The pulmonary ultrastructure in septic shock

Coalson, Jacqueline J.; Hinshaw, Lerner B.; Guenter, Clarence A.

doi:10.1016/0014-4800(70)90077-8

Cited by 80 publications

(17 citation statements)

References 22 publications

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“…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%

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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: Resultsmentioning

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%

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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“…Ultrastructurally, these leukocytes are seen degranulated and fragmented with r !ase of their lysosomal granules into the pulmonary capillaries (6). This phenomenon of pulmonary sequestration of leukocytes in response to certain stimuli was probably first described in This study evaluates t" role of sequestered leukocytes in the pathogenesis of the hemodynamic and pulmonary changes in endotoxic shock.…”

Section: Introductionmentioning

confidence: 84%

“…Endotoxin shock is characterized by an early fall in peripheral blood leukocyte count and sequestration of large numbers of polymorphonuclear leukocytes in the pulmonary cpillaries (6,15). Ultrastructurally, these leukocytes are seen degranulated and fragmented with r !ase of their lysosomal granules into the pulmonary capillaries (6).…”

Section: Introductionmentioning

confidence: 99%

Significance of Leukocytes in Endotoxin Shock

Pingleton¹,

Coalson²,

Guenter³

1974

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Office of Naval Research erpheral blood leukopenla and the sequestration of large numbers of polymorphonuclear leukocytes in pulmonary capillaries have been observed in experimental shock.-~j It h.is been suggested that release of leukocytic lysosomal enzyms contributes to sysitamic hypotension and pulmonary capillary damage. This study was undertaken to eval'iate the role of leukocytes in endotoxin shock. Six rhesus monkeys rendered leukopenic by total body irradiation (me~an white blood cells, 358/cu mmn) were comIpared with 6 normal mcnkeys (mean white blood cells, 10,550/cu mmn) for 2 hrs after Sinjection of I". coli endotoxin. The effects of irradiation wore evaluated in 3 additicnal animals which did not receive endotoxin. Following the injection of endotoxin, the mean cardiac output and systemic pressure decreased more than 50Y% in bath the leukopenic and normal groups. Metabolic acidosis developed in both groups. The mean arteriftl P0 1 2 was unchanged, however, the alvzvilar-arterial 02 gradients increased. Oifferences between the groups were not significant in these parameters. * .Light and electron microscopy demonstrated sequestered polymorphonuclear leukocytes * ari olatelets in Pulmonary capillaries in the non-radiated group, but leuikocytes Swere virtually absent in sections from lungF of the leukopenic animals. In spite Sof tnis difference, significant endothelial swelling and perivascular edema were demronstrahie in both groups. No significant histologic abnormalities wtvre noted in the three radiated leukopenic control animals who did not receive endotoxifl. Le,.kopenia provided no protection from the he-)dynamic effects or the histological damiage in puliionary capillaries observed after admini -rationi of endotoxin. This study was undertaken to evaluate the role of leukocytes in endotoxin shock.Six rhesus monkeys rendered leukcopenlc by total body irradiation (mean white blood cells, 358/cu mi) were -4npared with six normal monkeys (mean white blood cells, 10,550/cu m)for 2 hours after injection)f E. celi endotoxin. The effects of irradiation were evaluated in 3 aditional animals Whichd id not receive endotoxin.Following the injection of endotoxin, the mean cardiac output and systewlc pressure decreased more than~ 5fj% in both the loukopenic and noraal groups.Metabolic acidosis developed in both groups. The mean arterial p02 was unchanged, however, the alveolar-arterfal 02 gradfents increased. Diffeyrences between the 4roups were not significant in these parameters.Light and electron micrascapy d~nstrated sequestered polyorphonuclear leukocytes and platelets in pulmonary capillories in the-non-radiated group, but leukocytes were virtually atsent in sections from lungs of thp leukolnenic aoinials. in snite of this differenco, significant endothelial swlling and perivaicular adenw were deonstrable in both groups. No significant histologic abnormali!ties wot tioted in the three radlatel leukopenic conttol aniWmaIs WhO dica not receive enclotoxin. Leukopenia proyided no protection rm h hodnamicef...

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“…Platelet sequestration in lung capillaries during endotoxic shock is well documented [1][2][3], as well as leukopenia occurring in sev eral species [4], In 1961, Athens et al [5] hypothesized that the disappearance of neu trophils from circulation was the result of their sequestration in capillaries, but it was 10 years before it was described occurring in pulmonary capillaries, causing injury and possibly leading to the adult respiratory dis tress syndrome (ARDS) [6], Several in vitro studies confirmed these findings [7][8][9], There are no published in vivo studies on the dynamic behavior of leukocytes in the lungs or other organs during endotoxin-inbe the pathogenic factor for lung, liver and duced shock, although Cooper et al [10] recently reported in vivo radiolabeled leuko cyte kinetics in sheep after thrombin-in duced intravascular coagulation.…”

Section: Introductionmentioning

confidence: 99%

Multiorgan Leukocyte Sequestration during Endotoxic Shock in Sheep

Christenson¹,

Al-Sarraf²,

Owunwanne

et al. 1989

Med Princ Pract

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Following injection with indium-Ill-oxine-labeled leukocytes and Escherichia coli lipopolysaccharide, leukocyte sequestration was observed in the lungs, liver and kidneys in 6 sheep with a corresponding decrease in measured indium-Ill oxine leukocytes in the spleen and circulating blood, and a decrease in the leukocyte count in peripheral blood. In the lungs and kidneys, early leukocyte sequestration was followed by a decrease in activity in these organs, with a second phase of continuous leukocyte sequestration beginning 90 min after shock. A steady increase in leukocyte activity was observed in the lungs until the end of the experiment. Leucocyte sequestration may be the pathogenic factor for lung, liver and kidney injury in endotoxin-induced shock.

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The pulmonary ultrastructure in septic shock

Cited by 80 publications

References 22 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.

Significance of Leukocytes in Endotoxin Shock

Multiorgan Leukocyte Sequestration during Endotoxic Shock in Sheep

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