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At least 19 recordsLinked to original sources
PubMed2006

Role of angiotensin II in retinal leukostasis in the diabetic rat.

To study if the endogenous renin-angiotensin system affects diabetic retinal leukostasis, rats with streptozotocin-induced diabetes were treated with an ACE inhibitor (ramipril), an angiotensin II AT(1) receptor antagonist (losartan) and the Ca channel blocker, (nifedipine). In the diabetic rats, these drug treatments reduced systolic blood pressure by approximately 16 mmHg but did not change blood glucose. After 2 weeks, the rats were examined for retinal leukostasis in vivo with a scanning laser ophthalmoscope (SLO). Retinal leukostasis, which was defined as no movement of arrested leukocytes over 2 min, was markedly higher in diabetic rats than normal controls (P<0.01). Leukostasis was significantly decreased by ramipril and losartan (P<0.01 vs. untreated diabetic rats) but was still higher than normal. Retinal leukostasis after nifedipine treatment was not significantly different than in untreated diabetic rats. The same trend was observed when leukostasis was analyzed on retinal flat mounts with concanavalin A and CD45 immunofluorescence; ramipril and losartan treatment, however, decreased leukostasis to values no different than controls. Retinal leukostasis was lowered by nifedipine (P<0.05, untreated diabetes vs. nifedipine-treated) but was still higher than in normal, ramipril-, or losartan-treated rats. Assays of gene expression of retinal intercellular adhesion molecule (ICAM-1) by semi-quantitative RT-PCR indicated that ICAM-1 mRNA was increased in diabetic rats but was decreased markedly by treatment with losartan or ramipril, and modestly by nifedipine. In summary, suppressing the activity of the endogenous renin-angiotensin system markedly decreases, perhaps even normalizes, the retinal leukostasis that accompanies type I diabetes in rats. These effects seem to be partly independent of blood pressure and to be associated with a decrease in ICAM-1 gene expression. Angiotensin II may, thus, mediate retinal leukostasis in early diabetes.

Angiotensin II↗
PubMed2006

Correlation between expression of CD56/NCAM and severe leukostasis in hyperleukocytic acute myelomonocytic leukaemia.

OBJECTIVE: The possible contribution of surface molecules to the development of leukostasis syndrome in hyperleukocytic acute myeloid leukaemia (AML) was assessed by routine immunophenotyping and grading of the probability of clinical leukostasis. METHODS: Fifty-three patients (23 women, 30 men, median age 59 yr) with hyperleukocytic AML [white blood count (WBC) above 50 x 10(9)/L] were graded for the probability of clinical leukostasis according to the severity of neurologic, pulmonary and other symptoms possibly caused by leukostasis using a recently published scoring system. Age, WBC, absolute blast count, haemoglobin, cytogenetic risk group, infection, relative CD56 expression and absolute count of CD56 positive blasts were analyzed in multivariate stepwise backward logistic regression analysis. RESULTS: In patients with acute monocytic leukaemia (AML M4/M5) the absolute count of leukaemic blasts expressing CD56/NCAM was highly associated with the development of symptoms graded as highly probable leukostasis and all three patients succumbing to early death were CD56 positive. Only the absolute count of CD56 positive blasts was a significant predictor of risk of severe leukostasis (P = 0.020). This was not found in AML without monocytic involvement (AML M1, M2, M3v). CONCLUSIONS: The expression of CD56/NCAM, a surface marker used in routine immunophenotyping of AML, may help to predict severe and potentially fatal leukostasis in hyperleukocytic acute myelomonocytic leukaemia. These results emphasize the usefulness of this four-stage clinical grading scale for analysing the factors, which lead to severe leukostasis in hyperleukocytic patients. We extend previous findings that the mechanisms of leukostasis are different depending on the involvement of the monocytic lineage.

Adult↗
PubMed1985

Pulmonary leukostasis as the single worst prognostic factor in patients with acute myelocytic leukemia and hyperleukocytosis.

