Middle Hepatic Artery Research Articles

Hepatic falciform ligament artery: angiographic anatomy and clinical importance.

The hepatic falciform ligament artery (HFLA) was evaluated by angiography and also by dissections. Based on the findings, the mechanism of the post-chemoembolization skin rash was studied. A total of 340 liver cirrhosis patients who underwent hepatic artery chemoembolization for hepatocellular carcinoma were reviewed in terms of the angiographic incidence of the HFLA, variations in its origin, and the incidence of skin rash. The HFLA was demonstrated in 26 (7.6%) of the 340 patients on angiography. Two HFLAs were observed in one patient. The origin was the middle hepatic artery (A4) in 16 cases, the superior branch of the middle hepatic artery in three, the inferior branch of the middle hepatic artery in two, the inferior branch of the left hepatic artery (A3) in three, and the confluence of A3 and A4 in three cases. There were no patients who developed post-chemoembolization skin rash. Two cadavers were dissected to investigate the anastomosis between the HFLA and the subcutaneous artery. Two different anastomoses were found: (1) direct and (2) via the ensiform branch of the internal thoracic artery. These were located at the lower and upper part of the falciform ligament, respectively. The distribution of a chemotherapeutic agent through these anastomoses is the likely cause of post-chemoembolization skin rash. If prophylactic embolization of the proximal portion of the HFLA using a metallic coil is performed, the skin rash will be prevented.

Endothelin release is augmented with captopril in rat ischemia-reperfusion injury of the liver.

The reactive oxygen metabolites (ROMs) and the vascular endothelial factors such as endothelins (ETs) and thromboxane A2 (TxA2) were found to be mediators of the reperfusion component of ischemia-reperfusion (I/R) injury. Captopril (CPT), a sulfydryl (-SH) group containing angiotensin-converting enzyme inhibitor, has been shown to reverse I/R injury by its ROM scavenging effect. In this experimental study, the effects of CPT and BM 13.177 (a TxA2 receptor antagonist) were assessed on liver I/R injury in rats. Four groups of Wistar albino rats were either sham-operated, control, CPT or BM 13.177-treated. The middle and left lateral hepatic arteries and portal veins were occluded in each group but the sham and the corresponding agents were given to the animals prior to I/R injury. After I/R injury, blood was drawn from the suprahepatic inferior vena cava for ET-1-like activity assay and liver tissue samples were obtained for the determination of prostaglandin E2 (PGE2), leukotriene C4 (LTC4) and histopathologic examination. PGE2 and ET-1 levels were increased significantly in the control group compared with the sham-operated group. In the CPT group, LTC4, PGE2 and ET-1 levels were significantly increased compared with the control group, while only ET-1 levels were not different from those of the control group in the BM 13.177-treated group. It is concluded that ET-1 release increases in response to I/R injury in rat liver and CPT further increases this release. It also appears that CPT has a stimulatory effect on arachidonic acid metabolism in addition to its free radical scavenging effect.

The effect of isradipine in acute altitude hypoxia on cerebral, renal, and splanchnic blood flow evaluated by Doppler measurements

Recent studies have suggested that calcium antagonists may have a beneficial effect on high altitude pulmonary edema, but the effect on regional blood flow distribution is unknown. This study by transcranial and duplex Doppler evaluated the effect of the calcium antagonist isradipine on cerebral, renal, and splanchnic blood flows in acute altitude hypoxia. Twelve healthy subjects were investigated at sea level and repeatedly after 3–56 hours at high altitude (4350 m). Before the ascent, the subjects were randomized to treatment with isradipine 5 mg/day (n = 6) or placebo (n = 6). We measured flow velocities in middle cerebral arteries; flow rates in internal carotid arteries, portal vein, and right renal artery; and resistance indices in middle cerebral, internal carotid, renal, superior mesenteric, and hepatic arteries. Hypoxia increased middle cerebral artery flow velocity by 30% (placebo, p < 0.05) and 39% (isradipine, p < 0.01); increased internal carotid artery flow rate by 57% (placebo, p < 0.01) and 55% (isradipine, p < 0.05); and decreased middle cerebral and internal carotid artery resistance indices without differences between placebo and isradipine groups. Superior mesenteric artery resistance index was lower in hypoxia with isradipine compared with placebo (p < 0.05), suggesting a higher splanchnic blood flow. In conclusion, acute hypoxia induced an increase in cerebral blood flow. Besides decreasing superior mesenteric artery resistance index, prophylactic isradipine did not modulate the circulatory responses to acute hypoxia. The clinical significance of this increased splanchnic blood flow remains unclear.

