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At least 19 recordsLinked to original sources
PubMed1977

Glucagon inhibition of hepatic arterial responses to hepatic nerve stimulation.

The hepatic arterial vascular bed of the chloaralose-urethan-anesthetized dog was perfused with blood from a cannulated femoral artery. Hepatic arterial blood flow and perfusion pressure were measured. The hepatic periarterial postganglionic sympathetic nerves were stimulated supramaximally at 0.1, 0.5, 1, 2, 5, 10, and 20 Hz; this caused frequency-dependent rises in the calculated hepatic arterial vascular resistance at all frequencies above the threshold of 0.1 or 0.5 Hz. Glucagon was infused intra-arterially in dosese from 0.25 to 10 microgram/min; glucagon antagonized both the vasoconstrictor effects of hepatic nerve stimulation and of intra-arterial injections of norepinephrine. The degree of antagonism of these responses was significantly correlated with the calculated hepatic arterial glucagon concentration. It is possible that glucagon released physiologically in stress and hypoglycemia may protect the hepatic arterial vasculature from the effects of increased sympathetic discharge.

Animals↗
PubMed1978

The effects of intraportal infusions of glucagon on the hepatic arterial and portal venous vascular beds of the dog: inhibition of hepatic arterial vasoconstrictor reponses to noradrenaline.

The sympathetically-innervated hepatic arterial and portal venous vascular beds of the dog were perfused simultaneously in situ. Glucagon was infused into the hepatic portal vein (1--10 microgram/min); it caused increases in hepatic portal vascular resistance and tended to reduce the hepatic arterial vascular resistance. Extrahepatic effects of intraportal infusions of glucagon included increases in superior mesenteric blood flow and heart rate and falls in systemic arterial pressure. A test dose of noradrenaline (10 microgram) injected into either the hepatic artery or the portal vein caused both hepatic arterial and portal venous vasoconstriction. The hepatic arterial constrictor responses to noradrenaline were antagonized by intraportal infusions of glucagon. In contrast, intraportal glucagon did not antagonize the portal constrictor responses to intraarterial or intraportal noradrenaline. Elevated portal blood glucagon concentrations may "protect" the hepatic arterial blood flow from vasoconstriction due to elevated systemic levels of vasoactive substances including catecholamines.

Animals↗
PubMed1979

Bile duct cysts secondary to liver infarcts: report of a case and experimental production by small vessel hepatic artery occlusion.

Hepatic bile duct cysts were demonstrated on an abdominal CT scan and confirmed at autopsy in a patient with polyarteritis nodosa. The cysts developed in close proximity to hepatic artery aneurysms and occlusions visualized at hepatic arteriography and confirmed postmortem. The development of similar bile duct cysts following hepatic artery occlusion was demonstrated in 13 Rhesus monkeys.

Aneurysm↗
PubMed1975

Changes in lactic dehydrogenase isoenzymes after hepatic artery ligation in patients with hepatic carcinoma.

Serum activities of LDH isoenzymes as well as total LDH, GOT and GPT were determined after hepatic artery ligation in five patients with primary or metastatic liver cancer. Transaminases and total LDH activities were raised after the operation showing their peaks on the first or third postoperative days. LDH2, LDH3 and LDH5 increased substantially during the first three postoperative days. These changes became nearly normalized within two weeks after hepatic artery ligation. As control the same enzymatic activities were measured in eight patients after usual laparotomies but no significant abnormalities were observed postoperatively. Thus, liberation of not only cathodic but also anodic migrating LDH isoenzymes seems to ensue possibly after acute liver damage induced by hepatic artery ligation. This study also suggests that serial determination of LDH isoenzymes as well as its total activity could be a valuable assessment for evaluating the anti-tumor effect of hepatic artery ligation.

Adenocarcinoma, Papillary↗
PubMed1977

The role of beta-adrenoceptors in the responses of the hepatic arterial vascular bed of the dog to phenylephrine, isoprenaline, noradrenaline and adrenaline.

