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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In vagotomized rats, cerebral compression (CC) produced marked increase in arterial pressure and pulmonary hemorrhagic edema (PHE). We studied the effects of a vasodilator and an oxidant scavenger to delineate the role of hemodynamic and permeability factors in this type of neurogenic PHE. Infusion of sodium nitroprusside at a dose of 5 micrograms/kg/min significantly reduced the CC-induced pressor response by 14% and the lung edema by 41%. A dose of 10 micrograms/kg/min blocked the pressor response by 51%, and completely prevented the lung injury. Dimethylthiourea (DMTU), a potent scavenger for oxidants such as hydroxyl radical and hydrogen peroxide, in doses of 300 and 600 mg/kg was pretreated 15 min before CC. Although DMTU was shown to block the permeability lung damage caused by phorbol myristate acetate (a neutrophil activator), this agent did not exert any effect on the CC-induced pressor response and lung injury. The data indicate that granulocyte-mediated oxidants such as hydroxyl radical and hydrogen peroxide do not appear to be involved in this type of neurogenic lung pathology. The results support the concept that PHE induced by intracranial hypertension is initiated by hemodynamic changes in the systemic and pulmonary circulation. Hydrostatic effect plays a major role in this type of neurogenic lung pathology.
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PMID:Vasodilator and oxidant scavenger in the neurogenic pulmonary edema induced by cerebral compression. 145 71

Sixteen patients with relapsed non-Hodgkin's lymphoma underwent autologous bone marrow transplantation and infusion of recombinant human granulocyte-macrophage colony-stimulating factor (rhGM-CSF). Treatment consisted of involved-field radiotherapy, cyclophosphamide 60 mg/kg/d intravenously (IV) for 2 days, and fractionated total body irradiation (1,200 cGy). Autologous bone marrow was thawed and infused IV, followed 3 hours later by the first infusion of IV rhGM-CSF 11 micrograms/kg/d over 4 hours. Infusions of rhGM-CSF were continued daily until either both neutrophil count exceeded 1,500/microL and platelet count exceeded 50,000/microL, or until 30 days after marrow re-infusion. Toxicities encountered were mild and included fever, chills, hypertension, alopecia, rash, diarrhea, stomatitis, myalgias, and synovial (knee) effusions. Neutrophil recovery greater than 500/microL occurred a median of 14 days (range, 9 to 30 days) after marrow infusion, significantly earlier than in a comparable group of historic controls who recovered counts at a median time of 20 days (range, 12 to 51 days) (P = .00002). Median time to self-sustaining platelet counts greater than 20,000/microL was 23.5 days (range, 12 to 100 days), comparable with the historic group (P = .38). One bacteremia (central venous catheter exit site infection with Staphylococcus epidermidis) and one local infection (Giardia lamblia in stool) occurred. Patients received a median of 11.4 (range, 4.4 to 20.2) x 10(4) colony-forming unit granulocyte-macrophage (CFU-GM) progenitors per kg. Stem cell progenitors CFU-GM, CFU-granulocyte, erythroid, monocyte, megakaryocyte (CFU-GEMM), and burst-forming unit-erythroid (BFU-E) were detected in the bone marrow as early as 7 days after marrow re-infusion, and increased in proportion to peripheral blood counts, but by 30 to 60 days still remained much lower than before transplant. Neutrophils transiently decreased in 13 of 16 patients (median decrease, 42%) within 24 to 72 hours of discontinuing rhGM-CSF infusions. These data suggest that rhGM-CSF therapy enhances neutrophil recovery by forcing stem cells to produce mature elements at an enhanced rate but may not affect marrow stem cell and early progenitor population sizes.
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PMID:Recombinant granulocyte-macrophage colony-stimulating factor after autologous bone marrow transplantation for relapsed non-Hodgkin's lymphoma: blood and bone marrow progenitor growth studies. A phase II Eastern Cooperative Oncology Group Trial. 185 94

The etiology for the progressive organ injury in hypertension is largely speculative. Recent studies have shown that leukocytes play a key role in several cardiovascular diseases. As an initial step toward investigating the role of leukocytes in hypertension, we measured leukocyte counts and spontaneous activation of granulocytes of freshly drawn unseparated blood samples in spontaneously hypertensive rats and in their normotensive counterpart, Wistar-Kyoto rats. The animals were derived from one breeder in the United States and from two breeders in Europe. Total leukocyte counts in young, mature, and old hypertensive rats were 50-100% above the controls. The number of granulocytes in mature and old spontaneously hypertensive rats in more than 100% elevated compared with control rats. In young hypertensive rats the mean granulocyte count was only slightly elevated. The number of spontaneously activated granulocytes, as detected by the nitroblue tetrazolium reduction, increases with age in both species; in mature spontaneously hypertensive rats, it is more than 300% above the values in the controls. Furthermore, in mature hypertensive rats the number of monocytes, activated monocytes, and the lymphocyte count are also significantly elevated over the values in the normotensive controls. It is proposed that these elevated leukocyte counts may constitute an enhanced risk for organ injury in the spontaneously hypertensive rat.
Hypertension 1991 Mar
PMID:Leukocyte counts and activation in spontaneously hypertensive and normotensive rats. 199 64

