Hepatic arterial perfusion regulates portal venous flow between hepatic sinusoids and intrahepatic shunts in the normal rat liver in vitro

Berndt, Alexander; Cottam, Howard B.; Naftalin, Richard J

doi:10.1007/s004240100682

Cited by 18 publications

(24 citation statements)

References 29 publications

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“…The present study demonstrated near complete sorbitol uptake in the portal vein when intrahepatic shunts are closed. Once the shunts are induced to open either via reductions in hepatic arterial blood flow 10 or by intraportal injections of microspheres, portal venous uptake of sorbitol decreases to extremely low values (13% in the present study) and 4.3% following hepatic arterial ligation. Therefore, the potential for increased uptake is high and would not be significantly reduced by increases in portal venous flow either by deliberate manipulation or through the buffer response.…”

Section: Discussionmentioning

confidence: 43%

Location and function of intrahepatic shunts in anaesthetised rats

Benjamin²,

Naftalin³

et al. 2003

Gut

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Background: In the present study we determined the proportion of shunt flow due to patent intrahepatic portal systemic shunts in the normal rat liver and its relationship with microsphere induced portal hypertension. Methods: Systemic and hepatic haemodynamics were measured continuously before, during, and after intraportal injection of 15 µm diameter microspheres in anaesthetised male Wistar rats. Functional hepatic blood flow and intrahepatic shunt flow were determined by the use of constant intraportal infusion of sorbitol and simultaneous measurements in the portal vein, hepatic vein, and carotid artery. The percentage of large shunts of diameter >15 µm were estimated by intraportal injection of 51 Cr labelled 15 µm diameter microspheres. Results: Hepatic sorbitol uptake was 97.9 (0.5)% in normal control rats, with functional hepatic blood flow equalling total hepatic blood flow (2.52 (0.23) ml/min/100 g body weight). Microsphere injection decreased sorbitol uptake to 12.8 (4.3)% and further to 4.1 (0.7)% when followed by hepatic arterial ligation. In the latter two groups, intrahepatic shunt flow (1.46 (0.15) and 1.16 (0.19) ml/min/100 g body weight, respectively) was not significantly different from portal venous flow (1.36 (0.20) and 1.20 (0.20) ml/min/100 g body weight, respectively). Portal venous flow remained at 70% of basal values and portal venous pressure only increased by 50% from baseline. 51 Cr labelled microsphere shunt fraction through large shunts (>15 µm) was less than 1.0%. Conclusion: The site of confluence between the hepatic artery and portal vein is in zone II. Intrahepatic shunts originate in presinusoidal regions in zone I in the normal liver and, when activated by intraportal injection of microspheres, divert 70% of the total portal blood flow away from zone III and thereby reduce acute increases in portal venous pressure.

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Section: Discussionmentioning

confidence: 43%

Location and function of intrahepatic shunts in anaesthetised rats

Benjamin²,

Naftalin³

et al. 2003

Gut

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“…However, intrahepatic shunting of portal venous blood is another complication of portal hypertension and is also characterised by the entry of essentially unprocessed portal venous blood into the systemic circulation [24,27,28,30]. Our previous experiments demonstrated that intrahepatic shunts occur in the normal rat liver [7,21] and suggested that the shunt vessels have a wide diameter, ranging from 15-90 µm [25]. However, their location or the magnitude of intrahepatic shunt flow in the normal or diseased liver remains uncertain [7,25].…”

Section: Introductionmentioning

confidence: 99%

“…Our previous experiments demonstrated that intrahepatic shunts occur in the normal rat liver [7,21] and suggested that the shunt vessels have a wide diameter, ranging from 15-90 µm [25]. However, their location or the magnitude of intrahepatic shunt flow in the normal or diseased liver remains uncertain [7,25]. Their function in the regulation of intrahepatic blood flow distribution in the developing and diseased liver, where hepatic morphology undergoes dramatic changes, remains unknown [4,8].…”

Section: Introductionmentioning

confidence: 99%

“…Their function in the regulation of intrahepatic blood flow distribution in the developing and diseased liver, where hepatic morphology undergoes dramatic changes, remains unknown [4,8]. Moreover, the factors that control their opening, the mechanisms regulating their activity and their role in the development of portal hypertension and in the normal liver remain to be fully elucidated [6,7,25].…”

Section: Introductionmentioning

confidence: 99%

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Hepatic arterial perfusion decreases intrahepatic shunting and maintains glucose uptake in the rat liver