1 The sympathetically-innervated hepatic arterial vascular bed of the dog was perfused from a femoral artery. Hepatic arterial blood flow and perfusion pressure were recorded continuously, and the hepatic arterial vascular resistance (HAVR) calculated from these measurements.2 Intra-arterial injections of phenylephrine caused dose-dependent rises in HAVR, indicating hepatic arterial vasoconstriction, at all doses above threshold. No secondary reductions in HAVR followed these responses.3 Intra-arterial injections of isoprenaline caused only dose-dependent reductions in HAVR at doses above threshold.4 Intra-arterial injections of noradrenaline typically caused an initial increase in HAVR which was followed at all but the highest doses by a secondary, delayed, reduction in HAVR.5 Intra-arterial injections of adrenaline, like those of noradrenaline, resulted in hepatic arterial vasoconstriction followed by hepatic arterial vasodilatation.6 On a molar basis, the most potent hepatic arterial vasoconstrictor was noradrenaline, followed by adrenaline and phenylephrine.7 The maximum reductions in HAVR caused by adrenaline (mean reduction = 21.9%) and noradrenaline (16.9%) were significantly smaller than those due to isoprenaline ((P) < 0.001).8 Propranolol attenuated the hepatic arterial vasodilator responses due to isoprenaline, and the secondary falls in HAVR following intra-arterial adrenaline and noradrenaline.9 Propranolol did not modify the vasoconstrictor responses to phenylephrine.10 Both adrenaline and noradrenaline were more potent hepatic arterial vasoconstrictors after propranolol than in the absence of beta-adrenoceptor blockade. The potentiation of the vasoconstrictor effects of adrenaline was statistically significant.11 After propranolol, adrenaline was a more potent hepatic arterial vasoconstrictor than noradrenaline.12 Since the beta-adrenoceptors in the hepatic arterial vasculature were not blocked by atenolol, but were stimulated by salbutamol, it is concluded that they are predominantly of the beta(2)-type.13 The vasoconstrictor actions of phenylephrine, noradrenaline and adrenaline were all antagonized by the systemic administration of phentolamine, all three dose-response curves being shifted to the right.14 The results are discussed with regard to the possible control of the hepatic arterial vasculature by naturally-occurring catecholamines.

Albuterol↗
PubMed1978

The effects of intra-arterial and intraportal injections of vasopressin on the simultaneously perfused hepatic arterial and portal venous vascular beds of the dog.

The hepatic arterial and hepatic portal venous vascular beds of the chloralose-urethane anesthetized dog were perfused simultaneously in situ. Vasopressin (10 mU = 1 unit) was injected in graded increasing doses into the hepatic artery and into the portal vein. Both intra-arterial and intraportal vasopressin elicited both hepatic arterial vasoconstriction and hepatic venous dilation; the delay in onset of both hepatic vascular effects was significantly shorter than that for any succeeding systemic effects (a rise in systemic arterial pressure and fall in heart rate), showing that they were not attributable to recirculation or to arterial baroreceptor reflexes. Injections of vasopressin into the inferior vena cava at the level of the hepatic veins consistently produced smaller hepatic vascular effects than either intra-arterial or intraportal injections of the same doses. The results are discussed in the context of the therapeutic role of vasopressin in controlling gastrointestinal bleeding and portal hypertension.

Animals↗
PubMed1979

Hepatic artery ligation.

The use of hepatic artery ligation (HAL) in various clinical situations is illustrated by presenting a series of eight patients. The indications for HAL included ruptured hepatic tumors, spontaneous liver rupture, delayed hemorrhage after liver trauma, hematobilia, hepatic artery aneurysm, and hemorrhage after liver biopsy. Conventional methods of hemostasis had been used in some of these patients, but failed to control hemorrhage. The reasons for the relatively late adoption of hepatic artery ligation in treating liver hemorrhage are discussed and placed in proper prospective. Hepatic artery ligation has been shown to be such an effective method of controlling hemorrhage from the liver that other methods, such as packing and mass suture, which are unsafe and ineffective, should be abandoned. Major resection should be done only when an entire lobe of the liver is reduced to pulp or when exposure and repair of the retrohepatic vena cava are necessary.

Adult↗
PubMed1978

Liver necrosis following hepatic artery transection due to trauma.

