Various forms of the celiac trunk and its anastomoses with the superior mesenteric artery]

Three rare varieties of upper abdominal arteries were compared with similar cases in the anatomical literature. An attempt was made to obtain a classification of the supernumerary branches of the celiac trunk and of the anastomoses between the celiac trunk and the superior mesenteric artery. One or more supernumerary branches of the celiac artery can be observed: (1) the superior mesenteric artery; (2) an accessory hepatic artery; (3) a posterior pancreatic artery; (4) a colic artery; (5) an accessory splenic artery; (6) a connecting branch to the superior mesenteric artery, and (7) an inferior phrenic artery. The following types of anastomoses between the celiac artery and the superior mesenteric artery can be distinguished: (1) direct connection; (2) anastomoses within the hepatic artery; (3) anatomoses following pre- or postnatal stenosis, and (4) the pancreatic arcades. For the first type the theory of TANDLER (longitudinal anastomosis) is abandoned. The development of the second type is as yet unresolved. In the case of the last two types a postembryonal formation is possible.     

The blood supply of the stomach

156 abdominal preparations were explored by arteriography, corrosion and dissection. The stomach is vascularized by four well-anastomosed main arteries: the arteria gastrica dextra and sinistra and the arteria gastroepiploica dextra and sinistra. Other important vessels include: the arteria gastroduodenalis, the arteriae gastricae breves for the upper half of the greater curvature, a posterior gastric artery (36%), an accessory left gastric artery (12%) and an arteria supraduodenalis. The main vessels give rise to some very specific collaterals, e.g. the omental arteries that may form an omental arcade (44%), supra- and infra-pyloric branches, retroduodenal branches, rami cardiaci, esophagei and tuberales and an accessory left hepatic artery. The gastroduodenal artery always arises at a fixed point.     

Transhepatic approach for catheter ablation of accessory pathway in a child with complex congenital heart disease

We report on a 22-month-old boy with drug-resistant atrioventricular reentrant tachycardia and complex structural heart disease consisting of right atrial isomerism, mirror image orientation of the intrathoracic veins, hemi-azygos continuation to the left superior vena cava, separate drainage of the hepatic veins into the left-sided atrium, congenitally corrected transposition, pulmonary atresia, and atrial and ventricular septal defects.Access to the heart for radiofrequency (RF) ablation was obtained by percutaneous puncture of a hepatic vein, the left internal jugular vein, and femoral artery. The accessory pathway was localised to the free wall of the left-sided AV groove and successfully ablated. There were no procedure-related complications.RF ablation of an accessory pathway is feasible in young children with complex structural heart disease and abnormal systemic venous return. In such patients access to the heart must be planned with knowledge of the anatomy and judicious use of the hepatic venous approach.     

Accessory arteries supplying the human transverse colon

An accessory colic artery which arose from the superior mesenteric artery more proximally than the first jejunal artery and met the marginal artery at the splenic flexure was observed in 32 of 65 subjects (49.2%). Considering its constant morphological features, this accessory colic artery was given the new nomenclature 'superior left colic artery (arteria colica sinistra superior; CSS)'. The unusual middle colic artery arising from the celiac trunk was supposed to be caused by the anastomosis between the dorsal pancreatic artery from the CSS and that from the celiac trunk. An additional epiploic branch derived from the pancreatic branch (posterior epiploic branch) also sent an accessory colic artery in 2 subjects. But judging from its origin and area of distribution which overlaps with that of the middle colic artery, this accessory colic artery is not equivalent to CSS.     

Diminished hyperaemic response of the hepatic artery to portal venous occlusion (the buffer response) in Asian hybrid minipigs: a comparison of the response to that observed in dogs

The hyperaemic response of the hepatic artery to portal vein occlusion (the buffer response) and the action of exogenous adenosine upon hepatic artery blood flow was studied in Asian hybrid minipigs as a potential alternative experimental model to that previously developed in dogs. Adenosine produced a dose-dependent hepatic artery vasodilatation, but of lesser extent than that observed in dogs. A greatly diminished buffer response was observed in the pigs compared to that seen in dogs, and could not be replicated consistently. The adenosine uptake inhibitor dipyridamole did not potentiate responses to adenosine or the buffer response. It is concluded that the minipig is an unsuitable alternative model for the study of the hepatic artery buffer response.Abbreviations bw body weight - DPD dipyridamole - GDV gastroduodenal vein - HA hepatic artery - PV portal vein - PVO portal venous occlusion - PVP portal venous pressure - SE standard error     

