in vivo rabbit model. During control conditions, the prosthesis is clamped across the horizontal limb at "a". Portal-systemic diversion is achieved by removal of the clamp from "a" and cross-clamping at point "b", distal to the point of entry of the splenic vein into the portal vein.
Mentions: The experimental preparation was based upon a model we have previously established in the dog [21,30]. After cannulation of the carotid artery for blood pressure monitoring, a midline laparotomy was performed and the inflow vessels to the liver dissected. The gastroduodenal artery and vein were ligated and divided. A prosthetic (H-shaped) mesocaval shunt, constructed from 3.0 mm internal diameter silicone rubber tubing, was inserted proximal to the splenic vein after heparinisation (300 iu. kg-1 i.v.). This allowed diversion of mesenteric blood flow to the systemic circulation as required. A clamp was placed on the cross limb of the "H" to restore portal flow. Pre-calibrated electromagnetic flow probes (Statham) were applied to the common hepatic artery and portal vein (1 and 3 mm diameter respectively) (Figure 1).

Bottom Line: RESULTS: Hepatic arterial (HA) blood flow increased in response to reduced portal venous (PV) blood flow, the "buffer response", from 19.4 (3.3) ml min-1 100 g-1 to 25.6 (4.3) ml min-1 100 g-1 (mean (SE), p < 0.05, Student's paired t-test).Intra-portal injections of ATP or adenosine (1 micrograms kg-1-0.5 mg kg-1) elicited immediate increases in HA blood flow to give -log ED50 values of 2.0 and 1.7 mg kg-1 for ATP and adenosine respectively.Injection of ATP and adenosine had no measurable effect on PV flow.

View Article: PubMed Central - HTML - PubMed

Affiliation: Liver Sciences Unit, Academic Department of Surgery, GKT School of Medicine and Dentistry, St Thomas' Hospital, Lambeth Palace Road, London SE1 7EH, UK. barry.alexander@kcl.ac.uk

ABSTRACT
BACKGROUND: The role of adenosine and ATP in the regulation of hepatic arterial blood flow in the "buffer response" was studied in vitro and in a new in vivo model in the rabbit. The model achieves portal-systemic diversion by insertion of a silicone rubber prosthesis between the portal vein and inferior vena cava and avoids alterations in systemic haemodynamics. RESULTS: Hepatic arterial (HA) blood flow increased in response to reduced portal venous (PV) blood flow, the "buffer response", from 19.4 (3.3) ml min-1 100 g-1 to 25.6 (4.3) ml min-1 100 g-1 (mean (SE), p < 0.05, Student's paired t-test). This represented a buffering capacity of 18.7 (5.2) %. Intra-portal injections of ATP or adenosine (1 micrograms kg-1-0.5 mg kg-1) elicited immediate increases in HA blood flow to give -log ED50 values of 2.0 and 1.7 mg kg-1 for ATP and adenosine respectively. Injection of ATP and adenosine had no measurable effect on PV flow. In vitro, using an isolated dual-perfused rabbit liver preparation, the addition of 8-phenyltheophylline (10 MicroMolar) to the HA and PV perfusate significantly inhibited the HA response to intra-arterial adenosine and to mid-range doses of intra-portal or intra-arterial ATP (p < 0.001). CONCLUSIONS: It is suggested that HA vasodilatation elicited by ATP may be partially mediated through activation of P1-purinoceptors following catabolism of ATP to adenosine.

No MeSH data available.


Related in: MedlinePlus