Effect of aprotinin on neutrophil function after major vascular surgery

Lord, RJ; Roath, O.S.; Thompson, John F.; Chant, A.D.B.; Francis, John L.

doi:10.1002/bjs.1800790614

Cited by 41 publications

(11 citation statements)

References 29 publications

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“…Lord et al. studied the effects of aprotinin in human neutrophils in vivo 31 . When compared to controls, neutrophils obtained from patients undergoing major operations and who were treated with aprotinin demonstrated reduced activation, preserved ability to undergo chemotaxis, and decreased superoxide production.…”

Section: Discussionmentioning

confidence: 99%

Protective effect of aprotinin on ischemia–reperfusion injury in rat ovary

Şahin

Çoşar

Köken

et al. 2008

J of Obstet and Gynaecol

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Section: Discussionmentioning

confidence: 99%

Protective effect of aprotinin on ischemia–reperfusion injury in rat ovary

Şahin

Çoşar

Köken

et al. 2008

J of Obstet and Gynaecol

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“…1-3 Neutrophil function after aprotinin administration is also protected and the degree of superoxide production is reduced, 6,7 although whether this is a direct effect or is mediated by coagulant/fibrinolytic/platelet-receptor pathways is unclear. A better understanding of the effect of aprotinin on neutrophils could help address this question.…”

Section: Brian C Cooley*mentioning

confidence: 94%

Aprotinin in Ischemia-Reperfusion injury: Flap survival and neutrophil response in a rat skin flap model

Cooley

1998

Microsurgery

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Finding a pharmacologic avenue for preventing ischemia/ reperfusion injury remains a continuing quest. Both old and new agents have been investigated in this search. Dr. Stadelmann et al. have explored the use of a relatively old but important compound, aprotinin, for preventing ischemiarelated flap necrosis. A broad-spectrum serine protease inhibitor, aprotinin has achieved clinical status for its hemostatic effects when given during cardiovascular surgery [1][2][3] and hip replacement surgery. 4 Despite its efficacy in reducing blood loss during these procedures, surgeons and scientists have not ascertained the mechanism of action for aprotinin.Dr. Stadelmann's group has found that preischemic (but not postischemic) treatment with aprotinin leads to greater survival territory in ischemic rat flaps. The flap model, originally described by Finseth and Cutting, 5 is an axialpattern island groin flap with a connecting random-pattern (contralateral groin) flap territory. The present authors modified this flap model by applying a 10-hour ischemic episode through clamping of the pedicle. Thus, the model has overlapping elements of both global and marginal ischemia. Along with this modification, these authors have reduced the flap dimensions of the original design from a 9 × 9 to a 6 × 6-cm flap in the same-sized rats. It would be helpful to know the area of flap survival without the ischemic interval in the smaller-dimensioned flaps. Finseth and Cutting describe this survival as (40.5 cm 2 + 10.4 cm 2 ) of an 81-cm 2 flap-62.8% total survival. 5 If a similar pattern/area of survival can be assumed in the present model, then the effect of preischemically administered aprotinin (with 52.3 ± 5.4% survival, close to 62.8%) simply may be negating the global ischemic episode. Further study is warranted to investigate separately these different sides of the ischemia question, using purer models for each type of ischemia (e.g., nonischemic Finseth and Cutting flap or unilateral 10-hour ischemic flap).Dr. Stadelmann et al. have highlighted neutrophils as the potential targets for the beneficial effects of aprotinin. A rigorous control for the myeloperoxidase assay was not applied in their study, specifically, evaluation of the effect of aprotinin administration on neutrophil myeloperoxidase activity. Without this control, we can only assume that aprotinin did not interfere with the assay and that the assay accurately reflected the proportion of retained neutrophils in the biopsied flap tissue. The biopsy site was also located in an area where the effects of marginal and global ischemia may have been overlapping. This may account for the large scatter in the data among groups and time points, i.e., slight variations in the biopsy sites could lead to major differences in neutrophil levels.Clinical use of aprotinin in coronary bypass surgery has emphasized its role in inhibiting enzymes of the coagulation cascade, fibrinolysis, and/or platelet adhesion/aggregation.1-3 Neutrophil function after aprotinin administration is also pro...

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“…33 Aprotinin, a nonspecific serine protease enzyme inhibitor with broad-spectrum anti-inflammatory properties, has been proved to significantly decrease white cell activation and transmigration during CPB. 34 Low-dose aprotinin administration was found to have an anti-inflammatory effect similar to that of methylprednisolone, in blunting release of systemic tumor necrosis factor and neutrophil integrin CD11B upregulation, in comparison to untreated controls. 35 Additionally, after major vascular surgery, activation of neutrophils, manifested by increased superoxide production and impaired chemotaxis, has been shown to be significantly suppressed by aprotinin administration.…”

Section: (B) Aprotininmentioning

confidence: 96%

Pharmacological Neuroprotection During Cardiac Surgery

Kikuchi

2007

Asian Cardiovasc Thorac Ann

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Despite more than 30 years of aggressive neuroprotective research by many investigators, neuropsychological deficit after cardiac surgery remains an important cause of postoperative morbidity. Although the neurological outcome is a result of a multifactorial etiology, many physicians world-wide have recognized the importance of this problem, and extensive efforts have been made in attempting to minimize the incidence of neurological and neurocognitive dysfunction. Pharmacological intervention is one of the important potential methods of neuroprotection during cardiac surgery. In vitro studies have identified drugs that are effective protectants against focal cerebral ischemia, hemorrhage, and global ischemia. However, at present there is no solid agreement on the need for prophylactic neuroprotectants in cardiac surgery. Researchers and clinicians must become more cognizant of the pitfalls and paradoxes that have arisen in attempting to translate the results of animal studies into clinical trial, with regard to neuroprotective therapy during cardiac surgery. There is an extensive need for new pharmacological approaches directed at reducing neurologic and neurocognitive injury during cardiac surgery. This article reviews past and present neuroprotective efforts and interventions during cardiac surgery.

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Effect of aprotinin on neutrophil function after major vascular surgery

Cited by 41 publications

References 29 publications

Protective effect of aprotinin on ischemia–reperfusion injury in rat ovary

Protective effect of aprotinin on ischemia–reperfusion injury in rat ovary

Aprotinin in Ischemia-Reperfusion injury: Flap survival and neutrophil response in a rat skin flap model

Pharmacological Neuroprotection During Cardiac Surgery

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