Pressure‐flow relationships and effects of noradrenaline and isoprenaline on the hepatic arterial and portal venous vascular beds of the dog.

Richardson, P. D.; Withrington, P.G.

doi:10.1113/jphysiol.1978.sp012475

Cited by 53 publications

(29 citation statements)

References 19 publications

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“…Studies in vivo indicate that there is intrinsic vasomotor tone in the portal vein (Johansson & Ljung, 1967) and that carotid sinus baroreceptors and noradrenaline have sizeable effects on portal venous tone (Alexander, 1954 ;Brooksby & Donald, 1971;Auden & Donald, 1975;Carneiro & Donald, 1977;Richardson & Withrington, 1978 …”

Section: Discussionmentioning

confidence: 99%

Capacitance of the rabbit portal vein and inferior vena cava.

Brown¹,

Heistad²

1986

The Journal of Physiology

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SUMMARY1. We used vessel strips and whole vessels in vitro to determine the length-tension and pressure-volume relationships of two veins with similar diameter and wall thickness, the portal vein and inferior vena cava of rabbits.2. Length-tension studies indicate that longitudinal and circular strips of the portal vein have significantly smaller elastic moduli than similar strips of the inferior vena cava (P < 0 05).3. Pressure-volume relationships of intact vessels indicate that pressures greater than 5 mmHg do not produce significant increases in volume of the inferior vena cava, whereas volume of the portal vein increases significantly over a range of pressures from 2 to 15 mmHg. 1 4. Activation of smooth muscle with noradrenaline reduces the volume of the vena cava at distending pressures < 5 mmHg. In contrast, noradrenaline reduces the volume of the portal vein at pressures up to 10 mmHg. During inactivation in calcium-free solution and activation with noradrenaline, the portal vein is more compliant than the inferior vena cava (P < 0 05).5. Morphometric studies demonstrate more collagen in the inferior vena cava than in the portal vein. Differences in capacitance of the vessels may be related, in part, to greater collagen content in the inferior vena cava.

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Section: Discussionmentioning

confidence: 99%

Capacitance of the rabbit portal vein and inferior vena cava.

Brown¹,

Heistad²

1986

The Journal of Physiology

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“…These effects are not dependent upon a purely hydrodynamic response of one inflow circuit to altered perfusion in the other, since although such interactions do occur, they are quantitatively extremely small, and could not account for the effects described in this paper (Richardson & Withrington, 1978b).…”

Section: Discussionmentioning

confidence: 90%

“…Such an analysis of the temporal relationship of the responses to 5-HT is more difficult since they are both very small and of prolonged time-course, compared with histamine or with either noradrenaline or isoprenaline (Richardson & Withrington, 1978b). However, both the intra-arterial and intraportal injection of 100 jg 5-HT caused significant changes in the resistance of the hepatic inflow circuit not receiving the direct injection, whilst there were no significant changes in BP, HR or SMVF, this indicates that the transhepatic effects must arise from access within the liver rather than from elevated levels of systemic arterial 5-HT.…”

Section: Discussionmentioning

confidence: 99%

Responses of the Simultaneously‐perfused Hepatic Arterial and Portal Venous Vascular Beds of the Dog to Histamine and 5‐hydroxytryptamine

Richardson

Withrington

1978

British J Pharmacology

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1 The sympathetically-innervated hepatic arterial and portal venous vascular beds of the dog were perfused simultaneously in situ. 2 Histamine and 5-hydroxytryptamine (5-HT) were injected intra-arterially and intraportally in graded, increasing doses. 3 Intra-arterial histamine evoked decreases in hepatic arterial vascular resistance (HAVR) and increases in hepatic portal vascular resistance (HPVR). 4 Intraportal injections of histamine caused increases in HPVR and decreases in HAVR. 5 The time courses of the arterial responses to intraportal histamine and of the portal responses to intra-arterial histamine, compared with any systemic effects, showed that these effects on the liver vasculature could not be the result of recirculation of histamine. 6 Intra-arterial 5-HT evoked biphasic changes in HAVR and small falls in HPVR. Intraportal 5-HT caused falls in HPVR at low doses and rises at high doses, together, typically, with biphasic effects on HAVR. 7 It is unlikely that the arterial effects of intraportal 5-HT and the portal effects of intra-arterial 5-HT were due to recirculation of the vasoactive material. 8 Pathophysiologically, both histamine and 5-HT are released from the gastrointestinal tract into the portal vein. These experiments show that such release may affect the hepatic arterial vascular resistance (and therefore blood flow) even though vasoactive levels of the autacoids are not attained in the systemic circulation.

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“…Many other vasoactive substances, particularly peptides of gastrointestinal origin (see review, Withrington & Richardson, 1989) enter the liver in the portal inflow principally during digestion. It is now established that vasoactive substances present in the portal inflow alone may nevertheless have access to hepatic arterial resistance sites by 'transhepatic routes' (Richardson & Withrington, 1978;Lautt et al, 1984). It remains an important aspect of hepatic circulatory physiology to establish any interactions, on the liver vasculature, between substances of primarily systemic origin (i.e.…”

Section: Discussionmentioning

confidence: 99%

The actions of human atrial natriuretic factor on hepatic arterial and portal vascular beds of the anaesthetized dog

Withrington

Dhume

Croxton

et al. 1990

British J Pharmacology

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The vascular actions of atrial natriuretic factor (ANF) have been assessed with other vasoactive agents on the hepatic arterial and portal vascular beds of the anaesthetized dog. Intra‐arterial bolus injections of ANF (0.1–50 nmol) caused graded increases in hepatic arterial blood flow representing a vasodilatation of relatively short duration. Vasoconstriction was never observed. The maximum increase in hepatic arterial blood was the same for ANF and isoprenaline (Iso) i.e. approximately 60–70% increase over control flow. On a molar basis, ANF was less potent than Iso although over the higher dose range (10−9−10−7 mol) its vasodilator activity exceeded that of the endogenous vasodilator adrenaline. Intraportal bolus injections (1.0–50 nmol) of ANF did not alter portal inflow resistance since no changes in portal inflow pressure occurred when the portal circuit was perfused at constant inflow volume. This differential action of ANF on the hepatic arterial and portal vascular beds may provide a change in total liver blood flow in favour of the arterial component. ANF, by altering hepatic haemodynamics to favour formation of trans‐sinusoidal fluid exchange, may provide a temporary expansion of the extravascular fluid reservoir to buffer any increased venous pressure. However, chronically elevated plasma levels of ANF would encourage the formation of ascitic fluid.

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Pressure‐flow relationships and effects of noradrenaline and isoprenaline on the hepatic arterial and portal venous vascular beds of the dog.

Cited by 53 publications

References 19 publications

Capacitance of the rabbit portal vein and inferior vena cava.

Capacitance of the rabbit portal vein and inferior vena cava.

Responses of the Simultaneously‐perfused Hepatic Arterial and Portal Venous Vascular Beds of the Dog to Histamine and 5‐hydroxytryptamine

The actions of human atrial natriuretic factor on hepatic arterial and portal vascular beds of the anaesthetized dog

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