Mechanism of the protective effects of prostaglandins E1 and F2α in canine endotoxin shock

Raflo, Gary T; Wangensteen, Stephen L.; Glenn, Thomas M.; Lefer, Allan M.

doi:10.1016/0014-2999(73)90117-9

Cited by 52 publications

(14 citation statements)

References 21 publications

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“…29 However, indo- phosphokinase, and decreased myocardial lysosomal activity in comparison to controls. 34 ' 35 Recent reports have suggested that release of cardiac lysosomal hydrolases may signal irreversible cell death. They also have been implicated in the development of collateral blood flow.…”

Section: Discussionmentioning

confidence: 99%

Regional cardiac prostaglandin release during myocardial ischemia in anesthetized dogs.

Berger¹,

Zaret²,

Speroff³

et al. 1976

Circulation Research

114

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SUMMARY Cardiac prostaglandin release was studied in closedchest dogs during acute coronary occlusion. Aortic and coronary sinus blood was obtained before, and at intervals after, balloon occlusion of the left anterior descending artery in seven dogs. Samples were assayed for prostaglandins F, E, and A by radioimmunoassay. All dogs demonstrated prostaglandin F release. Mean ± SE postocclusion aortic levels were 0.26 ± 0.01 ng /ml; coronary sinus levels were 0.67 ± 0.01 ng/ml [P < 0.001). In six dogs, prostaglandin E also was released. Mean postocclusion aortic levels were 0.24 ± 0.01 ng/ml; coronary sinus, 0.44 ± 0.01 ng/ml (P < 0.001). There was no release of prostaglandin A. To examine the site of prostaglandin release, simultaneous samples from the aorta, the coronary sinus, and the great cardiac vein were obtained before and after left circumflex artery occlusion in six additional studies. The great cardiac vein drained effluent from nonischemic myocardium, whereas the coronary sinus drainage included blood from both ischemic and nonischemic zones. All six dogs demonstrated prostaglandin F release from the ischemic region. Mean postocclusion aortic prostaglandin F was 0.32 ± 0.01 ng/ml. Coronary sinus prostaglandin F was 1.69 ± 0.03 ng/ml (P < 0.001), whereas the great cardiac vein level remained at 0.34 ± 0.01 ng/ml (P > 0.05). Prostaglandin E was released from both ischemic and nonischemic regions. Mean aortic prostaglandin E was 0.21 ± 0.01 ng/ml; great cardiac vein, 0.55 ± 0.02 ng/ml (P < 0.001); and coronary sinus, 1.07 ± 0.04 ng/ml (P < 0.001). These results have led us to conclude that the different local availability of prostaglandins E and F may influence the cardiac response to ischemia.

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Section: Discussionmentioning

confidence: 99%

Regional cardiac prostaglandin release during myocardial ischemia in anesthetized dogs.

Berger¹,

Zaret²,

Speroff³

et al. 1976

Circulation Research

114

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“…generated after cell exposure to such stimuli, or whether endotoxin-induced T F activity might be reduced by prior cell exposure t o these compounds. Disodium cromoglycate was also tested since it has been shown t o stabilize lysosomal membranes and to protect animals from endotoxin induced shock and death (28); prior treatment of animals with PGE, has also been shown to have a similar protective effect (24). The data presented here show that T F production was markedly inhibited by prior exposure of the cells to PGEl and to some extent by Lepinephrine; n o T F was generated on stimulation of the cells with these agents in the absence of endotoxin.…”

Section: Discussionmentioning

confidence: 99%

Studies on Tissue Factor Activity and Production by Leukocytes of Human Umbilical Cord and Adult Origin

Rivers¹,

Hathaway²

1975

Pediatr Res

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“…PGs also stimulate adenyl cyclase enzyme on the hepatocyte membrane and raise the intracellular levels of cAMP (48) . cAMP appears to inhibit the liberation of lysosomal enzymes (24,60) , reducing in this way one of the main components of cell lesion by H and H+R injury.…”

Section: Discussionmentioning

confidence: 99%

“…PGs derive from arachidonic acid through the action of phospholipase A2 (PLA2) on the membrane phospholipids. PGs seem to stabilize the lysosomal membrane (31,48,52) and may also preserve the cell membranes as a whole. It is possible that PGs are produced in the cells by hypoxic stress.…”

Section: Discussionmentioning

confidence: 99%

Study of rat hepatocytes in primary culture submitted to hypoxia and reoxygenation: action of the cytoprotectors prostaglandin E1, superoxide dismutase, allopurinol and verapamil

Andrade

Santos

2009

Arq. Gastroenterol.

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-Context -Exposure of hepatocytes to pathological conditions in a microenvironment of hypoxia and reoxygenation is very frequent in hepatic diseases. Several substances present perspectives for cytoprotective action on hepatocyte submitted to reoxygenation after hypoxia and simple hypoxia. Objective -We research therapeutic options for hepatocytes submitted to hypoxia and hypoxia + reoxygenation injury. Methods -Primary culture of rat hepatocytes was submitted to hypoxia (2 hours) plus reoxygenation (2 hours) and simple hypoxia (4 hours) in the presence or the absence of cytoprotectors. The hepatocyte lesion was evaluated by functional criteria through percentage of lactate dehydrogenase released and cell viability. The effects of the cytoprotectors prostaglandin E1 3 ηg/mL, superoxide dismutase 80 μg/mL, allopurinol 20 μM and verapamil 10 -4 M were studied in this model of injury. Results -Reoxygenation after hypoxia induced more significant lesion in cultured hepatocytes compared to simple hypoxia, detected by analysis of functional criteria. There was a significant reduction of percentage of lactate dehydrogenase released and a significant increase of percentage of cell viability in the hypoxia + reoxygenation + cytoprotectors groups compared to hypoxia + reoxygenation groups. Prostaglandin E1, superoxide dismutase and verapamil also protected the group submitted to simple hypoxia, when evaluated by functional criteria. Conclusions -We conclude that reoxygenation after hypoxia significantly increased the lesion of cultured rat hepatocytes when compared to simple hypoxia. Prostaglandin E1, superoxide dismutase, allopurinol and verapamil acted as cytoprotectors to the rat cultured hepatocytes submitted to hypoxia + reoxygenation in vitro. The substances prostaglandin E1, superoxide dismutase and verapamil protected hepatocytes submitted to simple hypoxia on the basis of all the criteria studied in this experimental model.

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Mechanism of the protective effects of prostaglandins E1 and F2α in canine endotoxin shock

Cited by 52 publications

References 21 publications

Regional cardiac prostaglandin release during myocardial ischemia in anesthetized dogs.

Regional cardiac prostaglandin release during myocardial ischemia in anesthetized dogs.

Studies on Tissue Factor Activity and Production by Leukocytes of Human Umbilical Cord and Adult Origin

Study of rat hepatocytes in primary culture submitted to hypoxia and reoxygenation: action of the cytoprotectors prostaglandin E1, superoxide dismutase, allopurinol and verapamil

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