Patients with acute myelocytic leukemia and hyperleukocytosis have a poor prognosis due to vascular leukostasis and infiltration in the central nervous system and lungs. The clinical records of all patients with a new diagnosis of acute myelocytic leukemia and initial white blood cell count greater than 100,000 X 10(9)/liter admitted to the Mount Sinai Medical Center between the years 1974 and 1983 were examined. Forty-three patients were identified, 22 of whom had clinical and/or pathologic evidence of leukostasis of the central nervous system and/or lung. All patients received induction chemotherapy with daunorubicin and a continuous infusion of cytosine arabinoside. Thirty-five patients also underwent therapeutic leukapheresis prior to induction chemotherapy. The overall remission induction rate in these 43 patients was 51 percent. Fifteen patients had lung leukostasis; the remission rate for these patients was 27 percent (three complete remissions, one partial remission), as compared with a remission rate of 64 percent (18 of 28) for those without pulmonary leukostasis (chi 21 = 5.53; p = 0.02). Thirteen patients had central nervous system infiltration; the remission rate for these patients was 46 percent (five complete remissions, one partial remission), as compared with 53 percent (16 of 30) for patients without central nervous system involvement (chi 21 = 0.19; p = 0.67). The median survival of 21 patients without leukostasis was 10.8 months, as compared with 15.4 months for seven patients with central nervous system involvement and no lung leukostasis and 0.2 months for 15 patients with pulmonary leukostasis (chi 22 = 19.9; p less than 0.001). Thus, pulmonary leukostasis was found to be the single worst prognostic factor in this group of patients.

Adolescent↗
PubMed1995

Central nervous system leukostasis in patients with leukemias and lymphomas.

The clinical and neuropathological investigations have been done on 133 autopsied patients died of leukemia or non-Hodgkin's lymphoma of high malignancy. A study was performed to analyse the role of various factors particularly with respect to adhesion and aggregation in the CNS leukostasis development. The findings were also designated to evaluate the distribution of leukostasis in different CNS regions and to recognize its intensity in various CNS vessels. Basing on the studies the authors conclude that the risk of CNS leukostasis increases evidently when the leukocyte counts are elevated above 50 G/l. The adhesion and aggregation of leukemic and lymphomatous cells as well as local anatomical factors in the CNS vessels play and important role in the CNS leukostasis development, which is more intensive in the white matter and leptomeninges. The medium-sized vessels are much involved, whereas cortical capillaries are relatively less affected by leukostasis. The CNS leukostasis appears to be dynamic and reversible phenomenon, which undergoes fluctuations according to the leukocyte counts increase or decrease.

Adolescent↗
PubMed2005

Grading of symptoms in hyperleukocytic leukaemia: a clinical model for the role of different blast types and promyelocytes in the development of leukostasis syndrome.

OBJECTIVE: Patients with hyperleukocytic leukaemia were graded according to the severity of symptoms possibly caused by leukostasis to evaluate the effectiveness of therapy and to test the relative contribution of blast type and count of blasts and promyelocytes in the development of leukostasis syndrome. METHODS: Ninety-five patients (59 male, 36 female, median age 52 yr) with hyperleukocytic leukaemia [leukocytes above 50 x 10(9)/L, 48 acute myeloid leukaemia (AML), 31 chronic myeloid leukaemia (CML), 13 acute lymphoblastic leukaemia (ALL), three chronic myelomonocytic leukaemia (CMML)] were grouped according to the presence or absence and severity of neurologic, pulmonary and other symptoms into four categories (no, possible, probable and highly probable leukostasis syndrome). Age, white blood count (WBC), haemoglobin, blast count and total of blasts plus promyelocytes of these groups were compared by Mann-Whitney U-test. RESULTS: Patients with myeloid leukaemia (AML M1/M2, CML) which scored as highly probable leukostasis showed significantly higher WBC (P = 0.011), lower haemoglobin (P = 0.004), higher peripheral blast counts (P = 0.004) and higher total of peripheral blasts plus promyelocytes (P < 0.001) compared with the lower probability groups. In leukaemia involving the monocytic lineage (AML M4/M5, CMML) no significant differences were found in any of these factors between patients with highly probable leukostasis and the other patients. CONCLUSIONS: Our results show that a four-stage clinical grading scale is a valuable tool for analysing hyperleukocytic patient populations and evaluate the effectiveness of therapy more precisely. We further demonstrate that the mechanisms of leukostasis are different in myeloid leukaemia as compared with leukaemia with involvement of the monocytic lineage.

Adolescent↗
PubMed1993

Endothelial activation antigens in pulmonary leukostasis in leukemia.