Pathological induced changes in beta-adrenoceptor function occur in diseases such as asthma and hypertension. The mechanism(s) of this dysfunction is at present unclear. In the present study, the effect of lymphokines on beta-adrenoceptor agonist induced cAMP production in peripheral blood mononuclear cells (PBMC) is investigated. Pre-incubation of PBMC during 20 h with interleukin-2 (IL-2, 100 u ml-1) and granulocyte/macrophage-colony stimulating factor (GM-CSF, 100 u ml-1) significantly decreases beta-adrenoceptor agonist induced cAMP production by 35 +/- 8% and 37 +/- 11% respectively. IL-3 and IL-4 do not affect beta-adrenoceptor agonist induced cAMP production in PBMC. It can be concluded that IL-2 and GM-CSF, mediators derived from T-lymphocytes, can induce beta-adrenoceptor dysfunction in PBMC.
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PMID:Effect of lymphokines on beta-adrenoceptor function of human peripheral blood mononuclear cells. 217 22

Thirteen HLA-identical bone marrow donors served as the sole source of daily granulocyte transfusions for respective marrow recipients during the period of severe neutropenia between transplantation and engraftment. They experienced 12 to 29 (median, 17) daily, continuous flow centrifugation leukapheresis procedures using hydroxyethyl starch, but no corticosteroids, with little serious difficulty. No immediate clinical reactions occurred in 90 percent of 228 procedures. Mild citrate reactions were noted in 9 percent, and only two procedures (0.8%) were discontinued due to severe reactions. Ten donors (77%) answered a questionnaire mailed weeks later, and six reported transient, late clinical adverse effects. Five had moderate dermatologic problems; one had minimal hypertension requiring no therapy. Donors were monitored daily for laboratory abnormalities while donating granulocytes. Hemoglobin concentration and platelet counts remained stable (autologous red cell transfusions had been given). Blood leukocyte counts gradually fell (p less than 0.05), particularly after 10 or more daily granulocyte donations, and this fall was associated with a decrease of about 33 percent in leukocyte yields. No attempts were made to improve yields by giving higher doses of hydroxyethyl starch or by corticosteroid stimulation. With primary emphasis on donor safety, it seems feasible for a few compatible donors to provide prolonged granulocyte transfusion support for designated patients. However, diminishing leukocyte yields may result from intensive, repeated leukapheresis.
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PMID:Effects of intensive granulocyte donation on donors and yields. 242 11

Seventy-five patients, 13 to 49 years of age, with acute nonlymphoblastic leukemia in first remission were treated with cyclophosphamide, fractionated total body irradiation, and marrow transplantation from an HLA-identical sibling and randomized to receive either cyclosporine (CSP) (n = 36) or methotrexate (MTX) (n = 39) as prophylaxis for graft-v-host disease (GVHD). All patients engrafted, and 22 who were given CSP and 21 who were given MTX, are alive at 20 to 47 (median, 35) months (P = .5). Engraftment as assessed by granulocyte recovery (P less than .0005) and platelet transfusion requirement (P = .01) was faster in patients on CSP. Twelve patients (33%) on CSP and 22 (56%) on MTX developed acute GVHD of grades II through IV (P = .07) and 15 of 30 on CSP and 14 of 32 on MTX that were at risk developed chronic GVHD. The most frequent causes of death were interstitial pneumonitis and marrow relapse of leukemia, which occurred with similar frequency in both groups. Beneficial effects observed in patients on CSP included less severe mucositis and shorter duration of hospitalization; adverse effects included renal function impairment and hypertension. These data confirm that CSP is a useful immunosuppressant in patients undergoing marrow transplantation but fail to show a significant improvement in survival as compared with the standard regimen of MTX.
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PMID:Cyclosporine as prophylaxis for graft-versus-host disease: a randomized study in patients undergoing marrow transplantation for acute nonlymphoblastic leukemia. 388 12