Berndt

Rogers

Naftalin

2002

Pflügers Arch - Eur J Physiol

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Intrahepatic shunts have an important function in the regulation of portal venous pressure in the normal rat liver. The present study determined their location, the region of confluence between the hepatic arterial and portal venous vasculatures, regions within the liver that are bypassed and the effects of hepatic arterial perfusion upon the intrahepatic redistribution of portal venous flow. Livers of male Sprague-Dawley rats were excised and perfused in vitro. Hepatic bromosulphthalein (BSP) and glucose uptake were measured in hepatic venous samples. Diversion of the hepatic arterial supply into the portal venous vasculature opened the portal venous intrahepatic shunts and resulted in a 50% reduction in portal venous glucose uptake from 29.6+/-1.6% to 14.9+/-0.9% ( P<0.0001 Student's paired t-test). Portal venous injection of 15-microm-diameter microspheres also opened the intrahepatic shunts and reduced portal venous glucose uptake to 10% from 29.0+/-1.6% to 7.8+/-0.9% ( P<0.0001 Student's paired t-test). No significant reductions in portal venous BSP uptake (43.0+/-6.9 to 48.0+/-4.8%) or hepatic arterial glucose uptake, from an average value of 94.0%, occurred. Therefore, cessation of hepatic arterial perfusion or portal venous injection of microspheres reduced portal venous glucose uptake without affecting BSP uptake. It is concluded that intrahepatic shunts divert perfusate away from the perivenous, sinusoidal (zone III) regions and into the hepatic venous vasculature, distal to zone III. The microsphere data indicate that confluence between the hepatic arterial and portal venous vasculatures occurs mainly in sinusoidal zone II.

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“…No studies have been done with gradients as large as Ϫ163 mg/dl, however, so a bell-shaped response remains possible. A second likely explanation for the blunting of the response to the portal signal in the HAL po dogs may lie in the importance of the hepatic artery in regulation of hepatic circulation (4,5). It has been proposed that the architecture of the liver allows shunting of portal vein blood away from the areas of hepatic glucose uptake (zone III), and the presence of hepatic artery flow decreases intrahepatic shunting and thus stimulates glucose uptake (5).…”

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confidence: 99%

Chronic hepatic artery ligation does not prevent liver from differentiating portal vs. peripheral glucose delivery

Moore

Burish

Farmer

et al. 2003

American Journal of Physiology-Endocrinology and Metabolism

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Chronic hepatic artery ligation does not prevent liver from differentiating portal vs. peripheral glucose delivery. Am J Physiol Endocrinol Metab 285: E845-E853, 2003. First published May 28, 2003 10.1152/ajpendo.00130.2003.-Infusion of glucose into the hepatic artery blocks the stimulatory effect of the "portal signal" on net hepatic glucose uptake (NHGU) during portal glucose delivery. We hypothesized that hepatic artery ligation (HAL) would result in enhanced NHGU during peripheral glucose infusion because the arterial glucose concentration would be perceived as lower than that in the portal vein. Fourteen dogs underwent HAL ϳ16 days before study. Conscious 42-h-fasted dogs received somatostatin, intraportal insulin, and glucagon infusions at fourfold basal and at basal rates, respectively, and peripheral glucose infusion to create hyperglycemia. After 90 min (period 1), seven dogs (HAL po) received intraportal glucose (3.8 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 ) and seven (HALpe) continued to receive only peripheral glucose for 90 min (period 2). These two groups were compared with nine non-HAL control dogs (control) treated as were HALpe. During period 2, the arterial plasma insulin concentrations (24 Ϯ 3, 20 Ϯ 1, and 24 Ϯ 2 U/ml) and hepatic glucose loads (39.1 Ϯ 2.5, 43.8 Ϯ 2.9, and 37.7 Ϯ 3.7 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 ) were not different in HALpe, HAL po, and control, respectively. HALpo exhibited greater (P Ͻ 0.05) NHGU than HAL pe and control (3.1 Ϯ 0.3, 2.0 Ϯ 0.4, and 2.0 Ϯ 0.1 mg ⅐ kg Ϫ1 ⅐ min Ϫ1 , respectively). Net hepatic carbon retention was approximately twofold greater (P Ͻ 0.05) in HAL po than in HALpe and control. NHGU and net hepatic glycogen synthesis during peripheral glucose infusion were not enhanced by HAL. Even though there exists an intrahepatic arterial reference site for the portal vein glucose concentration, the failure of HAL to result in enhanced NHGU during peripheral glucose infusion suggests the existence of one or more comparison sites outside the liver. liver glucose uptake; portal vein NET HEPATIC GLUCOSE UPTAKE (NHGU) is enhanced approximately twofold when glucose is delivered via the hepatic portal vein vs. a peripheral vein (29,34). This "portal signal" appears to be neurally mediated (1). When glucose is delivered via the portal vein, the portal venous glucose concentration is greater than the glucose concentration in the arterial circulation, i.e., a negative arterial-portal (A-P) gradient exists. The rate of NHGU is related not to the portal vein glucose level per se (29) but instead to the magnitude of the negative A-P glucose gradient, up to approximately Ϫ18 mg/dl (35). This implies that the portal vein glucose concentration is compared with the arterial concentration at some site, triggering a neural response that includes enhancement of NHGU. The most likely reference sites for comparison with the portal vein glucose concentration would appear to be arteries perfusing the brain (specifically the hypothalamus; see Refs. 33 and 38), the carotid bodies (6,7,36), and the liver itself (14,4...

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Hepatic arterial perfusion regulates portal venous flow between hepatic sinusoids and intrahepatic shunts in the normal rat liver in vitro

Cited by 18 publications

References 29 publications

Location and function of intrahepatic shunts in anaesthetised rats

Location and function of intrahepatic shunts in anaesthetised rats

Hepatic arterial perfusion decreases intrahepatic shunting and maintains glucose uptake in the rat liver

Chronic hepatic artery ligation does not prevent liver from differentiating portal vs. peripheral glucose delivery

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