Adhesion between leukemic cells and the vascular endothelium has been suggested to play a role in the development of leukostasis in myelocytic leukemia. To define the role of adhesion molecules on the surface of endothelial cells in leukostasis, we used immunohistochemistry to study the expression of endothelial leukocyte adhesion molecule-1 (ELAM-1), vascular cell adhesion molecule-1 (VCAM-1), and intercellular adhesion molecule-1 (ICAM-1) in lung tissue of 4 patients with pulmonary leukostasis. Lung tissue of 2 patients with myelocytic leukemia without leukostasis and 4 patients with irrelevant nonpulmonary disease was used as a negative control. Positive control tissues included a lymph node with angioimmunoblastic lymphadenopathy and a hyperplastic tonsil. Weak positive staining for ELAM-1 was found in 1 patient in vessels, both with and without leukostasis. Expression of VCAM-1 and ICAM-1 in all patients tested was similar to that in the negative controls. The results of this study suggest that activation of endothelium, with increased expression of the endothelial adhesion molecules under study, is not a prerequisite for the development of pulmonary leukostasis in leukemia.

Adolescent↗
PubMed1983

Pneumococcal sonicate-induced biphasic granulocytopenia and its dissociation from pulmonary leukostasis. The contribution of pneumococcal products and complement to early and late granulocytopenic phases.

The pathogenesis of pneumococcus (PNC)-induced granulocytopenia is unclear. We studied its relationship to pulmonary leukostasis and the possible roles of PNC constituents and complement. Nonviable PNC was infused into normal and 99% C3-depleted rabbits. PNC challenge induced both granulocytopenia and pulmonary leukostasis in normal animals; complement-depleted animals displayed granulocytopenia without pulmonary leukostasis. Therefore an intact complement system was not essential to the granulocytopenia, whereas pulmonary leukostasis was complement-dependent. Rabbits infused with serum, plasma, or nonpyrogenic normal saline, each after in vitro incubation with PNC, developed significant granulocytopenia (p less than 0.001, p less than 0.01, and p less than 0.001, respectively) with maximal mean percent decreases of -98%, -97%, and -91%, respectively. When the animals were sacrificed at 3 hr, no pulmonary leukostasis was found. The granulocytopenia persisted for 3 hr after infusion of either PNC-exposed serum or plasma, whereas the granulocytopenia induced by PNC-exposed saline was of less than or equal to 1 hr duration. If serum or plasma complement was inactivated prior to PNC incubation, subsequent infusion also induced significant granulocytopenia of less than 1 hr duration (p less than 0.05 and p less than 0.01). PNC-exposed saline that was subsequently heat-treated induced this same early (less than or equal to 1 hr) granulocytopenia (p less than 0.05). Control animals infused with serum, plasma, or saline unexposed to PNC displayed neither granulocytopenia nor pulmonary leukostasis. Therefore neither prior in vitro complement inactivation nor heat treatment after PNC incubation prevented the early granulocytopenic phase; in vitro complement inactivation totally aborted the late phase. The complement-independent, heat-stable early granulocytopenic phase was further investigated. Its granulocytopenia-inducing activity did not require the presence of PNC capsular polysaccharide and was resistant to trypsin treatment. With ultrafiltration, its molecular weight was 100,000 to 300,000. Thus PNC-induced granulocytopenia is a multifactorial phenomenon involving both complement-dependent and complement-independent mechanisms as well as contribution by PNC constituents or by-products.

Agranulocytosis↗
PubMed2002

Effective and selective prevention of retinal leukostasis in streptozotocin-induced diabetic rats using gliclazide.

AIMS/HYPOTHESIS: Early stage leukocyte entrapment in the retinal microcirculation (retinal leukostasis) is considered to be one of the important pathogenetic events in diabetic retinopathy. Gliclazide, a sulphonylurea, was reported to reduce leukocyte adhesion to endothelial cells in hyperglycaemia in vitro, thus suggesting possible selective efficacy of this sulphonylurea in preventing leukostasis in diabetic patients. This study evaluated the effectiveness and selectivity of gliclazide treatment on retinal leukostasis of diabetic rats in vivo. METHODS: Streptozotocin (STZ) (65 mg/kg)-induced diabetic rats were divided into three groups (n = 8 each): an untreated diabetic group, a gliclazide-treated diabetic group, and a glibenclamide-treated diabetic group. Gliclazide or glibenclamide was administered orally during a 3-week period. Non-diabetic rats were used as a control (n = 8). Retinal leukostasis was quantitatively evaluated in vivo by acridine orange leukocyte fluorography using a scanning laser ophthalmoscope. RESULTS: The number of leukocytes trapped in the area around the optic disc in the untreated diabetic group (36.9 +/- 5.1 cells) increased significantly compared with the non-diabetic control group (21.9 +/- 2.9 cells; p = 0.0007). The number of leukocytes trapped in the gliclazide-treated diabetic group (23.5 +/- 4.0 cells) decreased significantly compared with untreated diabetic group ( p = 0.0008). In contrast, no reduction of retinal leukostasis was found in the glibenclamide-treated diabetic group (37.8 +/- 5.8 cells; p = 0.7923). CONCLUSION/INTERPRETATION: This suggests that gliclazide could directly improve abnormalities in the retinal microcirculation independent of blood glucose control and possibly have selective therapeutic benefits in preventing early, critical events in diabetic retinopathy compared with other sulphonylurea drugs.

