Blood mobilization from the liver of the anaesthetized dog (original) (raw)
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Experimental physiology, 1997
This study was designed to determine the extent to which the decrease in volume of blood in the abdominal circulation in response to sympathetic stimulation was due to a passive effect of decreasing flow rather than active constriction of the capacitance vessels. In dogs anaesthetized with alpha-chloralose (100 mg kg-1 i.v.) the abdominal circulation was vascularly isolated and perfused either at constant flow or at constant pressure, and drained at constant pressure from the inferior vena cava. Changes in volume were determined by integration of the differences between inflow and outflow. Supramaximal stimulation of both splanchnic (sympathetic) nerves at 1 Hz decreased abdominal volume during constant pressure perfusion (active and passive components) by 3.04 +/- 0.58 ml kg-1 and at constant flow (active responses only) by 2.30 +/- 0.49 ml kg-1 (means +/- S.E.M.). The responses at 8 Hz were respectively 9.52 +/- 0.91 and 5.09 +/- 0.49 ml kg-1. The proportion of the responses calcu...
Hepatology, 1984
Compounds reaching the liver do so via either the hepatic artery or the portal vein. This paper reports on the effectiveness of administration of compounds into these alternate routes for their effects on the hepatic parenchymal cells, the hepatic arterial resistance vessels (blood flow) and hepatic capacitance (blood volume responses). All tests were done on cats under pentobarbital anesthesia. Perfusion of the parenchymal cell mass was assessed by comparing the hepatic elimination of indocyanine green (ICG) administered via the two vascular routes. The ICG uptake was assessed by measuring relative areas under the hepatic venous outflow curve obtained following bolus injections of ICG into the artery and portal vein. In a separate series, using different methods, the hepatic venous levels reached early (2 min) and later (5 min) during a constant infusion were compared during administration via the two routes and found to be equal. Parenchymal cell functions (ICG extraction, bile salt stimulation of bile flow) indicate that blood from the artery and portal vein supplies the hepatic parenchymal cells equally well. This suggests a well-mixed blood supply prior to exposure of either blood stream to parenchymal cells. Substances being processed by the liver are thus equally well handled if reaching the liver via either the arterial or portal blood stream. This has significance in validating the use of some isolated liver perfusion methods that perfuse only via the portal vein. Access of vasoactive compounds in the two blood streams to hepatic arterial resistance vessels was assessed using electromagnetic flow probes. The infusion of adenosine and angiotensin produced dilation and constriction respectively of the hepatic artery with the effect being about 3 times as large at a given dose when infused via the artery. The data show that vasoactive substances in the portal blood can affect the hepatic arterial blood flow by Utransvascular" route and that portal blood has quite a high access to hepatic arterial resistance vessels. It does indicate, however, that the arterial resistance sites are not being perfused with mixed portal and arterial blood. The hepatic blood volume changes in responses to intraportal and intraarterial infusions of angiotensin and noradrenaline were measured using an in vivo plethysmograph assembled around the intact liver. Constriction of hepatic blood volume was equal with administration via the two routes indicating that the capacitance vessels are perfused by well-mixed blood and are, therefore, likely to consist mostly of sinusoidal and postsinusoidal vessels with presinusoidal roles being minor or absent. The hepatic acinus is the functional unit of the liver (1). The acinus represents a cluster of hepatic parenchymal cells roughly 2 mm in diameter that is perfused by a
Microvascular Research, 1987
Portal venous pressure was controlled by resistance localized to specific sites in hepatic lobar veins in cats. All of the pressure drop from the portal vein to the vena cava occurred across postsinusoidal vessels; portal pressure, lobar venous pressure, and, therefore, sinusoidal pressure were not significantly different. Norepinephrine and angiotensin infusions (intraportal) caused elevation in portal pressure due to constriction of hepatic venous resistance sites as well as some constriction of presinusoidal (portal or sinusoidal) resistance sites. At low doses of norepinephrine presinusoidal constriction dominated whereas at higher doses the postsinusoidal constriction increased proportionately more. Hepatic nerve stimulation produced a similar response measured at an early time (1 min), but by 3 min the presinusoidal constriction showed complete escape so that elevated portal pressure was entirely due to hepatic venous constriction. The same site that provided basal vascular resistance also provided the increased hepatic venous resistance with nerve stimulation and infusion of angiotensin and norepinephrine. Rapid elevation of central venous pressure (CVP) caused elevated sinusoidal pressure. At high CVP (16 mm Hg), 75% of a rise in CVP was transmitted whereas at normal CVP (<4.5 mm Hg) less than 20% transmission occurred. The presence of a high resistance in the hepatic veins protected intrahepatic pressure from the effects of normal fluctuation of CVP.
