Granulocytes and no-reflow phenomenon in irreversible hemorrhagic shock

Barroso-Aranda, Jorge; Schmid-Sconbein, G.W.; Zweifach, BW; Engler, Robert L.

doi:10.1016/0300-9572(89)90127-5

Cited by 22 publications

(31 citation statements)

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“…Furthermore, in a rat model of irreversible hemorrhagic shock, the no-reflow phenomenon was prevented by rendering the animals neutropenic. 41 Leukocytes may interfere with blood flow by mechanical plugging and perhaps by their release of oxygen free radicals that will add further injury to the capillary endothelium. [42][43][44][45][46] Thus, the no-reflow phenomenon is likely multifactorial.…”

Section: Pathophysiologymentioning

confidence: 99%

No-Reflow Phenomenon

2002

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Section: Pathophysiologymentioning

confidence: 99%

No-Reflow Phenomenon

2002

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“…First, it is the neutrophil count within an organ and the degree of activation and not the circulating count that is important in causing injury. 47 Second, it appears that the state of activation or priming of the circulating neutrophil pool before the ischemia is a more important determinant of injury than the total number of cells.48 Third, the relation between neutrophils, activation, and myocardial injury is nonlinear49; it likely shows thresholds or bifurcations. (A bifurcation, characteristic of a nonlinear system is an abrupt change in the dependent variable.)…”

Section: Residual Variancementioning

confidence: 99%

Can superoxide dismutase alter myocardial infarct size?

Engler

Gilpin

1989

Circulation

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superoxide was xanthine oxidase.17 Supportive evidence from other laboratories19-23 led to experimental attempts to reduce ischemic and reperfusion injury in animal models of myocardial infarction. In several studies, the addition of catalase was not felt to be necessary in vivo because of the presence of significant amounts in erythrocytes. Myocardial Infarct Size: Independent VariablesTo test the hypothesis that SOD will reduce infarct size in an animal model, all other significant independent variables must be known and measured. The Animal Models for Protecting Ischemic Myocardium (AMPIM) cooperative study in dogs found that the anatomic area at risk, collateral blood flow, and hemodynamic determinants of myocardial oxygen demand (measured as the ratepressure product) could explain most of the variance in infarct size with the protocol used.24 However, indexes of contractility were not measured. There were small, unexplained differences in infarct size between participating laboratories, and there was lower collateral blood flow in anesthetized than in conscious dogs. The unexplained differences in infarct size and collateral flow suggest the existence of other unmeasured independent variables that may alter collateral flow and thereby explain some of the residual variance. Also, the preparatory surgery may have induced collateral development in the conscious model, in which 80% of the variability could be explained by the measured indexes (including collateral blood flow). The AMPIM study concluded that a 10% (in unconscious animals) to 13% (in conscious animals) reduction in infarct size (p<0.05) would be detected only 50% of the time with 15 animals each in the control and treatment groups. Statistical ConsiderationsThe AMPIM study clearly shows that in the dog model considerable variation exists in area at risk, collateral flow, and hemodynamic indexes (rate pressure product); thus, any intervention trial should measure and include these variables in the analysis of the results. Several published SOD trials involving animals did not measure collateral blood flow,2,3 whereas in pigs5 and rabbits,13 flow measurements

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“…12 " 14 More specifically, global cerebral ischemia, induced by air embolism 3 and hypotension, 13 have implicated the presence of PMN leukocytes during the ischemia process. The presence of PMN leukocytes in the microvasculature immediately following focal cere- •See "Materials and Methods."…”

mentioning

confidence: 99%

Polymorphonuclear leukocytes occlude capillaries following middle cerebral artery occlusion and reperfusion in baboons.

Zoppo

Schmid‐Schönbein

Mori

et al. 1991

Stroke

661

406

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Background and Purpose: Microvascular perfusion defects may accompany sustained occlusion and subsequent reperfusion of the middle cerebral artery; however, the nature of such "no-reflow" defects remains unclear.Methods: In the absence of antithrombotic pretreatment, we documented lenticulostriatal microvascular flow integrity following 3-hour middle cerebral artery occlusion and 1-hour reperfusion in a baboon occlusion/reperfusion model by two methods identifying 1) microvascular occlusion and 2) microvascular patency.Results: Microvascular "no-reflow" involved capillaries (vessels of 4.0-7.5 /un diameter) of the lenticulostriatal territory. Capillary reflow included 27-39% of all capillaries in two subjects, indicating a significant reduction of perfusion from normal (2p=0.045). In identical experimental preparations, single polymorphonuclear leukocytes completely occluded 4.7% of microvessels of capillary diameter in randomly selected fields, partially occluded 33% of postcapillary venules, and occluded 40% (four of 10) of capillaries in linear reconstruction along a 110 /*m length. Circumferential contact between polymorphonuclear leukocytes and the luminal endothelial cell membranes was documented, with an intercellular gap of, at most, 160 nm. Fibrin was found with degranulated platelets when the latter were associated with granulocytes, but not with polymorphonuclear leukocytes alone.Conclusions: The rinding of capillary-obstructing polymorphonuclear leukocytes in the microvascular bed following middle cerebral artery reperfusion in focal ischemia in this model satisfies an essential requirement for postulating their role in early microvascular injury and the "no-reflow" phenomenon. {Stroke 1991 ;22:1276-1283)

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Granulocytes and no-reflow phenomenon in irreversible hemorrhagic shock

Cited by 22 publications

References 0 publications

No-Reflow Phenomenon

No-Reflow Phenomenon

Can superoxide dismutase alter myocardial infarct size?

Polymorphonuclear leukocytes occlude capillaries following middle cerebral artery occlusion and reperfusion in baboons.

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