Anatomical variations of the arterial pattern in the left hemiliver

The arterial supply to the left hemiliver was studied in 70 liver casts. The arteries were divided into 15 groups according to their origin and branching pattern. The left hemiliver was supplied by one artery in 53% of cases, by two arteries in 40% and by three arteries in 7%. The left hepatic artery, which originated from the proper hepatic artery, supplied all three left segments in 39% of specimens. The replacing left hepatic artery, which originated from the left gastric artery, supplied the whole left hemiliver in 3% of cases. The incomplete, replacing left hepatic artery supplied segments 2, 3 and a part of segment 4 in 6% of cases, and only segments 2 and 3 in 11%. There was one segmental artery for segment 2 in 86%, and two in 14%. Segment 3 was supplied by one artery in 87%, and by two in 13%. Segment 4 was supplied by one artery in 39% of cases, by two arteries in 43%, by three in 14% and by four arteries in 4%.     

Anatomical variations of the cystic artery

Thorough knowledge about the origin of the cystic artery is surgically important, especially when intraoperative or post-operative bleeding occurs in the gallbladder fossa. The arterial supply of the gallbladder was studied in 81 livers. The gallbladder was supplied by one cystic artery in 86% and by two arteries in 14% of cases. When a single artery was present, it originated from the right hepatic artery in 53% of livers. Other origins included the anterior or the posterior sectional hepatic artery, the replacing right hepatic artery, and in 5% of cases, segmental arteries for segments 4, 5, 6 and 8. When two cystic arteries supplied the gallbladder, both most commonly originated from the right hepatic artery (7% incidence). In 1% of cases, a subsegmental branch for segment 6 and a subsegmental branch for segment 5 respectively, originated from the cystic artery.     

Effect of the ligation of hepatic artery on the microcirculation in the cirrhotic liver in the rat.

The significance of the hepatic arterial supply in the intrahepatic microcirculation in normal and carbon tetrachloride-induced cirrhotic livers was studied by dye injection method and by ligation of the hepatic artery. The in vivo distribution of dye injected into the hepatic artery evidenced the presence of arterio-venous shunts in the cirrhotic liver. When the hepatic artery of the cirrhotic liver was ligated, the elevated portal venous pressure dropped significantly, and the fast-flowing population of microvessels and sinusoids in the bimodal frequency distribution plot disappeared. The fast-flowing microvessel and sinusoids appeared to be the "arterial" microvessels and sinusoids, and they were converted into the slow-flowing venous channels after hepatic arterial ligation. The transmission of arterial pressure via the A-V shunts may be of greater significance in the pathophysiology of portal hypertension than previously believed.     

Anatomical variations of the arterial pattern in the right hemiliver

The arterial supply to the right hemiliver was studied in 80 liver casts. The arteries were divided into 10 groups according to their origin and branching pattern. The right hemiliver was supplied by one artery in 96% of cases and by two arteries in 4%. When there was only one artery it originated from the proper hepatic artery in 73/77 cases and from the superior mesenteric artery in 4/77 cases. The replacing right hepatic artery which originated from the superior mesenteric vessel supplied the whole right hemiliver in 5% of cases. The incomplete replacing right hepatic artery which supplied only a part of the right hemiliver was found in 4% of cases. The anterior section (segments 5 and 8) was supplied by one artery in 61%, by two arteries in 30% and by three arteries in 9% of cases. The posterior section (segments 6 and 7) was supplied by one artery in 66%, by two arteries in 31% and by three arteries in 3% of cases. Segments 5 and 7 were predominantly supplied by one artery, whereas segments 6 and 8 by two arteries.     

Patterns of arterial supply of the human fetal liver. The significance of the accessory hepatic artery

One or two aberrant hepatic arteries were found in 30% of human fetal livers. The liver received a triple or double arterial supply. The aberrant artery arises from the left gastric or superior mesenteric arteries and supplies an entire lobe or more without joining the branches of the usual hepatic artery in 38.5%. The artery has an important significance for the arterial supply of the fetal liver.     

