Effects of increased pulmonary vascular tone on gas exchange in canine oleic acid pulmonary edema

Leeman, Marc; Lejeune, Philippe; Hallemans, Roger; Mélot, Christian; Naeije, Robert

doi:10.1152/jappl.1988.65.2.662

Cited by 33 publications

(23 citation statements)

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“…There were 15 preclinical studies (26–40) identified in this systematic review (Table 1). In 10 studies the antiplatelet drug was ASA (26–31, 35–38) in three studies ASA-triggered lipoxin (32, 33, 38) , and in three studies ASA-triggered resolving D 1 (34, 39, 40) were studied.…”

Section: Resultsmentioning

confidence: 99%

Prevention or Treatment of Ards With Aspirin

Panka

Grooth

Man

et al. 2017

Shock

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Background The acute respiratory distress syndrome (ARDS) is a life-threating disorder that contributes significantly to critical illness. No specific pharmacological interventions directed at lung injury itself, have proven effective in improving outcome of patients with ARDS. Platelet activation was identified as a key component in ARDS pathophysiology and may provide an opportunity for preventive and therapeutic strategies. We hypothesize that use of acetyl salicylic acid (ASA) may prevent and/or attenuate lung injury. Methods We conducted a systematic review of preclinical studies and meta-analysis of clinical studies investigating the efficacy of ASA in the setting of lung injury. MEDLINE, EMBASE AND COCHRANE databases were searched. Results The literature search yielded 1314 unique articles. Fifteen pre-clinical studies and eight clinical studies fulfilled the in- and exclusion criteria. In the animal studies, the overall effect of ASA was positive, e.g. ASA improved survival and attenuated inflammation and pulmonary edema. Mechanisms of actions involved, among others, are interference with the neutrophil-platelets interaction, reduction of leukotrienes, neutrophil extracellular traps and prostaglandins. High dose ASA may be the drug of choice. A meta-analysis of 3 clinical studies showed an association between ASA use and a reduced incidence of ARDS (OR 0.59, 95% CI 0.36–0.98), albeit with substantial between-study heterogeneity. All studies had their own shortcomings in methodological quality. Conclusion This systematic review of preclinical studies and meta-analysis of clinical studies suggests a beneficial role for ASA in ARDS prevention and treatment. However, the currently available data is insufficient to justify an indication for ASA in ARDS. The body of literature does support further studies in humans. We suggest clinical trials in which the mechanisms of action of ASA in lung injury models is being evaluated to guide optimal timing and dose, before prospective randomized trials.

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Section: Resultsmentioning

confidence: 99%

Prevention or Treatment of Ards With Aspirin

Panka

Grooth

Man

et al. 2017

Shock

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“…During lung injury, the pulmonary circulation is exposed to the widespread release of these constricting and dilating mediators, the net effect is an increase in the vascular tone. Inhibitors of COX [25,26] and of NO synthesis or their effects, have been shown to further increase Ppa in experimental lung injury [27]. Intravenous infusion of endotoxin in sheep causes Ppa to rise within several minutes, which remains raised for hours [28].…”

Section: Discussionmentioning

confidence: 99%

“…inhibiting HPV) [19]. Blockade of COX and NO have been shown to improve Pa,O 2 by reducing intrapulmonary shunt in animals with oleic acid-induced pulmonary oedema [19,[25][26][27]. In clinical practice, several intravenous vasodilators have been administered in patients with ARDS, with the aim of increasing cardiac output and hence oxygen delivery.…”

Section: Intravenous Vasodilatorsmentioning

confidence: 99%

Pathophysiology and pharmacological treatment of pulmonary hypertension in acute respiratory distress syndrome

Moloney

Evans²

2003

Eur Respir J

112

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Pulmonary hypertension (PH) is a characteristic feature of the acute respiratory distress syndrome (ARDS). The magnitude of PH has been shown to correlate with the severity of lung injury in patients with ARDS independently of the severity of associated hypoxaemia and has an adverse prognostic significance.Early in the histopathological evolution of ARDS, pulmonary vasoconstriction, thromboembolism and interstitial oedema contribute to the development of PH, although pulmonary vascular remodelling probably occurs eventually. Intravenous vasodilator agents lead to an increase in intrapulmonary shunting and systemic hypotension, which can limit their therapeutic use, and have not been shown to improve survival. By contrast, rapidly metabolised vasodilators administered by inhalation induce selective pulmonary vasodilatation and decrease shunting, but again do not appear to confer a survival benefit.Research aimed at further understanding the mechanisms that underlie pulmonary hypertension, a characteristic feature of the acute respiratory distress syndrome, are expected to provide improvements in pharmacological interventions for the treatment of pulmonary hypertension in the acute respiratory distress syndrome.

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“…These results are consistent with potentiation of HPV in shunt regions and enhanced diversion of perfusion to ventilated lung. In animal models of ALI/ARDS, these effects of almitrine were shared by antagonists of cyclooxygenase (33, 1058,1060,1738) but not by antagonists of NOS (1058,1415,1555,1668), which increased PVR but did not alter P a O 2 or shunt. These results suggest that endogenous production of vasodilator prostaglandins such as PGI 2 , and thus their inhibition of HPV and other vasoconstrictor mechanisms, may have been greater in more injured nonventilated lung than in less injured ventilated lung, whereas endogenous production of NO and NO-dependent inhibition of vasoconstriction was similar in ventilated and nonventilated lung.…”

Section: Vi) Chronic Obstructive Pulmonary Diseasementioning

confidence: 95%

Hypoxic Pulmonary Vasoconstriction

Sylvester

Shimoda

Aaronson

et al. 2012

Physiological Reviews

599

621

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It has been known for more than 60 years, and suspected for over 100, that alveolar hypoxia causes pulmonary vasoconstriction by means of mechanisms local to the lung. For the last 20 years, it has been clear that the essential sensor, transduction, and effector mechanisms responsible for hypoxic pulmonary vasoconstriction (HPV) reside in the pulmonary arterial smooth muscle cell. The main focus of this review is the cellular and molecular work performed to clarify these intrinsic mechanisms and to determine how they are facilitated and inhibited by the extrinsic influences of other cells. Because the interaction of intrinsic and extrinsic mechanisms is likely to shape expression of HPV in vivo, we relate results obtained in cells to HPV in more intact preparations, such as intact and isolated lungs and isolated pulmonary vessels. Finally, we evaluate evidence regarding the contribution of HPV to the physiological and pathophysiological processes involved in the transition from fetal to neonatal life, pulmonary gas exchange, high-altitude pulmonary edema, and pulmonary hypertension. Although understanding of HPV has advanced significantly, major areas of ignorance and uncertainty await resolution.

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Effects of increased pulmonary vascular tone on gas exchange in canine oleic acid pulmonary edema

Cited by 33 publications

References 0 publications

Prevention or Treatment of Ards With Aspirin

Prevention or Treatment of Ards With Aspirin

Pathophysiology and pharmacological treatment of pulmonary hypertension in acute respiratory distress syndrome

Hypoxic Pulmonary Vasoconstriction

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