Hepatic artery ligation for control of bleeding liver wounds has gained widespread acceptance. Hepatic necrosis is rarely seen after this procedure has been performed. Recently, a patient with multiple organ injuries secondary to a gunshot wound to the abdomen underwent hepatic artery ligation and hepatic necrosis developed even though the portal venous system was normal.

Adult↗
PubMed1977

A comparison of the effects of bradykinin, 5-hydroxytryptamine and histamine on the hepatic arterial and portal venous vascular beds of the dog: histamine H1 and H2-receptor populations.

1 The hepatic arterial and hepatic portal venous vascular beds of anaesthetized dogs were separately perfused in different experiments.2 From measurements of perfusion pressures and blood flows in the two series of experiments, hepatic arterial vascular resistance (HAVR) and hepatic portal venous vascular resistance (HPVR) respectively were calculated.3 Bradykinin, 5-hydroxytryptamine (5-HT) and histamine were injected intra-arterially and intra-portally and dose-response curves constructed from these data.4 Bradykinin injected intra-arterially caused dose-dependent hepatic arterial vasodilatation, and with an ED(50) of 2.66 x 10(-13) mol was more potent than any other vasodilator agent yet examined on this vascular bed.5 Bradykinin injected intraportally at doses up to 10 times those which were maximal on the arterial circuit did not alter the calculated HPVR.6 5-HT injected intra-arterially caused weak and variable rises in HAVR, indicating vasoconstriction. The maximum rise in HAVR was much less than that attained with noradrenaline in the same preparations.7 5-HT injected intraportally caused dose-dependent rises in HPVR indicating portal constriction at doses above 15-100 mug: in some experiments small doses of 5-HT resulted in reductions in calculated HPVR.8 Histamine has previously been shown to cause hepatic arterial vasodilatation: by intraportal injection, it caused dose-dependent rises in HPVR.9 In order to examine the receptors responsible for the effects of histamine, dose-response curves were constructed before and after mepyramine and metiamide.10 On the hepatic arterial vascular bed, metiamide did not antagonize the vasodilator effects of intra-arterial histamine, but these effects were antagonized by mepyramine.11 Similarly on the hepatic portal bed, the rises in HPVR due to histamine were antagonized by mepyramine but not by metiamide.12 The effects of histamine on both the hepatic arterial and portal venous vascular beds of the dog are therefore mediated predominantly by histamine H(1)-receptors.

Animals↗
PubMed1978

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

1. The innervated hepatic arterial and portal venous vascular beds of the dog were perfused simultaneously, in situ. Under control conditions, the pressures, blood flows and calculated vascular resistances in these beds were similar to those previously reported in preparations where one bed was perfused alone. 2. The pressure-flow curves in both the hepatic arterial and portal venous vascular beds were almost linear over the pressure ranges 30--200 and 2.5--12.0 mmHg respectively. There was no evidence of pressure-induced autoregulation of flow in either circuit. 3. Increases in hepatic arterial blood flow and perfusion pressure were associated with a linearly related increase in hepatic portal vascular resistance. Occlusion of the hepatic artery caused a mean fall of 21.3% in portal vascular resistance. 4. Increases in hepatic portal blood flow and perfusion pressure were associated with a linearly related incease in hepatic arterial vascular resistance. Occlusion of the hepatic portal vein caused a mean fall of 16.0% in hepatic arterial vascular resistance. 5. Intra-arterial injections of noradrenaline (0.1--50 microgram) caused biphasic changes in hepatic arterial vascular resistance, and a rise in hepatic portal vascular resistance. Both hepatic vascular effects had a significantly shorter latency than any succeeding systemic cardiovascular effects. 6. Intraportal injections of noradrenaline (0.1--50 microgram) caused hepatic portal vasoconstriction, and a biphasic change in the hepatic arterial resistance. Both of these effects had a significantly shorter latency than any succeeding systemic effects. 7. Intra-arterial injections of isoprenaline (0.1--10 microgram) caused dose-dependent hepatic arterial vasodilatation but little change in portal vascular resistance. Intraportal isoprenaline caused little change in portal resistance but elicited dose-dependent hepatic arterial vasodilatation. 8. The time courses of the responses to intra-arterial and intraportal noradrenaline and isoprenaline indicate that the responses of the liver vascular bed which does not receive the direct injection were not due to recirculation of the vasoactive material. 9. It is postulated that vasoactive material injected into one inflow circuit of the liver elicits changes in the vascular resistance of the other inflow circuit by an intrahepatic effect.

