Limits...
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 changes in (a) hepatic arterial pressure responses (Δ HAP) and (b) portal venous pressure responses (Δ PVP) to intra-portal injection of ATP. The adenosine receptor antagonist 8-phenyltheophylline (10 μM) significantly decreased hepatic arterial responses to ATP, while portal venous responses were unaffected (** p < 0.01, compared with before 8-SPT). The error bars in the graphs represent the SE.
© Copyright Policy
Related In: Results  -  Collection


getmorefigures.php?uid=PMC305370&req=5

Figure 5: The changes in (a) hepatic arterial pressure responses (Δ HAP) and (b) portal venous pressure responses (Δ PVP) to intra-portal injection of ATP. The adenosine receptor antagonist 8-phenyltheophylline (10 μM) significantly decreased hepatic arterial responses to ATP, while portal venous responses were unaffected (** p < 0.01, compared with before 8-SPT). The error bars in the graphs represent the SE.

Mentions: Livers from another group of 6 rabbits [body weight 2.60 (0.14) kg, liver weight 98.8 (5.2) g] were perfused at raised tone [HAP 156.2 (4.8) and PVP 2.3 (0.7) mmHg]. The addition of 8-SPT to the hepatic arterial and portal venous perfusate significantly inhibited the HA response to 10-8 moles 100 g liver-1 intra-arterial adenosine from 33.2 (3.5) to 6.5 (3.8) mmHg (p < 0.001). The HA dose-related responses to mid-range doses of intra-portal ATP were also significantly reduced by 8-SPT, causing a non-significant right shift of the dose-response curve to ATP from -log Molar ED50 5.08 (0.15) to 4.97 (0.12) (p = 0.05) (Figure 5a). The portal venous responses to intra-portal injections of ATP were not significantly altered by 8-SPT (Figure 5b).


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 changes in (a) hepatic arterial pressure responses (Δ HAP) and (b) portal venous pressure responses (Δ PVP) to intra-portal injection of ATP. The adenosine receptor antagonist 8-phenyltheophylline (10 μM) significantly decreased hepatic arterial responses to ATP, while portal venous responses were unaffected (** p < 0.01, compared with before 8-SPT). The error bars in the graphs represent the SE.
© Copyright Policy
Related In: Results  -  Collection

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

Figure 5: The changes in (a) hepatic arterial pressure responses (Δ HAP) and (b) portal venous pressure responses (Δ PVP) to intra-portal injection of ATP. The adenosine receptor antagonist 8-phenyltheophylline (10 μM) significantly decreased hepatic arterial responses to ATP, while portal venous responses were unaffected (** p < 0.01, compared with before 8-SPT). The error bars in the graphs represent the SE.
Mentions: Livers from another group of 6 rabbits [body weight 2.60 (0.14) kg, liver weight 98.8 (5.2) g] were perfused at raised tone [HAP 156.2 (4.8) and PVP 2.3 (0.7) mmHg]. The addition of 8-SPT to the hepatic arterial and portal venous perfusate significantly inhibited the HA response to 10-8 moles 100 g liver-1 intra-arterial adenosine from 33.2 (3.5) to 6.5 (3.8) mmHg (p < 0.001). The HA dose-related responses to mid-range doses of intra-portal ATP were also significantly reduced by 8-SPT, causing a non-significant right shift of the dose-response curve to ATP from -log Molar ED50 5.08 (0.15) to 4.97 (0.12) (p = 0.05) (Figure 5a). The portal venous responses to intra-portal injections of ATP were not significantly altered by 8-SPT (Figure 5b).

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