Idiopathic noncirrhotic portal hypertension in dogs: 33 cases (1982–1998)

Bunch, Susan E.; Johnson, Susan E.; Cullen, John M.

doi:10.2460/javma.2001.218.392

Cited by 53 publications

(75 citation statements)

References 34 publications

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“…Moreover, splenomegaly and intra-abdominal collaterals (eg splenorenal shunt, paraesophageal veins and esophageal varices) were never observed in this model. Portal hypertension has been shown to associate with hepatic dysfunc-tion, 15,17,18 but no abnormal levels of serum AST/ ALT in mice were observed following ST.…”

Section: Discussionmentioning

confidence: 99%

Splenic transposition is superior to caudal shunt as a model of murine total hepatic ischemia

Matsumoto

Efron

Tsujimoto

et al. 2005

Laboratory Investigation

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Murine total hepatic ischemia (THI) followed by reperfusion without shunting of the portal vein induces significant lethality in rodents due to intestinal congestion. Two methods have been promulgated to study THI and reperfusion in mice without intestinal congestion: subcutaneous splenic transposition which creates a portosystemic shunt via epigastric vessels, and a caudal shunt with 30% hepatectomy, which creates a portosystemic shunt via the small remnant of remaining caudal lobe. We compared outcome, inflammatory response and hepatic injury due to THI and reperfusion in these two models. Female C57BL/6 mice underwent ST, caudal shunt or no surgery prior to having 30 min of total hepatic ischemia followed by 60 min of reperfusion. Survival, surgical complications, serum AST/ALT and IL-6 were determined. Apoptotic and necrotic hepatocytes were identified by morphological criteria. Complication rates for the ST and caudal shunt procedures were 6.7 and 20%, respectively. Subsequent mortality rates following THI and 60 min reperfusion were 5.9 and 50% in mice with ST and caudal shunt, respectively. Both groups had elevated serum AST/ALT concentrations. However, in mice undergoing caudal shunt, AST/ALT levels were also significantly increased even without THI. The number of apoptotic hepatocytes after THI and reperfusion in mice following caudal shunt was significantly higher compared with those of ST (Po0.001). Both ST and caudal shunt can be used in models of THI and reperfusion to prevent significant lethality due to intestinal congestion. However, ST is a simple, safe and suitable model, whereas caudal shunt requires manipulation of the liver, and is associated with significant hepatic injury and morbidity. Keywords: intestinal congestion; mouse; portal hypertension; splenic transposition; total hepatic ischemia and reperfusion Total hepatic ischemia (THI) and reperfusion injury are inevitable consequences of various surgical maneuvers that occur during hepatobiliary surgery, liver transplantation and hepatic trauma surgery. 1 Models of hepatic warm ischemia in rodents have been instrumental in elucidating mechanisms of injury during liver transplantation and hepatic ischemic/reperfusion injury.In humans and primates, occlusion of the hepatoduodenal ligament (containing the portal vein, hepatic artery and the common bile duct) is well tolerated because of a more efficient portosystemic collateral network through which splanchnic blood can return to the heart (Pringle maneuver 2 ). Interruption of blood flow to the normothermic liver is safe for at least 60 min even without a venous bypass to decompress the vasculature proximal to the occlusion. 3 In contrast, THI in rodents has been shown to produce several pathologic events, including splanchnic congestion, severe intestinal ischemia, mesenteric congestion and systemic shock. 4 Consequently, these animals poorly tolerate even short periods of total hepatic ischemia. For example, 30 min of ischemia induces an immediate and delayed intestinal barrier failure, w...

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Section: Discussionmentioning

confidence: 99%

Splenic transposition is superior to caudal shunt as a model of murine total hepatic ischemia

Matsumoto

Efron

Tsujimoto

et al. 2005

Laboratory Investigation

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“…However, histopathologic liver changes may be identical in case of primary diseases causing PH (idiopathic non-cirrhotic PH (NCPH), portal venous hypoplasia, hepatic microvascular dysplasia and congenital arterioportal fistula) or in the case of reduced portal perfusion (congenital PSS). Thus, differentiation between PH with MAPSS due to primary liver disease and CPSS may not be possible based only on liver histopathologic findings ( Van den Ingh et al, 1995a, 1995bCenter, 1996;Bunch et al, 2001). Hence, based on the overall histopathologic and imaging findings in this patient, three diagnostic hypotheses may be reasonably considered:…”

Section: Discussionmentioning

confidence: 98%

Unusual haemodynamics in two dogs and two cats with portosystemic shunt - implications for distinguishing between congenital and acquired conditions

Ricciardi¹

2017

Open Vet J.

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Extrahepatic porto-systemic shunt (PSS) in small animals can be congenital (CPSS) or acquired (APSS) as a consequence of portal hypertension (PH), and are distinguished on the bases of their anatomical pattern. A precise morphologic imaging assessment, along with clinical and histopathologic findings, is important for distinguishing patients with PH from those with congenital PSSs, which require different therapeutic approach. Expected findings in patients with PH are presence of ascites, multiple APSS, and a confirmed cause of portal flow obstruction. On the other hand, a single PSS, absence of ascites and no evidence of portal vein, caudal vena cava or hepatic disorders are typical findings of CPSS patients. This paper describes four cases of PSSs in which the combination of the computed tomographic imaging findings did not match the standards for APSS nor for CPSS: one dog had chronic hepatitis causing PH and ascites and a splenoazygos PSS, to date considered a CPSS pattern. One dog showed a left splenogonadal PSS and porto-caval varices, to date considered an APSS pattern, without ascites, portal vein obstruction, primary structural hepatic disorders nor evidence of PH. Two cats, with and without diffuse hepatic structural disorders respectively, had a single left splenogonadal PSS without ascites. Possible interpretation of such unusual haemodynamic conditions and clinical repercussion, especially for orientation of treatment choice, are discussed.

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“…This results in distention and increased pulsatility in the hepatic veins during the cardiac cycle, as previously described. 301 In contrast, hepatic microvascular dysplasia (now known as hepatic portal venous hypoplasia) 278 is a disease where the portal blood is shunted through the liver bypassing the sinusoids and draining directly into the central veins of the liver. [328][329][330] The minimal degree of portal vein pulsatility that would allow diagnosis of right-sided heart failure has not been established in humans, but most agree that any evidence of reversed flow in the portal vein indicates severe right-sided heart dysfunction.…”

Section: Doppler Evaluation Of the Portal Vein Portal Vein Abnormalitmentioning

confidence: 99%

Liver

Nyland¹,

Larson²,

Mattoon³

2015

Small Animal Diagnostic Ultrasound

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Idiopathic noncirrhotic portal hypertension in dogs: 33 cases (1982–1998)

Cited by 53 publications

References 34 publications

Splenic transposition is superior to caudal shunt as a model of murine total hepatic ischemia

Splenic transposition is superior to caudal shunt as a model of murine total hepatic ischemia

Unusual haemodynamics in two dogs and two cats with portosystemic shunt - implications for distinguishing between congenital and acquired conditions

Liver

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