Early effects of ionizing radiation on pulmonary endothelial angiotensin-converting enzyme and 5′-nucleotidase, in vivo

Catravas, John D.; Burch, Sandra E.; Spurlock, Benjamin O.; Mills, Luther R.

doi:10.1016/0041-008x(88)90276-1

Cited by 22 publications

(9 citation statements)

References 21 publications

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“…Pulmonary endothelial ectoenzyme activity measurements have been shown to provide early and sensitive indices of radiationinduced endothelial lung injury. In this respect, rabbits exposed to 30 Gy of ionizing radiation produced early decreases of PCEB-ACE and -5′-Nucleotidase affinities for their substrates in vivo in the absence of structural endothelial damage (Catravas et al, 1988). The aforementioned early dysfunction of pulmonary endothelial ectoenzymes was further confirmed under a broad range of pulmonary blood flows in the rabbit heart-bypass model (i.e.…”

Section: Ionizing Radiation and Acute Lung Injurymentioning

confidence: 78%

Endothelial pathomechanisms in acute lung injury

Maniatis

Κοτανίδου

Catravas

et al. 2008

Vascular Pharmacology

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193

169

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Acute lung injury (ALI) and its most severe extreme the acute respiratory distress syndrome (ARDS) refer to increased-permeability pulmonary edema caused by a variety of pulmonary or systemic insults. ALI and in particular ARDS, are usually accompanied by refractory hypoxemia and the need for mechanical ventilation. In most cases, an exaggerated inflammatory and pro-thrombotic reaction to an initial stimulus, such as systemic infection, elicits disruption of the alveolo-capillary membrane and vascular fluid leak. The pulmonary endothelium is a major metabolic organ promoting adequate pulmonary and systemic vascular homeostasis, and a main target of circulating cells and humoral mediators under injury; pulmonary endothelium is therefore critically involved in the pathogenesis of ALI. In this review we will discuss mechanisms of pulmonary endothelial dysfunction and edema generation in the lung with special emphasis on the interplay between the endothelium, the immune and hemostatic systems, and highlight how these principles apply in the context of defined disorders and specific insults implicated in ALI pathogenesis.

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Section: Ionizing Radiation and Acute Lung Injurymentioning

confidence: 78%

Endothelial pathomechanisms in acute lung injury

Maniatis

Κοτανίδου

Catravas

et al. 2008

Vascular Pharmacology

Self Cite

193

169

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“…Pulmonary capillary endothelium–bound ACE (PCEB‐ACE) activity has been studied extensively in vivo and in situ, by means of indicator‐dilution techniques in numerous animal models. Under physiologic conditions, PCEB‐ACE activity allows estimations of the perfused capillary bed (10, 13, 14), while under pathologic conditions, PCEB‐ACE dysfunction is an early and sensitive index of lung vascular injury (9, 15–18). A similar indicator‐dilution technique for use in the study of humans has been recently introduced.…”

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confidence: 99%

Pulmonary capillary endothelial dysfunction in early systemic sclerosis

Orfanos

Psevdi

Stratigis

et al. 2001

Arthritis & Rheumatism

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Objective Pulmonary capillary endothelium–bound angiotensin‐converting enzyme (PCEB‐ACE) activity is a sensitive and quantifiable index of endothelial function in vivo. Systemic sclerosis (SSc) is characterized by endothelial damage and excess collagen formation, causing mainly pulmonary hypertension (PH) in the limited cutaneous SSc (lcSSc) subset and interstitial lung disease with pulmonary interstitial fibrosis (PIF) in the diffuse cutaneous SSc (dcSSc) subset. This study was undertaken to investigate the hypothesis that PCEB‐ACE activity is reduced early in SSc, in the absence of PH or PIF. Methods Applying indicator‐dilution techniques, we measured single‐pass transpulmonary hydrolysis and percent metabolism (%M) of a synthetic ACE substrate and calculated functional capillary surface area (FCSA) in 25 SSc patients and 11 controls. Substrate hydrolysis and %M reflect ACE activity per capillary; FCSA reflects ACE activity per vascular bed. Results PCEB‐ACE activity was decreased in both SSc subsets. Among patients without PH, substrate hydrolysis and %M were decreased in patients with lcSSc and more profoundly in those with dcSSc; loss of FCSA normalized to body surface area (FCSA/BSA) was observed in dcSSc, but not in lcSSc. High‐resolution computed tomography of the lung, performed in all SSc patients, revealed no correlation between substrate %M, hydrolysis, or FCSA/BSA and the degree of PIF; 5 dcSSc and 5 lcSSc patients with no detectable PIF exhibited decreases in hydrolysis and %M, while FCSA/BSA was decreased only in dcSSc. Conclusion Depression of PCEB‐ACE activity, indicating pulmonary endothelial dysfunction, occurs early in SSc, in the absence of PH or PIF, and is more pronounced, at this early pulmonary disease stage, in dcSSc than in lcSSc.

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“…Furthermore, dilution error appears to remain constant, at least within individual preparations, since repeated determinations of these parameters produce remarkably reproducible results (e.g. see Catravas et al, 1988).…”

Section: Discussionmentioning

confidence: 99%