The Journal of physiology, 1983
1. Dogs were anaesthetized with chloralose, ventilated artificially, and the regions of the aortic arch and carotid sinuses were isolated vascularly and perfused with blood. The abdominal circulation was isolated vascularly, perfused at constant flow and drained from the inferior vena cava at constant venous pressure. Changes in vascular resistance were determined by calculating changes in abdominal aortic perfusion pressure, and changes in capacitance by integrating the changes in venous outflow. 2. Stimulation of aortic body chemoreceptors, either by changing the aortic arch perfusate from arterial to venous blood at constant perfusion pressure or by injection of sodium cyanide into the aortic arch, resulted in an increase in abdominal vascular resistance and a decrease in abdominal vascular capacitance. 3. After both cervical vagosympathetic trunks had been cut, stimulation of aortic chemoreceptors no longer resulted in resistance or capacitance responses. 4. These results indica...
Hind-limb vascular-capacitance responses in anaesthetized dogs
The Journal of physiology, 1983
In anaesthetized dogs a hind limb was vascularly isolated, perfused through the femoral artery at either constant flow or constant pressure and drained from the femoral vein at constant pressure. Inflow and outflow were recorded. Vascular-resistance changes were calculated from changes in pressure or flow and volume changes from the differences between inflow and outflow. During constant-flow perfusion, both changes in carotid sinus pressure and direct stimulation of efferent sympathetic nerves resulted in large resistance responses. However, changes in carotid sinus pressure did not result in changes in limb blood volume and only small decreases were obtained in response to direct stimulation. During constant-pressure perfusion, both reflex and direct stimulation resulted not only in significant changes in resistance but also in significant volume changes which were much larger than those obtained during constant-flow perfusion. Similar responses were obtained when the flow rate wa...
The Journal of physiology, 1983
1. In anaesthetized dogs the regions of the carotid bifurcations were isolated vascularly and perfused at constant non-pulsatile pressures. The abdominal circulation was isolated vascularly, perfused at constant flow and drained through the inferior vena cava at constant pressure. Vascular resistance and capacitance responses were determined from the changes in perfusion pressure and changes in venous outflow. 2. Stimulation of carotid chemoreceptors with venous blood resulted in an increase in arterial perfusion pressure of 38% (S.E. +/- 4.6) and a decrease in vascular capacitance of 24.4 +/- 2.5 ml. (1.05 +/- 0.24 ml. kg-1). 3. When carotid perfusion pressure was higher than 17 kPa, stimulation of chemoreceptors resulted in significantly (P less than 0.05) smaller resistance responses but significantly (P less than 0.05) greater capacitance responses than those obtained at lower carotid pressures. 4. These results show that abdominal resistance and capacitance vessels constrict in...
Journal of Surgical Research, 1978
There is debate about the extent of mixing of hepatic arterial and portal venous blood in the liver parenchyma and also about the precise anatomical site at which this happens [81. Current concepts suggest that the two inflows of blood mix completely either before or in the sinusoids of the liver [ 151, and it is therefore presumed that the hepatic parenchyma has a completely mixed blood flow. This view is supported by investigations using labeled indicators which show that all but a very small fraction of the total hepatic vascular bed is common to both inputs [4, 71.
Experimental Physiology, 1997
The existence of abdominal arterial baroreceptors has long been controversial. Previously difficulties have been encountered in localizing a stimulus to abdominal arteries without affecting reflexogenic areas elsewhere. In these experiments, using anaesthetized dogs, the abdomen was vascularly isolated at the level of the diaphragm, perfused through the aorta, and drained from the inferior vena cava to a reservoir. Changes in abdominal arterial pressure were effected by changing the perfusion pump speed. During this procedure the flow back to the animal from the venous outflow reservoir was held constant. Increases and decreases in abdominal arterial pressure resulted, respectively, in decreases and increases in perfusion pressure to a vascularly isolated hindlimb and in some dogs also a forelimb. Responses were significantly larger when carotid sinus pressure was high (120-180 mmHg) than when it was low (60 mmHg). Responses were still obtained after cutting vagus, phrenic and splanchnic nerves, but were abolished by spinal cord lesion at T12. These experiments provide evidence for the existence of abdominal arterial baroreceptors. The afferent pathway for the reflex vasodilatation appears to run in the spinal cord.