Animals↗
PubMed1977

The effects of glucagon, secretin, pancreozymin and pentagastrin on the hepatic arterial vascular bed of the dog.

1 The sympathetically-innervated arterial vascular bed of the dog's liver was perfused from a femoral artery. Arterial blood flow and perfusion pressure were monitored continuously and the hepatic arterial vascular resistance (HAVR) calculated from these measurements. 2 Commercial preparations of secretin, pancroezymin, glucagon and pentagastrin were administered by intra-arterial (i.a.) injection and infusion. 3 Secretin and pancreozymin by injection caused dose-dependent hepatic arterial vasodilatation, and on a molar basis were both more potent than glucagon or pentagastrin. 4 Intra-arterial infusions of secretin and pancreozymin caused hepatic arterial vasodilatation at calculated blood concentrations close to those measured under physiological conditions by other investigators. The vasodilatation was of the same duration as that of the hormone infusions. 5 Pentagastrin by i.a. injection caused dose-dependent hepatic arterial vasodilatation; by i.a. infusion, vasodilatation occurred but there was marked 'escape' from the effects during the continued infusion. 6 As reported previously, glucagon by injection caused dose-dependent hepatic arterial vasodilatation of long duration; by infusion, glucagon caused vasodilatation that persisted after the cessation of the infusion. 7 Glucagon infused i.a. inhibited the vasoconstricter effects of i.a. noradrenaline, over the same range of infusions that caused hepatic arterial vasodilatation. 8 Secretin or pancreozymin did not antagonize the effects of noradrenaline on the hepatic arterial vascular bed at any doses used. 9 Pentagastrin did not antagonize the vasoconstrictor effect of noradrenaline whether hepatic arterial vasodilatation resulted from the pentagastrin infusion, or not. 10 These results are discussed with respect to the possible control of the hepatic arterial vascular bed by gastrointestinal hormones.

Animals↗
PubMed1979

Treatment of hepatic metastases by percutaneous hepatic arterial infusion.

Better palliation for patients with hepatic metastases requires improved quality and duration of survival with a low complication rate and acceptable expense. Eligible patients between 1967 and 1977 were treated with a program of systemic chemotherapy until progression of hepatic metastases, then hepatic arterial infusion and subsequent maintenance on systemic chemotherapy. The angiography department was able to place the infusion catheter into the common hepatic artery percutaneously in 85% of all patients. The reasons for failure appeared related to anatomic variations and not to the physical characteristics of the liver cancer. A group of 24 patients with colorectal cancer and another group of 28 patients with 13 different primaries were treated. The colorectal cancer patients attained a median treatment time of 8 months before hepatic arterial infusion, and 9 more thereafter. The median survival of 17 months is much better than that reported for systemic chemotherapy alone. In a group of 28 patients with various primaries treated in the same way, the median survival time was 10 months. The nature of complications and the 6% incidence were the same in both groups. In summary, this is a modality yielding improved quality of life and longer survival with a low complication rate and acceptable costs.

Antineoplastic Agents↗
PubMed1977

Hemobilia from ruptured hepatic artery aneurysm. Report of a case and review of the literature.

Hepatic artery aneurysm is a rare vascular disease associated with high mortality caused by massive hemorrhage or by complications following surgical treatment. Over the past twenty-five years it has been managed surgically with increasing success. Eighty reported cases of hepatic artery aneurysms ruptured into the biliary tree were reviewed and the etiology, clinical signs, diagnosis, and treatment of such an aneurysm are discussed. A personal case with an aneurysm of the right hepatic artery ruptured into the common hepatic duct is reported. The diagnosis was made before surgery by arteriography and the aneurysm was successfully managed by ligation of the right hepatic artery both proximal and distal to the aneurysm, closure of the communication between the common hepatic duct and the aneurysm, and choledochal drainage. Hemobilia secondary to hepatic artery aneurysm must be considered in thedifferential diagnosis of unexplained gastrointestinal hemorrhage.

Aneurysm↗