Animals↗
PubMed2006

Pigment epithelium-derived factor (PEDF) prevents diabetes- or advanced glycation end products (AGE)-elicited retinal leukostasis.

Pigment epithelium-derived factor (PEDF) is the most potent inhibitor of angiogenesis in the mammalian eye, suggesting that PEDF may protect against proliferative diabetic retinopathy. However, a role for PEDF in early diabetic retinopathy remains to be elucidated. Leukocyte adhesion to retinal capillary endothelium (leukostasis) is a critical event in early diabetic retinopathy, whose process is mainly mediated by intercellular adhesion molecule-1 (ICAM-1). We investigated here whether PEDF could prevent diabetes- or advanced glycation end products (AGE)-elicited retinal leukostasis by suppressing ICAM-1 expression. Immunohistochemistry of 8-hydroxydeoxyguanosine (8-OHdG), an oxidative stress marker, showed intense staining in the nuclei of cells in the inner and outer plexiform layers of streptozotocin-induced diabetic rat retinas. Administration of PEDF or pyridoxal phosphate, an AGE inhibitor, decreased retinal levels of 8-OHdG and subsequently suppressed ICAM-1 gene expression and retinal leukostasis in diabetic rats. Further, intravenous administration of AGE to normal rats increased ICAM-1 gene expression and retinal leukostasis, which were blocked by PEDF. PEDF also inhibited the AGE-induced T cell adhesion to microvascular endothelial cells by suppressing ICAM-1 expression. These results demonstrated that PEDF inhibited diabetes- or AGE-elicited retinal leukostasis by suppressing ICAM-1. Our present study suggests that PEDF may play a protective role against early diabetic retinopathy by attenuating the deleterious effect of AGE.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed2003

Characterization of retinal leukostasis and hemodynamics in insulin resistance and diabetes: role of oxidants and protein kinase-C activation.

Increases in leukostasis/monocyte adhesion to the capillary endothelium (leukostasis) and decreases in retinal blood flow may be causally associated and are implicated in the pathogenesis of diabetic retinopathy. In this study, we demonstrate that increases in leukostasis are observed in insulin-resistant states without diabetes, whereas decreases in retinal blood flow require diabetes and hyperglycemia. Microimpaction studies using beads mimicking retinal capillary obstruction by leukocytes did not affect retinal blood flow. In diabetic rats, treatment with the antioxidant alpha-lipoic acid normalized the amount of leukostasis but not retinal blood flow. In contrast, treatment with D-alpha-tocopherol and protein kinase-C beta-isoform inhibition (LY333531) prevented the increases in leukostasis and decreases in retinal blood flow in diabetic rats. Serum hydroxyperoxide, a marker of oxidative stress, was increased in diabetic rats, but normalized by treatment with antioxidants alpha-lipoic acid and D-alpha-tocopherol and, surprisingly, PKC beta-isoform inhibition. These findings suggest that leukostasis is associated with endothelial dysfunction, insulin resistance, and oxidative stress but is not related to retinal blood flow and is not sufficient to cause diabetic-like retinopathy. Moreover, treatment with PKC beta inhibition is effective to normalize diabetes or hyperglycemia-induced PKC beta-isoform activation and oxidative stress.

Animals↗
PubMed1993

Involvement of the complement system in the pathogenesis of pulmonary leukostasis in experimental myelocytic leukemia.

