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.
SUMMARY1. The splenic artery flow, the splenic weight and the arterial blood pressure were recorded in cats anaesthetized with sodium pentobarbitone.2. Oscillations in splenic artery flow and splenic weight were observed. Following occlusion and release of the splenic artery, there was a brief increase in flow to above the pre-occlusion level and the oscillations in flow were greatly increased in amplitude. It is suggested that the brief increase is a consequence of the reduction of arterial pressure and that the oscillations are due to synchronization of rhythmic activity of smooth muscle within the spleen.3. Stimulation of the splenic nerves resulted in decreases in splenic artery flow and splenic weight. The size of the responses varied with the frequency of stimulation and maximum responses in both flow and weight were obtained at about 3 impulses/sec. 4. After stimulation for 10 min, the splenic weight response was maintained while the flow response showed some recovery towards the control level.5. When the splenic artery flow was reduced to about half the control level for periods up to 2 hr, the flow and weight responses to stimulation of the splenic nerves remained unchanged; the significance of this after a haemorrhage is discussed.6. Intravenous administration of atropine or propranolol did not affect the responses to nerve stimulation. After phenoxybenzamine, nerve stimulation caused a smaller decrease in splenic weight, while the splenic artery flow increased to above the control level. this increase was unaffected by atropine but abolished by propranolol.
The hepatic arterial blood flow of cats anesthetized with pentobarbital was recorded with an electromagnetic flowmeter. Administration of isoprenaline by close arterial infusion caused a vasodilatation which was blocked after propranolol. Adrenaline caused a variable change but after propranolol it consistently produced vasoconstriction, and after phenoxybenzamine, vasodilatation. One hour after phenoxybenzamine, stimulation of the sympathetic nerves caused a marked vasodilatation which was blocked by propranolol. It is concluded that both α and β adrenergic receptors are present in the hepatic arterial bed. However, β receptor responses may be difficult to elicit if the basal tone of the vascular bed is already reduced by prior procedures.
SUMMARY1. In cats, a venous long-circuit technique was used to measure the blood flows in the superior vena cava and the hepatic, renal and iliac segments of the inferior vena cava. The sum of these flows gave the venous return (minus coronary and bronchial flows). In further experiments using an electromagnetic flowmeter, flow in the portal vein and in the superior mesenteric and coeliac arteries was measured.2. Approximately two-thirds of the hepatic blood flow is derived from the portal vein.3. After block of conduction in the cervical region of the spinal cord, the proportions of the venous return coming from each region during the control periods were not significantly altered although the arterial pressure and total venous return were decreased.4. Intravenous infusions of adrenaline caused an increase in venous return which was associated with a marked increase in hepatic blood flow. The increase in hepatic blood flow was due to an increase in flow in the superior mesenteric artery and portal vein. Flow in the coellac artery remained unchanged. This response was unaffected by block of the cervical region of the spinal cord and by atropine or pentolinium.5. Intravenous infusions of noradrenaline caused little change in venous return or regional blood flows. Small increases in superior mesenteric artery flow were occasionally seen and on cessation of the infusion a large but brief increase occurred. These facts suggest that noradrenaline has a similar action to adrenaline but this is masked by concomitant vasoconstriction.
SUMMARY1. In cats under pentobarbitone anaesthesia, a venous long-circuit technique was used to measure the blood flows in the superior vena cava and the hepatic, renal and iliac segments of the inferior vena cava. The sum of these flows gave the venous return (minus coronary and bronchial flows).2. In these preparations, the mean venous return was 130 ml./kg. Of this 28 % came from the superior vena cava and 37 % from the hepatic, 23 % from the renal and 12 % from the iliac segments of the inferior vena cava.3. After haemorrhage, the flows from all the venae cavae segments decreased. The quantitative changes varied with the particular cat, the degree and duration of the haemorrhage and whether the animal had been subjected to a previous haemorrhage.4. The proportion of the reduced venous return draining from the superior vena cava and the hepatic segment increased, that draining from the renal and iliac segments decreased. Vasoconstriction occurred in all vascular beds, but was greatest in the kidney and hind limbs. Thus the blood flow through the head and liver was partially maintained at the expense of that through the kidneys and hind limbs.5. Autoregulation of blood flow in the kidneys was usually seen immediately after the first removal of blood but with the onset of renal vasoconstriction it was reduced or abolished for the remainder of the experiment.
A / b e~m Received Marcla 23, 1968 GREENWAY, C. V.. ANLB LAWSON, A. E. 1968. Effect of adrenaline and propranolol on the superior ~nesealkeric artery blood flow. Can. 3. Physiol. Pharmasol. 46, 986-908.Adrenaline infusions into the sa~pesior rnesenteric artery caused a marked increase in sa~perior mcsenteris arlery blond flow with little change in arterial pressure. This vasodilation was blocked after the intraveaaous administration of propranolor. e'crr'diO/ogy Deparfmertt, W~qk'ul Vicforio ffos~~irnl. /kgorrirerrl, QtdebecReceived h'larclt 22, 1968 ~%NLPERXXJ, W. h4., AND BRAKDH, G. 1968. Regional myoglobin concentration in the myocardium of the dog. Caw. J. Physiol. Phar~nacol. 46, 908-910.It has been demonstrated previously that chronic ltyposia leads to an iancrease in tnyog8obin concentration, Evidence of differences in Po2 and blood flow in deep and siiperficia1 layers of cardiac rnalscle suggest that there naight be a corresponding difTcrcnce in tnyoglobin concentration in the anyscar'diiam.Kesults showed an even distrib~~tiasn of rrzyoglobin concentration in inner and outer layers of the: left ventricular wall, right ventricle, and septiam, suggestiaag that &, in inner layers of the left ventricular wall is not sufficiently diminished to stimulate an increase in myoglobin concentration.
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