Significance of leukocytes in endotoxic shock

Pingleton, William W.; Coalson, Jacqueline J.; Guenter, Clarence A.

doi:10.1016/0014-4800(75)90062-3

Cited by 43 publications

(8 citation statements)

References 19 publications

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“…Previous studies attempting to implicate granulocytes as mediators of the pulmonary vascular reaction to endotoxin have been inconclusive (2)(3)(4). We showed, in sheep, that granulocyte depletion prevented increased pulmonary vascular permeability after autologous complement-activated plasma infusion (9).…”

Section: Introductionmentioning

confidence: 69%

“…Hydroxyurea primarily depleted granulocytes; granulocyte depletion required [4][5][6][7][8][9][10][11] d. The effects of hydroxyurea on blood leukocyte and platelet counts are shown in Fig. 1.…”

Section: Resultsmentioning

confidence: 99%

“…We also put catheters through neck vessels into the superior vena cava and aortic arch. The initial experiments were performed [3][4][5] In all experiments, we used the same lot of endotoxin prepared according to the Westphal method by Difco Laboratories from E. coli 0127:B8. We dissolved endotoxin in 20 ml sterile pyrogen free 0.89% NaCl for each series ofexperiments.…”

Section: Methodsmentioning

confidence: 99%

“…During the early part of this reaction leukocytes, primarily granulocytes, are sequestered in pulmonary vessels (2)(3)(4)(5)(6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

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Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Heflin¹,

Brigham²

1981

J. Clin. Invest.

394

116

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A B S T R A C T To see whether circulating granulocytes are necessary for the lung vascular reaction to endotoxin, we measured the endotoxin response in chronically instrumented sheep before and after granulocyte depletion with hydroxyurea. Granulocyte depletion did not affect the pulmonary hypertension caused by endotoxin (peak mean pulmonary artery pressures = 38+2 cm H20 before depletion and 42+2 after depletion, P = NS). The late phase increase in lung lymph flow after endotoxin was significantly lower in the granulocytopenic animals as reflected by lung lymph flow (mean steady state lymph flow before depletion = 30.6+2.0 SE ml/h; mean steady state lymph flow after granulocyte depletion = 15.4+1.0; P < 0.01) even though late phase pulmonary vascular pressures were similar before and after granulocyte depletion. Lung lymph protein clearance (lymph flow x lymph/plasma protein concentration) was also significantly lower after granulocyte depletion (mean steady state before depletion = 21.4 + 1.4 SE ml/h; and after depletion = 10.4+ 1.0; P < 0.01). We conclude that circulating granulocytes are necessary for the development of increased lung vascular permeability to fluid and protein following endotoxin. The pulmonary vasopressor effects of endotoxin in sheep are independent of granulocytes.

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Section: Introductionmentioning

confidence: 69%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

“…During the early part of this reaction leukocytes, primarily granulocytes, are sequestered in pulmonary vessels (2)(3)(4)(5)(6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Heflin¹,

Brigham²

1981

J. Clin. Invest.

394

116

View full text Add to dashboard Cite

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“…For example, experiments in granu locyte-depleted animals suggest that the in crease in vascular permeability in response to endotoxin is attenuated (14), whereas in leukopenic animals (15,16), it has been shown that endothelial damage still occurs. Addi tionally, in the animal given a single infusion of complement-activated plasma, only a mod est increase in vascular permeability occurs, and the accompanying endothelial damage is transient (17).…”

mentioning

confidence: 99%

Hydroxyl radical participation in the in vitro effects of Gram-negative endotoxin on cardiac sarcolemmal Na,K-ATPase activity.

Taga

Okabe

1991

Jpn.J.Pharmacol

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ABSTRACT-The effect of in vitro exposure of sarcolemmal membrane (SL) vesicles to Gram-negative endotoxin lipopolysaccharides (LPS) was studied. LPS decreased the Na,K-ATPase activity of SL vesicles; this effect was inhibited by hydroxyl radical (' OH) scavengers such as dimethylthiourea and dimethyl sulfoxide, but not by super oxide dismutase, a scavenger of superoxide anion radicals or by the hydrogen perox ide scavenger catalase. ESR spin-trapping with 5,5-dimethyl-l-pyrroline N-oxide veri fied the generation of *OH from LPS itself under the conditions used; *OH gener ated from LPS was not affected by deferoxamine, a powerful iron chelator. The Na,K-ATPase activity was reduced by an 'OH radical generating system consisting of dihydroxyfumarate and Fe 3+-ADP. Furthermore, exposure of SL vesicles to LPS caused an increase in malondialdehyde formation. It can be concluded that LPS dam ages cardiac SL by an oxygen free radical mechanism by the generation of 'OH, due to inhibition of Na,K-ATPase activity and peroxidation of lipids, and that the effect of LPS is not dependent on the presence of contaminating iron.Endotoxins are lipopolysaccharides located in the outer membrane of Gram-negative bac teria. Much of the morbidity and mortality associated with Gram-negative infections is thought to be due to release of endotoxin (1). Injection of microgram amounts of endotoxin into susceptible experimental animals produces a number of biological effects. These include multiple hematologic events such as comple ment activation, disseminated intravascular coagulation, and intestinal bleeding. Injection of larger doses of endotoxin frequently results in shock and death (2).A current hypothesis for the mechanism underlying the cardiovascular collapse of Gram-negative septic or endotoxin shock be gins with the observation of Jacob, et al. (3) that endotoxin within the vascular space acti vates complement and leads to the production of complement components; most importantly, C5a. C5a activates polymorphonuclear leuko cytes (4) which become adherent to endothe lial surfaces and other leukocytes and subse quently release oxygen free radicals, lysosomal hydrolases, and arachidonic acid derivatives. These oxygen free radicals (superoxide anion, Oz ; hydroxyl radical, *OH; singlet oxygen, 1O 7; and hydrogen peroxide, H202) are ca pable of extensive endothelial cell (5) and car diac cell damage (6-9) and could potentially produce the loss of contractility in vascular smooth muscle and cardiac muscle which is * To whom reprint requests should be addressed .

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Role of the neutrophil in adult respiratory distress syndrome

Windsor

Mullen

Fowler

et al. 1993

Journal of British Surgery

252

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Adult respiratory distress syndrome (ARDS) remains a significant cause of morbidity and mortality in surgical practice. Despite the continued advance of surgical technique and therapy, the mainstay of treatment of ARDS remains supportive. In the past decade cytokines have been found to be primary chemical mediators of the host response to inflammatory disease. The polymorphonuclear leucocyte has also emerged as a possible cellular mediator of the end-organ damage that characterizes these inflammatory processes. The role of the neutrophil as the primary cellular mediator of alveolar capillary membrane injury in ARDS remains controversial. This article reviews the relevant current literature and considers the implications of the prevailing evidence on future management of this syndrome.

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Significance of leukocytes in endotoxic shock

Cited by 43 publications

References 19 publications

Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Prevention by granulocyte depletion of increased vascular permeability of sheep lung following endotoxemia.

Hydroxyl radical participation in the in vitro effects of Gram-negative endotoxin on cardiac sarcolemmal Na,K-ATPase activity.

Role of the neutrophil in adult respiratory distress syndrome

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