The role of the complement system in the pathogenesis of pulmonary leukostasis in myelocytic leukemia was studied in a rat model. Acute myelocytic leukemia was induced in six Brown-Norway rats, and complement levels were assayed during the course of the disease. Whole complement activity (CH50) and hemolytic activity of C1q, C3, and C4 decreased from day 16 after induction of the leukemia, when the rats developed pulmonary leukostasis. In addition, local complement activation was established in the lung vessels by immunofluorescence microscopy in advanced stages of pulmonary leukostasis. Finally, following systemic activation of the complement system by injection of cobra venom factor (CVF), leukemic rats (n = 6) died of pulmonary leukostasis 4.5 days earlier than did leukemic controls (n = 6). These findings suggest that, in acute myelocytic leukemia in Brown-Norway rats, pulmonary leukostasis is induced by activation of the complement system. This finding could lead to new modes of treatment for a life-threatening complication of leukemia.

Animals↗
PubMed2000

Hyperleukocytic leukemias and leukostasis: a review of pathophysiology, clinical presentation and management.

Acute hyperleukocytic leukemias (AHL) are associated with a very high early mortality rate mostly due to respiratory failure or intracranial bleeding. The pathophysiological process leading to these complications is called leukostasis but the biological mechanisms underlying its development and progression remain unclear. Although traditionally related to "over-crowding" of leukemic blasts in the capillaries of the microcirculation, leukostasis is likely to result from direct endothelial cell damage. This damage is probably mediated by soluble cytokines released during the interaction between leukemic cells and vascular endothelium and by the subsequent migration of leukemic blasts in the perivascular space. Leukemic cell's ability to respond to chemotactic cytokines and their expression of specific adhesion molecules are probably more important in determining whether leukostasis will develop than the number of circulating blasts. This could explain why leukostasis does not develop in all patients with AHL. The identification of the adhesion molecules, cytokines and receptors mediating endothelial cell damage in AHL should become a priority if therapeutic improvements are desired. Leukapheresis is widely used but it is unclear whether it provides additional benefit to a simpler and less invasive intervention with allopurinol, hydroxyurea and intravenous fluids. Cranial irradiation is not generally recommended. Induction chemotherapy should be started without delay. It is hoped that specific pharmacological inhibitors of the interaction between leukemic cells and vascular endothelium will result in an improved outcome for this very high-risk population.

Acute Disease↗
PubMed1990

[Postoperative pulmonary leukostasis responsible for fatal respiratory distress].

A case is reported of a 78-year-old woman with a history of chronic leukemia and who developed after emergency appendicectomy a fatal respiratory distress syndrome related to pulmonary leukostasis. Clinically, the patient had fever, dyspnea and severe hypoxaemia. Chest x-ray showed diffuse pulmonary infiltrates. The patient died from progressive respiratory failure despite ventilatory support. Post mortem lung biopsies were taken for pathologic examination. They showed thrombi composed of leukaemic blast cells which obstructed and distended the lumens of pulmonary arterioles and capillaries. The respiratory distress is attributed to pulmonary leukostasis. Toxic substances released from the leukostatic leukaemic cell or local hypoxia due to vascular occlusion produce this endothelial cell and basement membrane damage. An infectious origin or endogenous pyrogen substances released from leukaemic monocytes may explain the fever. The frequent occurrence of pulmonary leukostasis in patients with leukocyte count greater than 100,000/mm3 point out the need for prevention or therapy of pulmonary leukostasis in these high-risk patients. They need chemotherapy and, if rapid reduction is not observed, leukopheresis which may favourably influence the outcome of patients.

Aged↗
PubMed1986

Streptococcus pneumoniae-induced alterations in levels of circulating thromboxane and prostacyclin: dissociation from granulocytopenia, thrombocytopenia, and pulmonary leukostasis.

The role of thromboxane (Tx) A2 in Streptococcus pneumoniae-induced granulocytopenia, thrombocytopenia, and pulmonary leukostasis is unclear. Rabbits were injected with 0.85% NaCl, nonviable pneumococci, or nonviable pneumococci after pretreatment with TxA2 synthetase inhibition. Blood was obtained immediately before and at times after injection for granulocyte and platelet counts and assays of TxB2 and 6-keto prostaglandin F1 alpha (6-ketoPGF1 alpha). Animals were evaluated for pulmonary leukostasis histologically and biochemically (myeloperoxidase activity). Pneumococcal challenge induced significant granulocytopenia (P less than .001), thrombocytopenia (P less than .001), and elevations in levels of both TxB2 (P less than .05) and 6-ketoPGF1 alpha (P less than .001) as well as pulmonary leukostasis (P less than .001). TxA2 synthetase inhibition blocked the pneumococcus-induced elevation in level of TxB2 without significantly altering levels of circulating granulocytes, platelets, or 6-ketoPGF1 alpha. Pulmonary leukostasis was not blocked. In another group of pneumococcus-challenged animals, no significant transpulmonary gradients of either TxB2 or 6-ketoPGF1 alpha were found.