The use of 8-phenyltheophylline as a competitive antagonist of adenosine and an inhibitor of the intrinsic regulatory mechanism of the hepatic artery

Reduction of portal blood flow results in compensatory vasodilation of the hepatic artery, the hepatic arterial buffer response. The hypothesis tested is that the regulation of the buffer response is mediated by adenosine, where the local concentration of adenosine in the region of the hepatic arterial resistance vessels is regulated by washout of adenosine into portal venules that are in intimate contact with hepatic arterioles. In anesthetized cats, portal flow was reduced to zero by complete occlusion of all arterial supply to the guts. The resultant dilation of the hepatic artery compensated for 23.9 +/- 4.9% of the decrease in portal flow. Dose-response curves were obtained for the effect of intraportal adenosine infusion on hepatic arterial conductance in doses that did not lead to recirculation and secondary effects on the hepatic artery via altered portal blood flow. The dose to produce one-half maximal response for adenosine is 0.19 mg X kg-1 X min-1 (intraportal) and the estimated maximal dilation is equivalent to an increase in hepatic arterial conductance to 245% of the basal (100%) level. The adenosine antagonist, 8-phenyltheophylline, produced dose-related competitive antagonism of the dilator response to infused adenosine (but not to isoproterenol) and a similar, parallel antagonism of the hepatic arterial buffer response. If supramaximal blocking doses were used, the hepatic artery showed massive and prolonged constriction with blood flow decreasing to zero. The data strongly support the hypothesis that intrinsic hepatic arterial buffer response is mediated entirely by local adenosine concentration.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of glucagon on vasoconstriction and vascular escape from nerve- and norepinephrine-induced constriction of the hepatic artery of the cat

Glucagon, in the anesthetized cat, was capable of dilating the hepatic artery to the same extent and in a dose-dependent manner when administered directly into the hepatic artery or into the portal vein. Portal venous infusions of glucagon did not inhibit nerve- or norepinephrine-induced vasoconstriction of the hepatic artery in contrast to previous reports in the dog. Rather, at certain doses, glucagon mildly potentiated the vasoconstriction induced by both constrictor stimuli. Vascular escape from nerve- and norepinephrine-induced constrictor responses was found to be inhibited by glucagon in a dose-dependent manner. Glucagon infusion is the first intervention reported to modulate vascular escape in the hepatic artery. Owing to its similar effects on nerve- and exogenous norepinephrine-induced responses, glucagon appears to be acting at a postsynaptic site. Therefore, we suggest that in the cat, glucagon is not an inhibitory modulator of nerve- and norepinephrine-induced vasoconstriction, but rather may potentiate the constrictor response in a postsynaptic manner.     

Trehalases from the American cockroach,Periplaneta americana: multiple occurrence of the enzymes and partial purification of enzymes from male accessory glands

Trehalase activities were found in several tissues of the adult American cockroach, Periplaneta americana. Among these, male accessory glands, fat body, thoracic muscle, hepatic cecum, blood and mid-gut contained high trehalase activity; activity in the male accessory gland was especially high. The enzymic properties of soluble trehalases were investigated and the enzymes from the male accessory gland were highly purified.

The properties of these enzymes were electrophoretically and kinetically distinct from each other. The presence of enzymes with somewhat different properties in different tissues suggests that trehalose utilization and trehalase activity may be regulated by way of a tissue-specific mechanism. The detailed properties of these enzymes are presented with a discussion of their regulation.     

Blockade of nitric oxide synthase potentiates the suppression of vasodilators by norepinephrine in the hepatic artery.

