The effects of stimulation of the hepatic nerves, infusions of noradrenaline and occlusion of the carotid arteries on liver blood flow in the anaesthetized cat

Abstract

SUMMARY1. In anaesthetized cats, the hepatic artery, portal vein and inferior vena cava pressures and the hepatic artery and portal vein flows were recorded using pressure transducers and electro-magnetic flowmeters.2. The hepatic nerves were stimulated with maximal stimuli for periods of 2-5 min. The magnitude of the response varied with the frequency of stimulation over the range 1-10 impulses/sec. The resistance to flow increased in both the hepatic artery and the portal vein.3. In the hepatic artery, mean pressure remained virtually constant, while the flow showed an initial marked decrease followed by a return towards the control level. In the portal vein, the flow remained constant while portal pressure showed a maintained increase. These responses were unaffected by previous administration of atropine and propranolol, but were blocked by phenoxybenzamine.4. Infusions of noradrenaline into the hepatic artery produced changes similar to those following stimulation of the nerves. In contrast, when the hepatic arterial pressure was maintained constant, intravenous infusions of noradrenaline produced a maintained decrease in hepatic artery flow.5. The occurrence of autoregulation of the hepatic artery flow at arterial pressures above 80-100 mm Hg was confirmed.6. Occlusion of the carotid arteries caused a rise in arterial pressure with little change in hepatic artery flow, but when the hepatic artery pressure was maintained at the pre-occlusion level the flow showed an abrupt decrease, usually followed by a recovery towards the control level. This decrease was abolished by section of the hepatic nerves and removal of the adrenal glands.

Comparison of the effects of hepatic nerve stimulation on arterial flow, distribution of arterial and portal flows and blood content in the livers of anaesthetized cats and dogs

“…In both organs, escape occurs during constant flow perfusion and the initiating factor cannot be the decrease in total arterial flow (Dresel & Wallentin, 1966;Greenway et al 1967). However, as Dresel & Wallentin pointed out, these experiments did not exclude the possibility that a local accumulation of metabolites or the opening of shunt vessels results in a redistribution of the flow through certain areas of the organs.…”

“…This was not due to failure of the nerves since the increase in portal pressure was well maintained and we have since shown that the decrease in hepatic blood content during nerve stimulation was also maintained for at least 20 min (Greenway, Stark & Lautt, 1969). The escape was greater during hepatic nerve stimulation than during noradrenaline infusions and was not modified after fi-adrenergic blocking agents (Greenway et al 1967;Ross & Kurrasch, 1969). In a recent review, we placed considerable emphasis on this autoregulatory escape as a mechanism of protecting the liver from hypoxia due to sustained vasoconstriction ).…”

“…The methods have been discussed critically in previous papers (Greenway et al 1967;Greenway et al 1969;Greenway & Lautt, 1970;Greenway & Oshiro, 1972). In this comparison of the responses to nerve stimulation in cats and dogs, the methods used in each species were as similar as possible and the same equipment was used for both.…”

“…The mean responses expressed as percentage changes in hepatic arterial conductance (flow divided by arterial minus hepatic venous pressure) are shown in Fig. 3 was prolonged beyond 3 min, the flow continued to recover towards the control level as previously described (Greenway et al 1967). On cessation of stimulation, a small post-stimulatory hyperaemia occurred in both cats and dogs.…”

Further observations on mesenteric vasoconstriction, survival and the clotting defect after endotoxin administration

“…Superior mesenteric arterial flow or hepatic arterial flow was recorded with a non-cannulating flow probe connected to an electromagnetic flowmeter (Nycotron, Oslo) as previously described (Greenway, Lawson & Mellander, 1967;Greenway & Murthy, 1971). Renal flow was recorded by a long-circuit from the left renal vein to the left external jugular vein through an extracorporeal flow probe; these cats were given heparin (10 mg/kg) intravenously before the long-circuit was set up.…”