Decreased serum angiotensin converting enzyme in adult respiratory distress syndrome associated with sepsis

Casey, Larry C.; Krieger, Bruce P.; Kohler, John P.; Rice, Charles L.; Oparil, Suzanne; Szidon, Peter

doi:10.1097/00003246-198109000-00008

Cited by 57 publications

(38 citation statements)

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“…8 However, during sepsis there is also a decrease in circulating ACE activity, which correlates with systemic blood pressure. 12,13 These decreases in serum ACE activity during sepsis may reflect endothelial cell damage or inhibition of ACE activity by bacterial mediators such as lipopolysaccharide (LPS). 14 Because of the important role ACE plays in inflammatory responses, interindividual genetic variation in ACE activity may alter outcome in severe infections.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin Converting Enzyme Insertion/Deletion Polymorphism Does Not Alter Sepsis Outcome in Ventilated Very Low Birth Weight infants

2004

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OBJECTIVE:This study compared the effect of the angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphisms on the incidence and outcome of sepsis in ventilated very low birth weight infants. STUDY DESIGN:Infectious complications were retrospectively determined in 295 (234 African-American, 58 Caucasian and three Hispanic) mechanically ventilated very low birth weight (VLBW) infants (<1500 g at birth) and compared ACE I/D genotype. RESULTS:The incidence of the D allele in the study population was 0.60. A total of 113 (38.3%) infants were homozygous DD, 128 (43.4%) were heterozygous ID and 54 (18.3%) were homozygous II. One or more episodes of late BSI developed in 28 (52%) of 54 infants with the II genotype, 66 (52%) of 128 infants with the ID genotype and 52 (46%) of 113 infants with the DD genotype (p ¼ 0.618). Neither the rates of non-CONS BSI (II: 24%, ID: 23%, DD: 22%; p ¼ 0.937) nor multiple bacteremic/fungemic episodes (II: 13%, ID: 16%, DD: 12%; p ¼ 0.641) were different between genotype groups. The ACE I/D polymorphism had no effect on sepsis-related mortality (II: 7%, ID: 5%, DD: 4%; p ¼ 0.692). Sepsis mortality for infants with late BSI was 14% in infants with the II genotype, 9% with the ID genotype and 10% with the DD genotype (p ¼ 0.764). CONCLUSIONS:The ACE I/D polymorphism does not have a significant effect on the incidence or outcome of sepsis in ventilated VLBW infants.

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Section: Introductionmentioning

confidence: 99%

Angiotensin Converting Enzyme Insertion/Deletion Polymorphism Does Not Alter Sepsis Outcome in Ventilated Very Low Birth Weight infants

2004

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“…Furthermore, hypoxia is known to decrease lung angiotensin-converting enzyme (ACE) activity. For example, there is severe depression of lung ACE activity following acute lung injury, and the serum ACE level decreases in sepsis-induced ARDS in humans [6,7]. Thus, hypoxia may decrease BK degradation in the lung of ARDS patients, thereby potentiating the harmful effects of the peptide.…”

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confidence: 99%

Bradykinin stimulates IL-6 and IL-8 production by human lung fibroblasts through ERK- and p38 MAPK-dependent mechanisms

Hayashi¹,

Yamashita

Matsui

et al. 2000

Eur Respir J

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Bradykinin (BK) is a major kinin with well-documented pharmacological properties including vascular leakage and induction of a variety of cytokines. However, the intracellular signalling mechanisms by which BK induced proinflammatory cytokine production have not been fully elucidated. This study investigated the role of the extracellular signal-regulated protein kinase 1/2 (ERK 1/2) and p38 mitogen-activated protein kinase (p38 MAPK) in the BK-induced interleukin (IL)-6 and IL-8 production by human lung fibroblasts.Lung fibroblasts were stimulated with BK in the presence or in the absence of PD98059, a specific MAPK/ERK kinase-1 inhibitor, or SB203580, a specific p38 MAPK inhibitor, and IL-6 or IL-8 production and their gene expression was examined. BK-induced ERK 1/2 or p38 MAPK phosphorylation was also analysed by Western blot analysis.BK at nanomolar concentrations stimulated lung fibroblasts to produce IL-6 and IL-8 along with increased ERK 1/2 and p38 MAPK phosphorylation. BK-induced IL-6 and IL-8 synthesis was inhibited by a B2-type BK receptor antagonist. Furthermore, PD98059 or SB203580 significantly suppressed BK-induced IL-6 and IL-8 production and their gene expression.These results indicate that bradykinin-induced interleukin-6 and interleukin-8 production are at least partly mediated through the extracellular signal-related protein kinase 1/2 and p38 mitogen-activated protein kinase pathway-dependent activation in human lung fibroblasts, and suggest that bradykinin appears to be involved in the inflammatory reaction leading to acute lung injury through stimulating interleukin-6 and interleukin-8 production by lung fibroblasts. Eur Respir J 2000; 16: 452±458.

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“…AT-II has been shown to be involved in the development of pulmonary edema, increasing vascular tone and vascular permeability [31,32]. Several authors described a reduction in ACE plasma level in patients with ARDS [33][34][35][36], reflecting lung damage severity (decreased synthesis) and impairment of systemic release of the enzyme [25]. We found lower AT-II plasma levels at admission in subjects with ACE II genotype, being more strikingly reduced in ARDS patients.…”

Section: Discussionmentioning

confidence: 43%

Angiotensin-converting enzyme insertion/deletion polymorphism is associated with severe hypoxemia in pediatric ARDS

et al. 2011

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Decreased serum angiotensin converting enzyme in adult respiratory distress syndrome associated with sepsis

Cited by 57 publications

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Angiotensin Converting Enzyme Insertion/Deletion Polymorphism Does Not Alter Sepsis Outcome in Ventilated Very Low Birth Weight infants

Angiotensin Converting Enzyme Insertion/Deletion Polymorphism Does Not Alter Sepsis Outcome in Ventilated Very Low Birth Weight infants

Bradykinin stimulates IL-6 and IL-8 production by human lung fibroblasts through ERK- and p38 MAPK-dependent mechanisms

Angiotensin-converting enzyme insertion/deletion polymorphism is associated with severe hypoxemia in pediatric ARDS

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