We have previously shown that nitric oxide (NO) and adenosine suppress vasoconstriction induced by norepinephrine infusion and sympathetic nerve stimulation in the hepatic artery and superior mesenteric artery. NO is involved in the control of basal vascular tone in the superior mesenteric artery but not the hepatic artery. The vasodilation induced by adenosine is inhibited by NO in the superior mesenteric artery but not in the hepatic artery. Based on these known interactions of catecholamines, adenosine, and NO, the objective of this study was to test the hypothesis that NO modulates the interaction between vasoconstrictors and vasodilators in the hepatic artery. We examined the ability of norepinephrine to suppress adenosine-mediated vasodilation and the role of NO in this interaction. Hepatic arterial blood flow and pressure were monitored in pentobarbital-anesthetized cats. The maximum hepatic arterial vasoconstrictor response to norepinephrine infusion was potentiated by blockade of NO production using Nomega-nitro-L-arginine methyl ester (L-NAME), and the potentiation was reversed by L-arginine. The maximum dilator response to adenosine was only slightly suppressed (14.0+/-5.8%, P < 0.05) by norepinephrine infusion; however, after the NO blockade, the suppression by norepinephrine of the vasodilation induced by adenosine was substantially potentiated (45.2+/-9.1%, P < 0.05). Similar results were obtained for isoproterenol-induced vasodilation. We conclude that the interaction between these vasodilators and norepinephrine was modulated by NO which inhibited the vasoconstriction and the suppression of vasodilators caused by norepinephrine and that in the absence of NO production, norepinephrine-induced constriction and the ability to antagonize dilation is substantially potentiated.     

环颈雉胃的血供

用血管铸型法和大体解剖学方法对环颈雉胃动脉的起源、分布及胃静脉的回流情况进行了解剖学研究。结果表明,环颈雉的胃动脉均由腹腔动脉分出;腺胃由腺胃背侧动脉和腺胃腹侧动脉营养,腺胃背侧动脉直接起自腹腔动态的左侧,腺胃腹侧动脉起自腹腔动脉左支。腺胃血液的静脉有腺胃前静脉和腺胃后静脉,分别汇入后腔静脉和左肝门静脉。肌胃由肌胃左动脉、肌胃右动脉和肌胃背侧动脉营养,肌胃左动脉起自腹腔动脉的左支;肌胃右动脉起自腹腔动脉的右支;肌胃背侧动脉从腺胃背动脉分支而来。回流肌胃血液的静脉有胃右静脉、胃左静脉和胃腹侧静脉;胃右静脉汇入右肝门静脉,胃左静脉和胃腹侧静脉汇入左肝门静脉。另外腺胃和肌胃的表面缺乏主干动脉间的吻合。     

A portal-arterial glucose concentration gradient as a signal for an insulin-dependent net glucose uptake in perfused rat liver

Since in the usual perfusion of isolated rat liver via the portal vein an insulin-dependent increase of hepatic glucose uptake could not be demonstrated, the possibility was considered that hepatic glucose uptake might not be a function of the absolute concentration of this substrate but of its concentration gradient between the portal vein and the hepatic artery. Therefore a new method was established for the simultaneous perfusion of isolated rat liver via both the hepatic artery (20-35% flow) and the portal vein (80-65% flow). When glucose was offered in a concentration gradient, 9.5 mM in the portal vein and 6 mM in the hepatic artery, insulin given via both vessels caused a shift from net glucose release to uptake. This insulin-dependent shift was not observed when glucose was offered without a gradient or with an inverse gradient, 6 mM in the portal vein and 9.5 mM in the hepatic artery. Using a portal-arterial glucose gradient as a signal the liver might be able to differentiate between endogenous and exogenous glucose.     

The metabolism of fructose in the bivascularly perfused rat liver.