Analysis of branching patterns of middle hepatic artery using A-P and oblique view hepatic angiography

Analysis of branching patterns of middle hepatic artery using A-P and oblique view hepatic angiography

Experimental study on the pathogenesis of acute acalculous cholecystitis, with special reference to the roles of microcirculatory disturbances, free radicals and membrane-bound phospholipase A2

To elucidate the pathogenesis of acute acalculous cholecystitis, the gallbladder was subjected to ischemia-reperfusion by simultaneously occluding the middle hepatic artery and the superior mesenteric vein in dogs, and the degree of inflammation and biochemical changes in the gallbladder mucosa were studied by varying the duration of ischemia or reperfusion. Ischemia alone did not induce cholecystitis either macroscopically and histologically, although it increased phospholipase A2 (PLA2) activity, content of lipid peroxide, and superoxide dismutase (SOD) activity in the mucosa with prolongation of the ischemic time. Cholecystitis was produced in all animals by 45-min ischemia followed by 90-min reperfusion as the shortest ischemia and reperfusion times. In this model, prolongation of the ischemic time increased the area of mucosal inflammation horizontally with increases of the PLA2 activity, content of lipid peroxide, and SOD activity, whereas by prolonging the reperfusion time the inflammation area spread deeper vertically toward the serosal side with significant increase in the mucosal PLA2 activity, content of lipid peroxide, and SOD activity. These results revealed that ischemia-reperfusion plays an important role in the pathogenesis of acute acalculous cholecystitis, causing the generation of free radicals and the activation of membrane-bound PLA2.

Changes of Contractile and Endothelium-Dependent Relaxant Responses Following a 2-H Hemorrhagic Hypotension in Cats

The effect of hemorrhagic shock on the reactivity of feline middle cerebral (MCA), mesenteric (MES), brachial (BRACH), renal (REN), and hepatic (HEP) arteries was studied in vitro. In sodium pentobarbital-treated cats, a steady level of hypotension (50 mm Hg) was reached by bleeding into a reservoir and maintained by further bleeding or autotransfusion during 2 h (shock). Rings of the arteries (from control animals and from animals after shock) were suspended for isometric tension recording in organ chambers.

Surgical anatomy of the hepatic hilum with special reference to the caudate lobe.

AbstractThe portal triad around the hepatic hilum, including the caudate lobe, was investigated using 106 adult cadavers. The portal vein showed regular branching at the hepatic hilum. The round ligament was attached mainly to the pars umbilicalis of the left branch of the portal vein (81.3%), especially to its lower portion (64.6%). Typical extrahepatic branching of the hepatic artery was noted in 67% of the cadavers. Intrahepatic branching of the middle and left hepatic arteries showed some variations in 9.4% and 12.5% of the cadavers, respectively. The cystic artery originated from the right hepatic artery in 84.4% of the cadavers, and a dual cystic artery was observed in 30.2%.An aberrant hepatic duct, previously reported as an accessory hepatic duct, was observed in 9.0% of the cadavers; each entered the common hepatic duct on the right side. With reference to the course of bile duct and hepatic artery, the middle hepatic artery traversed the left main hepatic duct anteriorly in 13.5% of the cadavers, and ran partly in front of the duct in 52.0%. Furthermore, the right hepatic artery or its branches traversed the right main hepatic duct anteriorly in 9.4% of the cadavers and ran partly in front of the duct in 38.5%. The caudate lobe is supplied by both the right and left branches of the portal triad, mainly by the left. The caudate process is mainly supplied by the posterior branches of the portal triad, being continuous with the posterior segment of the liver.

Mycotic embolism and embolomycotic aneurysms. Neglected lessons of the past.

During the past decade, nine patients with bacterial endocarditis have required management of mycotic emboli and/or aneurysms in this center. In these patients, 25 separate mycotic emboli or aneurysms were identified. Among these were four visceral, 11 lower extremity, one aortic, one hypogastric, and eight cerebral lesions. Multiple sites were involved in seven of the nine patients (78%). Presenting symptoms were secondary to acute expansion of mycotic aneurysms in three patients and secondary to rupture of aneurysms in four patients. Mycotic emboli produced cerebral infarction in two patients and acute ischemia in six patients. Asymptomatic mycotic aneurysms of the middle cerebral, hepatic, hypogastric, and profunda femoris arteries and asymptomatic emboli to the profunda femoris and tibial arteries were found during angiographic study. Management included resection alone (7 aneurysms), resection and graft replacement (2 aneurysms and 2 emboli), embolectomy (2), or observation. There was no mortality or loss of limb in these patients. This experience underscores the frequent multiplicity of mycotic emboli and/or aneurysms and stresses the importance of empiric angiographic survey to exclude silent yet potentially lethal visceral and cerebral mycotic foci in patients with bacterial endocarditis and peripheral emboli or aneurysms.

Protean manifestations of mycotic aneurysms.

Nine patients examined by arteriography were shown to have mycotic aneurysms involving the thoracic aorta, subclavian artery, renal artery, middle cerebral artery, hepatic artery, and splenic artery. Patients presented with sepsis, chest pain, mediastinal mass, headache, hypertension, and intraperitoneal bleeding. Etiologic factors included endocarditis, septicemia, drug abuse, and poorly controlled soft-tissue infection. Most mycotic aneurysms were virulent processes with rapid progression and only three of the nine patients (33%) survived. Since mycotic aneurysms may be associated with rapid progression and poor prognosis, early recognition is mandatory.

Arterial collaterals in intrahepatic arterial occlusion.

Two cases are reported, where intrahepatic peripheral arterial collaterals were angiographically observed. In one case the collateral artery connected the subsegmental arteries of the dorso-caudal and ventro-cranial segments; in the other collateral circulation existed between the ventro-cranial segmental artery and the middle hepatic artery. Thus, the segmental arteries of the liver are not always end arteries. A schematic drawing of the hitherto angiographically confirmed collaterals is given.