6-Ketoprostaglandin F1 alpha↗
PubMed1976

The pathologic characteristics of leukostasis and leukemic nodules occurring in the central nervous system of guinea pigs with L2C/NB leukemia.

Leukostasis and leukemic nodules are found in the central nervous system (CNS) of at least 75% of guinea pigs during the terminal stages of untreated L2C/NB leukemia, a transmissible, acute lymphocytic leukemia. The CNS lesions develop after extensive visceral leukemic infiltration at a time when the white cell count is rising to 10(5)-5 x 10(5) cells/mm3, and the differential examination shows predominantly blasts. Leukostasis precedes formation of the nodule. Both lesions may be found in any part of the central nervous system including the spinal cord, but are most numerous in the diencephalon and rostral brain-stem. Ultrastructural studies demonstrate that parenchymal leukostasis develops chiefly within capillaries, and is associated with endothelial cell degeneration and necrosis. Fibrin deposits are not seen within affected capillaries. The sequence of development, pathologic and hematologic characteristics of leukostasiss and leukemic nodules in human and L2C/NB leukemia are virtually identical. The CNS lesions of untreated L2C/NB leukemia are a precise, convenient model for the study of intracerebral leukostasis and leukemic nodules.

Animals↗
PubMed1987

Pulmonary leukostasis: radiologic-pathologic study.

The terminal chest radiographs of ten patients with pulmonary leukostasis were correlated with the autopsy findings. In six patients, no abnormalities attributable to leukostasis were seen on chest radiographs. In four patients, diffuse alveolar consolidations were caused by alveolar edema following leukostasis. Leukostasis should be considered in leukemia patients with severe dyspnea who have normal chest radiographs or diffuse alveolar edema.

Cause of Death↗
PubMed1993

Pressure-related capillary leukostasis following ischemia-reperfusion and hemorrhagic shock.

Although the receptor-dependent venular adhesion of leukocyte adherence has been relatively well characterized, less is known about capillary leukostasis. With the use of fluorescence intravital microscopy, leukocyte behavior in the capillaries of rabbit tenuissimus muscle was evaluated after ischemia-reperfusion or hemorrhage. After fixed volume hemorrhage or 4 h of total ischemia, inflammatory injury was manifest by broken fibrils, edema, leukocyte infiltration, and margination along the postcapillary venular walls. Nevertheless, as long as arterial perfusion pressure was between 27 and 72 mmHg, the frequency of capillary leukostasis was low (4-8 cells/mm2) and similar in all groups, including animals treated with the antiadhesion antibody IB4. In contrast, when perfusion pressure decreased to 20 mmHg, capillary leukostasis increased similarly (to 16-21 cells/mm2) in controls (with or without IB4) and in those subjected to ischemia. Furthermore, when perfusion pressure was increased to more than 27 mmHg, (27-72 mmHg) stationary leukocytes returned to the original low level (4-5 cells/mm2). These results are consistent with the conclusion that during some inflammatory injuries, capillary leukostasis is a pressure-related phenomena that is not receptor dependent and is freely reversible with the early restoration of perfusion pressure.

Animals↗
PubMed1980

Pulmonary leukostasis and its relationship to pulmonary dysfunction in sheep and rabbits.

Pulmonary leukostasis, as a result of complement activation, has been invoked as a cause of pulmonary dysfunction. To investigate this phenomenon, we studied the pulmonary response to infusion of autologous complement-activated plasma in sheep and rabbits. Complement activation was produced by plasma incubation with zymosan. Leukopenia, with selective loss of polymorphonuclear leukocytes into the lungs, occurred in all animals immediately after the onset of plasma infusion. Complement-activated plasma infusion in sheep produced a significant fall in the arterial PO2 and a marked rise in pulmonary vascular resistance, whereas no such effects were observed in rabbits. Pretreatment of the sheep with sulfinpyrazone eliminated the pulmonary response to complement-activated plasma without altering the leukopenic response. Pulmonary histology in rabbits and sheep confirmed the presence of intracapillary leukostasis after the plasma infusions, whether or not sulfinpyrazone had been administered previously. The pulmonary response to complement activation is associated with pulmonary capillary leukostasis, but leukostasis alone is not an adequate explanation of the phenomenon.

Animals↗