The metabolism of fructose was investigated in the bivascularly and hemoglobin-free perfused rat liver. Anterograde and retrograde perfusions were performed. In anterograde perfusion, fructose was infused at identical rates (19 mumols min-1 g-1) via the portal vein (all liver cells) or the hepatic artery (predominantly perivenous cells); in retrograde perfusion fructose was infused via the hepatic vein (all liver cells) or the hepatic artery (only periportal cells). The cellular water spaces accessible via the hepatic artery were measured by means of the multiple-indicator dilution technique. The following results were obtained. (i) Fructose was metabolized to glucose, lactate and pyruvate even when this substrate was infused via the hepatic artery in retrograde perfusion; oxygen consumption was also increased. (ii) When referred to the water spaces accessible to fructose via the hepatic artery in each perfusion mode, the rate of glycolysis was 0.99 +/- 0.14 mumols min-1 ml-1 in the retrograde mode; and, 2.05 +/- 0.19 mumols min-1 ml-1 in the anterograde mode (P = 0.002). (iii) The extra oxygen uptake due to fructose infusion via the hepatic artery was 1.09 +/- 0.16 mumols min-1 ml-1 in the retrograde mode; and, 0.51 +/- 0.08 mumols min-1 ml-1 in the anterograde mode (P = 0.005). (iv) Glucose production from fructose via the hepatic artery was 2.18 +/- 0.18 mumols min-1 ml-1 in the retrograde mode; and, 1.83 +/- 0.16 mumols min-1 ml-1 in the anterograde mode (P = 0.18). (v) Glucose production and extra oxygen uptake due to fructose infusion did not correlate by a single factor in all perfusion modes. It was concluded that: (a) rates of glycolysis are lower in the periportal area, confirming previous views; (b) extra oxygen uptake due to fructose infusion is higher in the periportal area; (c) a predominance of glucose production in the periportal area could not be demonstrated; and (d) extra oxygen uptake due to fructose infusion is not a precise indicator for glucose synthesis.     

Hepatic heterogeneity in the response to ATP studied in the bivascularly perfused rat liver

The zonation of the purinergic action of ATP in the hepatic parenchyma was investigated in the bivascularly perfused rat liver by means of anterograde and retrograde perfusion. Livers from fed rats were used, and ATP was infused according to four different experimental protocols: (A) anterograde perfusion and ATP infusion via the portal vein; (B) anterograde perfusion and ATP via the hepatic artery; (C) retrograde perfusion and ATP via the hepatic vein; (D) retrograde perfusion and ATP via the hepatic artery. The following metabolic parameters were measured: glucose release, lactate production and oxygen consumption. The hemodynamic effects were evaluated by measuring the sinusoidal mean transit times by means of the indicator-dilution technique. ATP was infused during 20 min at four different rates (between 0.06-0.77 µmol min_-1 g liver_-1; 20-200 µM) in each of the four experimental protocols.The results that were obtained allow several conclusions with respect to the localization of the effects of ATP along the hepatic acini: (1) In retrograde perfusion the sinusoidal mean transit times were approximately twice those observed in anterograde perfusion. ATP increased the sinusoidal mean transit times only in retrograde perfusion (protocols C and D). The effect was more pronounced with protocol D. These results allow the conclusion that the responsive vasoconstrictive elements are localized in a pre-sinusoidal region; (2) All hepatic cells, periportal as well as perivenous, were able to metabolize ATP, so that concentration gradients were generated with all experimental protocols. Extraction of ATP was more pronounced in retrograde perfusion, an observation that can be attributed, partly at least, to the longer sinusoidal transit times. In anterograde perfusion, the extraction of ATP was time-dependent, a phenomenon that cannot be satisfactorily explained with the available data; (3) ATP produced a transient initial inhibition of oxygen uptake when protocols A and B were employed. These protocols are the only ones in which the cells situated shortly after the intrasinusoidal confluence of the portal vein and the hepatic artery were effectively supplied with ATP. The decrease in oxygen consumption was more pronounced at low ATP infusions when protocol B was employed. These observations allow the conclusion that the former phenomenon is localized mainly in cells situated shortly after the intrasinusoidal confluence of the portal vein and hepatic artery. Oxygen consumption in all other cells, especially the proximal periportal ones, is increased by ATP; (4) In agreement with previous data found in the literature, glycogenolysis stimulation by ATP was more pronounced in the periportal region. The cells that respond more intensively are not the proximal periportal ones, but those situated in the region of the intrasinusoidal confluence of the portal vein and the hepatic artery.     

Role of the hypothalamus in regulating liver circulation

In acute experiments on nembutal anesthetized dogs stimulation of anterior hypothalamus elicited changes in the hepatic artery blood flow, which followed those of arterial pressure; the vascular resistance remaining unchanged. The stimulation of medial and posterior hypothalamus led to decrease in flow and increase in the resistance of the hepatic artery. In most cases of hypothalamic stimulation the portal blood flow diminished, portal pressure and vascular resistance increased. The opposite reactions were observed during stimulation of sympathoinhibitory area, paraventricular and lateral hypothalamic nuclei. The conclusion is made that the hypothalamus participates in integrative and differential control of the hepatic circulation.