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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

The hepatic arterial buffer response during portal venous occlusion. There was a significant increase in hepatic arterial flow during portal venous occlusion (* p < 0.05) compared to basal hepatic arterial flow. HAF = hepatic arterial flow, PVF = portal venous flow and MAP = mean arterial pressure.
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Figure 2: The hepatic arterial buffer response during portal venous occlusion. There was a significant increase in hepatic arterial flow during portal venous occlusion (* p < 0.05) compared to basal hepatic arterial flow. HAF = hepatic arterial flow, PVF = portal venous flow and MAP = mean arterial pressure.

Mentions: In a number of experiments irreversible hypotension (n = 2), respiratory depression (n = 2) and acidosis (n = 2) occurred during the temporary occlusion of the portal vein for the insertion of the mesocaval shunt and data from these preparations have therefore not been included. It was imperative that haemodynamic stability should be attained before measurements were conducted and this was achieved in 5 preparations presented here. HA flow (HAF) was 19.4 (3.3) ml min-1 100 g-1, PV flow (PVF) 85.5 (19.3) ml min-1 100 g-1 and mean arterial pressure was 80.2 (5.8) mmHg. When the mesocaval shunt was opened and the mesenteric vein occluded PVF decreased to 38.5 (3.7) ml min-1 100 g-1 and HAF increased to 25.6 (4.3) ml min-1100 g-1 (p < 0.05, Figure 2a) a calculated buffering capacity of 18.7 (5.2) % (Table 1, n = 5). During portal venous flow reduction the mean arterial pressure consistently rose to 85.2 (5.2) mmHg, (p < 0.001). When the portal venous flow was re-established there was often a small rebound portal "hyperaemia" accompanied by a temporary fall in HA flow and a fall in systemic blood pressure (Figure 2b).


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)

The hepatic arterial buffer response during portal venous occlusion. There was a significant increase in hepatic arterial flow during portal venous occlusion (* p < 0.05) compared to basal hepatic arterial flow. HAF = hepatic arterial flow, PVF = portal venous flow and MAP = mean arterial pressure.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 2: The hepatic arterial buffer response during portal venous occlusion. There was a significant increase in hepatic arterial flow during portal venous occlusion (* p < 0.05) compared to basal hepatic arterial flow. HAF = hepatic arterial flow, PVF = portal venous flow and MAP = mean arterial pressure.
Mentions: In a number of experiments irreversible hypotension (n = 2), respiratory depression (n = 2) and acidosis (n = 2) occurred during the temporary occlusion of the portal vein for the insertion of the mesocaval shunt and data from these preparations have therefore not been included. It was imperative that haemodynamic stability should be attained before measurements were conducted and this was achieved in 5 preparations presented here. HA flow (HAF) was 19.4 (3.3) ml min-1 100 g-1, PV flow (PVF) 85.5 (19.3) ml min-1 100 g-1 and mean arterial pressure was 80.2 (5.8) mmHg. When the mesocaval shunt was opened and the mesenteric vein occluded PVF decreased to 38.5 (3.7) ml min-1 100 g-1 and HAF increased to 25.6 (4.3) ml min-1100 g-1 (p < 0.05, Figure 2a) a calculated buffering capacity of 18.7 (5.2) % (Table 1, n = 5). During portal venous flow reduction the mean arterial pressure consistently rose to 85.2 (5.2) mmHg, (p < 0.001). When the portal venous flow was re-established there was often a small rebound portal "hyperaemia" accompanied by a temporary fall in HA flow and a fall in systemic blood pressure (Figure 2b).

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