Alterations in Cell Function With Ischemia and Shock and Their Correction

Chaudry, Irshad H.; Clemens, Mark G.; Baue, Arthur E.

doi:10.1001/archsurg.1981.01380220053009

Cited by 75 publications

(17 citation statements)

References 56 publications

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“…Acute hepatic and renal ischemia may be the consequence of deteriorated hepatic and renal perfusion si multaneously when cardiac output falls be low a critical level. Alternatively, hepatic damage due to ischemia and hypoxemia could be the triggering mechanism for renal circulatory disorders, in a way similar to the mechanisms observed in hepatorenal syn drome in cirrhotic patients [19] or in acute hepatic failure [20], Our observations suggest that CSV3 is a severe, but potentially reversible, complica tion of congestive heart failure. The diffi culty is to anticipate which patients develop this complication.…”

Section: Discussionsupporting

confidence: 64%

Compensated Cardiogenic Shock: A Subset with Damage Limited to Liver and Kidneys

Naschitz¹,

Yeshurun²

1987

Cardiology

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A variant of compensated cardiogenic shock occurring in patients with chronic congestive heart failure following an episode of pulmonary edema, and in the absence of hypotension, is described. The clinical picture is characterized by combined renal and hepatic injury and a severe, often fatal, course and is distinct from other subsets of cardiogenic shock. When the splanchnic vasodilator dopamine was added to the patients’ management, the outcome was uniformly favorable. This variant of compensated cardiogenic shock requires early diagnosis and treatment. The apparently beneficial effect of low-dose dopamine needs further evaluation.

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Section: Discussionsupporting

confidence: 64%

Compensated Cardiogenic Shock: A Subset with Damage Limited to Liver and Kidneys

Naschitz¹,

Yeshurun²

1987

Cardiology

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“…Therefore, the study of any model of ischemic injury requires appraisal of the events which occur during both ischemia and reperfusion and should include ischemic periods of varying severity so as to properly categorize the importance of the damaging events. The mechanism of ischemic injury appears to be the gradual loss of normal cellular homeostasis and, in particular, membrane-associated processes which regulate ion concentrations within and between subcellular compartments [26][27][28][29][30][31].…”

Section: Discussionmentioning

confidence: 99%

Lipid peroxidation is a nonparenchymal cell event with reperfusion after prolonged liver ischemia

Walsh

Rao

Makowka

et al. 1990

Journal of Surgical Research

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A proposed mechanism for irreversible ischemic liver damage has been peroxidation of membrane phospholipids by free radicals. However, the hepatocyte is laden with enzymes which are antioxidants and, therefore, ought to be relatively resistant to oxidative injury. To test the hypothesis that free radical damage from ischemia and reperfusion of the liver is a non parenchymal cell process, we studied an in vivo model of ischemia. A point of transition from reversible to irreversible ischemia was defined at ≥60 min of total ischemia by serial measurements of ATP at control, end of ischemia, and end of reperfusion periods (n = 6 each). Nonparenchymal cells were separated out of 10 livers in each ischemic group using a Percoll gradient. Second derivative spectroscopy did not detect conjugated dienes in any hepatocellular fraction, total cellular, mitochondrial, or microsomal, but did in the nonparenchymal cell fractions of livers from the 60-and 90-min ischemia groups. This in vivo study shows that irreversible ischemia in the rat liver is associated with free radical lipid peroxidation, but that the non parenchymal cells rather than hepatocytes are the focus of this injury.

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“…Postischemic organ hypoperfusion designated as 'no reflow phenomenon' ap peared to be caused by the destruction of microvascular beds, microsludging and vas cular spasms, and would contribute to organ damage [26]. The effect of calcium channel blocker on portal pressure and hepatic blood flow is still debatable [27,28], but Reichen and Le [29] reported that verapamil could reduce the hepatic resistance and improve the hepatic microvascular circulation in an ex vivo liver perfusion model in rats with cirrhosis.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Verapamil on Ischemia-Induced Hepatic Damage in the Rat

Shinohara¹,

Kayashima²,

Konomi³

1990

Eur Surg Res

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The preventive effects of the calcium channel blocker, verapamil, on ischemic liver damage were studied using a rat total hepatic ischemic model. A marked improvement in the survival was obtained by verapamil administration. Following 90 min of hepatic ichemia, 8 of 9 rats (89%) survived in the verapamil-treated group compared to only a 50% survival rate in the saline-treated control group. Furthermore, 56% of the rats still survived after 120 min of ischemia, while there was no survivor in the control group. The recovery of hepatic ATP level following ischemia was significant in the verapamil-treated group, showing the well-preserved mitochondrial function afforded by verapamil administration.

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Alterations in Cell Function With Ischemia and Shock and Their Correction

Cited by 75 publications

References 56 publications

Compensated Cardiogenic Shock: A Subset with Damage Limited to Liver and Kidneys

Compensated Cardiogenic Shock: A Subset with Damage Limited to Liver and Kidneys

Lipid peroxidation is a nonparenchymal cell event with reperfusion after prolonged liver ischemia

Protective Effects of Verapamil on Ischemia-Induced Hepatic Damage in the Rat

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