Impaired neutrophil responses contribute to the neonate's increased susceptibility to infection. Because granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) enhance granulocyte and macrophage number and function, their use in the management of neonatal sepsis may be beneficial. Little is known about the endogenous levels of G-CSF and GM-CSF. In adults, raised values for G-CSF, but not GM-CSF, have been demonstrated in patients with infection, and conflicting data has emerged regarding CSF levels in neonates. We have used an ELISA to measure maternal and cord serum G-CSF and GM-CSF at the time of delivery, with gestational age between 25 and 42 wk. In mothers, an inverse linear relationship between gestational age and GM-CSF levels (p = 0.049) was found, but no association with G-CSF levels was observed. In neonates, a quadratic association was found between GM-CSF levels and gestational age (p = 0.019), whereas G-CSF levels showed an inverse linear association (p = 0.015). In addition, an association was found between maternal and cord GM-CSF (p = 0.007) but not G-CSF levels in paired samples. The effect of gestational age on the cytokine levels could not be explained by the white cell count, the absolute neutrophil count, pregnancy-induced hypertension, or the presence of infection.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Granulocyte and granulocyte-macrophage colony-stimulating factors in cord and maternal serum at delivery. 751 77

The leukocyte glycoprotein L-selectin mediates an early step in the recruitment of leukocytes to sites of inflammation. L-Selectin surface expression is rapidly down-regulated by inflammatory signals in vitro. In a prospective study, we found L-selectin expression on umbilical cord blood granulocytes and monocytes to be significantly decreased in newborn infants with acute bacterial infection compared with controls (p < 0.01). A significantly reduced L-selectin expression of both granulocytes and monocytes was also found to be associated with an increased neutrophil immature/total ratio (p < 0.01) but not with other laboratory markers of neonatal sepsis. There was no apparent impact of prematurity, low birth weight, gestational hypertension, or gestational diabetes on L-selectin expression. Although the mode of delivery did not affect granulocyte L-selectin expression, umbilical cord blood monocytes showed an increased L-selectin expression after emergency cesarean delivery compared with samples obtained after elective cesarean or vaginal delivery (p < 0.01). We conclude that acute systemic inflammation results in down-regulation of granulocyte and monocyte L-selectin expression in vivo similar to that observed in vitro.
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PMID:L-selectin is down-regulated in umbilical cord blood granulocytes and monocytes of newborn infants with acute bacterial infection. 753 4

G-CSF (granulocyte-colony stimulating factor) is one of the cytokines which increase and activate neutrophils. These effects have been confirmed by a lot of clinical studies. Although only few side effects have been reported so far, we saw a patient with hypertension, facial edema, and severe headache after G-CSF administration. We have measured the sticking strength of leukocytes to the walls of narrow pores in modified Nuclepore filtration method of Kikuchi, in various clinical situations, and we have denoted the pore filtration time as the rheological activity of leukocytes (RAL). In this study, we tried to measure RALs of patients after G-CSF administration (60-100 micrograms) and to compare them with those of non-treated normal individuals. We also checked serum levels of granulocyte elastase in the patients. In the static state (in which neutrophils were not stimulated), RALs of the patients were 8.0 +/- 1.5sec. [N = 8], and those of the controls were 3.8 +/- 1.6sec. [N = 21] (p < 0.001). In the activated state (in which neutrophils were stimulated by formyl-methionyl-leucyl-phenylalanine), PALs of patients were quite high, i.e. those of the patients and controls were 592 +/- 322sec. and 69 +/- 62sec., respectively (p < 0.001). In all cases given G-CSF, the serum levels of granulocyte elastase were above the normal range. In view of our results, we it is possible that highly activated leukocytes would injure tissue and then induce organ failure and several symptoms, as in this study.
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PMID:[Leukocyte activity and occurrence of tissue injury by G-CSF]. 768 59

Before and after venous stasis and upon recovery blood samples were drawn from the saphenous vein in 10 patients with varicose veins (Group 1), in 10 with venous hypertension (Group 2) and in 10 healthy controls. The total leucocyte count, the leucocyte filterability rate (LFR), superoxide dismutase blood concentrations (SOD) and the production of superoxide anions from granulocytes were determined. After stasis, the total leucocyte count increased significantly (p < 0.01) in both groups of patients and the LFR was significantly (p < 0.01) impaired. SOD blood concentrations fell significantly (p < 0.01) and oxygen free radical production dropped significantly (p < 0.01) in both groups. Upon recovery, all parameters returned to normal in Group 1 but significant differences remained in Group 2. No significant modification was observed at any stage of the study in the control group. These results suggest that impairments in leucocyte rheology and granulocyte production of oxygen free radicals cause capillary plugging and possibly damage to microcirculatory vessel walls in venous disease.
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PMID:Leucocyte activity in chronic venous insufficiency. 779 Jul 51


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