Acute occlusion of the portal vein in the calf

Battersby, Cameron; Balderson, Glenda A.; Winch, J. E.; Burnett, W.

doi:10.1016/0022-4804(71)90142-9

Cited by 11 publications

(7 citation statements)

References 7 publications

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“…These have included endotoxic shock (Battersby et al, 1971), hypovolaemia (Brunschwig, 1955), hepatic outflow block syndrome (Starzl et al, 1960) and the release of vasoactive substances (Joseph et al, 1968). In acute liver damage potassium is released from hypoxic liver cells (Stewart et al, 1953) and high values have been recorded during total hepatic ischaemia (Backlund et al, 1965).…”

Section: Ischaemia In Man Is Unknownmentioning

confidence: 99%

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Total hepatic ischaemia in the Rhesus monkey

McMaster

Medd

1977

Journal of British Surgery

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During operations for major hepatic trauma it may be necessary temporarily to deprive the liver of its blood supply by occlusion of the hepatic artery and portal vein. The maximum 'safe period' of total hepatic ischaemia in man is unknown. In the monkey the ischaemic liver 'leaks' potassium, and levels of this element in the hepatic veins rise during ischaemia reaching a peak immediately after blood supply to the liver is restored. However, critical systemic levels of potassium are never reached and severe biochemical disturbance does not occur until 2 h following revascularization in animals having experienced ischaemic periods of longer than 20 min.

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Section: Ischaemia In Man Is Unknownmentioning

confidence: 99%

“…The problem of hepatic congestion and outflow block syndrome (Starzl et al, 1960) and the liver's susceptibility to endogenous bacterial colonization leading to infection and endotoxic shock are well known (Ford, 1900;Battersby et al, 1971).…”

Section: Ischaemia In Man Is Unknownmentioning

confidence: 99%

Total hepatic ischaemia in the Rhesus monkey

McMaster

Medd

1977

Journal of British Surgery

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“…Unfortunately, this method has resulted in normothermic ischemiareperfusion injury of the liver. Many clinical observations indicate that prolonged intraoperative normothermic ischemia and succeeding reperfusion of the liver are the most significant disadvantages of Pringle's manever, and may cause postoperative functional disorder of the liver [2][3][4][5][6] . Although the process of ischemia reperfusion injury of the liver is complicated, it consists of three pathologic components: hepatic ischemia, portal congestion, and reinflow of arterial and congested portal blood.…”

Section: Introductionmentioning

confidence: 99%

Heat shock protein 72 normothermic ischemia, and the impact of congested portal blood reperfusion on rat liver

Dai¹

2001

WJG

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“…Recently, it has also been performed for cirrhotic liver resection. Although prolonged interruption of hepatic blood inflow is known to be fatal in many species [3,4,9,12], it is unclear whether the cause of death is due to prolonged hepatic warm ischemia or to recirculation of pooled-portal blood to the previously ischemic liver.…”

Section: Introductionmentioning

confidence: 99%

Is the deterioration of liver viability due to hepatic warm ischemia or reinflow of pooled-portal blood in intermittent portal triad cross-clamping?

et al. 1988

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The effects of hepatic warm ischemia and portal pooling on the viability of the liver were investigated with respect to hepatic energy metabolism by performing intermittent portal triad cross-clamping (Pringle's maneuver) on dogs with or without portosystemic shunt. The dogs were divided into two groups of five: Group 1, non-shunt group, underwent Pringle's maneuver performed for 30 min and declamping for 30 min, a process that was repeated five times; and Group 2, shunt group, underwent the same procedure as Group 1, except for portosystemic shunt using a heparinized hydrophilic catheter between the splenic and jugular veins. The shunt was opened during Pringle's maneuver and was closed immediately at declamping. In the non-shunt group, portal pooling increased and systemic blood pressure decreased when Pringle's maneuver was performed, but in the shunt group portal and systemic blood pressures remained within the normal range. In the non-shunt group, the initial velocity of arterial blood ketone body ratio (KBR) recovery after each declamping significantly (P less than 0.01) decreased from 0.122 +/- 0.016 (per min) after the first declamping to 0.028 +/- 0.017 (per min) after the fifth declamping. Hepatic energy charge [= (ATP + 1/2 ADP)/(ATP + ADP + AMP)] decreased from 0.840 +/- 0.003 before ischemia to 0.749 +/- 0.003 30 min after the fifth declamping (P less than 0.001). The concentrations of lactate and total amino acids in arterial blood increased. On the other hand, in the shunt group, the initial velocity of KBR recovery and hepatic energy charge showed little change even after the fifth declamping (0.081 +/- 0.016 per min and 0.851 +/- 0.009, respectively). The concentrations of lactate and total amino acids showed almost no increase. The impairment of hepatic energy metabolism by intermittent portal triad cross-clamping is mainly due to reinflow of pooled-portal blood to the previously ischemic liver, rather than hepatic warm ischemia. The KBR may be useful for determining the degree of impairment of hepatic energy metabolism.

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Acute occlusion of the portal vein in the calf

Cited by 11 publications

References 7 publications

Total hepatic ischaemia in the Rhesus monkey

Total hepatic ischaemia in the Rhesus monkey

Heat shock protein 72 normothermic ischemia, and the impact of congested portal blood reperfusion on rat liver

Is the deterioration of liver viability due to hepatic warm ischemia or reinflow of pooled-portal blood in intermittent portal triad cross-clamping?

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