Endothelin 1 concentrations in infants with meconium stained amniotic fluid

Yiğit, Şule; Tekinalp, Gülsevin; Oran, O; Yurdakök, Murat; Alíefendíoğlu, Didem; Gürgey, Aytemiz

doi:10.1136/fn.87.3.f212

Cited by 9 publications

(6 citation statements)

References 9 publications

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“…Therefore, our findings may reflect the reactive induction of such vasodilators to lower the pulmonary arterial pressure, which could be a possible compensatory mechanism to prevent the progression of PPHN. A previous study reported high plasma ET-1 levels in infants with MASF on day 0 [31] , in contrast with our finding. In that study, however, infants with MAS and MASF comprised a single group, and blood samples were collected within 6 h after birth.…”

Section: Discussioncontrasting

confidence: 56%

Meconium Aspiration Delays Normal Decline of Pulmonary Vascular Resistance Shortly after Birth through Lung Parenchymal Injury

Ban

Ogihara²,

Mori³

et al. 2010

Neonatology

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Background: Persistent pulmonary hypertension of the newborn is often associated with meconium aspiration syndrome (MAS) or perinatal asphyxia. Objective: To determine the effect of meconium or asphyxia on pulmonary arterial pressure and circulating levels of vasoactive substances, we conducted a prospective study of 54 term infants, including infants with meconium-stained amniotic fluid with normal (MSAF) or abnormal (MAS) chest X-ray findings, infants with perinatal asphyxia, and controls. The purpose of this study was to determine the group most likely to have elevated pulmonary arterial pressure and a disturbed balance between vasoactive substances. Methods: To estimate the pulmonary arterial pressure by echocardiography, we used the ratio of the right to left systolic ventricular pressure (RVP/LVP ratio). We measured the plasma concentrations of endothelin-1 (ET-1), cyclic guanosine monophosphate (cGMP) as an indicator of nitric oxide (NO) production, and 6-keto-prostaglandin F₁α (6-keto-PGF₁α) for the estimation of prostacyclin concentration. We also measured KL-6 as a marker of lung injury. Results:The RVP/LVP ratio was significantly higher in the MAS group than the other groups on day 0. Although ET-1 and 6-keto-PGF₁α levels were comparable among all groups, the cGMP level on days 3–5 and the KL-6 level throughout the first postnatal week were significantly higher in the MAS group. Conclusions: It is possible that meconium aspiration delays normal decline of pulmonary vascular resistance shortly after birth through lung parenchymal injury. The subsequent increase of cGMP in MAS may be an adaptive response to prevent further elevation of pulmonary arterial pressure by inducing NO.

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Section: Discussioncontrasting

confidence: 56%

Meconium Aspiration Delays Normal Decline of Pulmonary Vascular Resistance Shortly after Birth through Lung Parenchymal Injury

Ban

Ogihara²,

Mori³

et al. 2010

Neonatology

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“…Among multiple vasoactive mediators, ET-1 is an important modulator of fetal pulmonary vascular tone and may contribute to failure in postnatal pulmonary vascular adaptation [25]. In both newborns and experimental animals, meconium aspiration increased plasma levels of ET-1, associated with higher pulmonary artery pressure and vascular resistance [26,27]. The finding suggests that meconium-induced alterations in pulmonary vasoregulation may be superimposed on the transitional vascular changes of newborns [28].…”

Section: Endothelin-1 (Et-1)mentioning

confidence: 89%

Inflammation in Meconium Aspiration Syndrome: Targets for Pharmacological Modulation

Mokrá¹,

Mokrý

2007

CPR

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Pathophysiology of meconium aspiration syndrome (MAS) is complex and interactions between individual pathomechanisms are still not completely understood. As recently shown, inflammation plays a significant role in the pathogenesis of MAS. Activated cells release and stimulate production of a wide variety of mediators, including cytokines, enzymes, reactive species, and other biologically active substances in meconium-injured lungs. Anti-inflammatory drugs acting on different levels of inflammatory cascade may in combination with other treatment (exogenous surfactant, inhaled NO, liquid ventilation) improve the clinical status of newborns with MAS. For example, corticosteroids modulate activity of phospholipase A 2 and induced NO synthase, influence migration and activation of leukocytes, and reduce lung edema. Cyclooxygenase inhibitors modulate production of thromboxane and prostaglandins. Phosphodiesterase inhibitors have vasodilating, bronchodilating and anti-inflammatory effects. Antioxidants diminish formation of reactive species. However, there are many other drugs., e.g. anti-cytokine antibodies, inhibitors of complement, inhibitors of angiotensinconverting enzyme, anticoagulants, inhibitors of proteolytic enzymes, calcium-channel blockers etc. that may be beneficial in MAS. Nevertheless, further testing is necessary until the novel approaches may be recommended. In this article, authors reviewed main factors participating in meconium-induced inflammation and pointed out some targets for its pharmacological modulation.

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“…9 Endothelins have been implicated in the pathogenesis of pulmonary hypertension in neonates. [10][11][12] In preterm infants with RDS, studies have shown increased concentrations of ET-1 in the plasma and in tracheal aspirates.…”

mentioning

confidence: 99%

Endothelin-1 andL-Arginine in Preterm Infants with Respiratory Distress

Rifay¹,

Sherif²,

Said³

et al. 2010

Amer J Perinatol

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In addition to the immaturity of air sacs and surfactant deficiency, preterm infants with respiratory distress syndrome (RDS) have abnormalities in the pulmonary vascular bed. We aimed to study two known modulators of pulmonary vessels: endothelin-1 (ET-1) and L-arginine. We hypothesized that plasma concentrations of ET-1 and L-arginine could correlate with the severity of RDS. We prospectively studied 71 preterm infants (gestational age = 29 to 35 weeks) with and without RDS. We measured plasma ET-1 by enzyme-linked immunosorbent assay and L-arginine by spectrophotometry. Infants who continued to require oxygen support or died by day of life 28 were considered to have bronchopulmonary dysplasia (BPD). ET-1 concentrations were significantly higher in RDS infants ( p = 0.039) than controls. Among infants with RDS, it was significantly higher in those who later developed BPD ( p = 0.026). L-arginine was significantly lower in RDS infants ( p = 0.001), but did not differ between BPD and non-BPD infants ( p = 0.19). There was no correlation between L-arginine and ET-1 ( r = 0.1, p = 0.41). The acute phase of RDS is associated with increased plasma concentrations of ET-1 and decreased L-arginine. Infants who later developed BPD had higher plasma ET-1 at birth. Concentrations of ET-1 and L-arginine did not correlate.

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Endothelin 1 concentrations in infants with meconium stained amniotic fluid

Cited by 9 publications

References 9 publications

Meconium Aspiration Delays Normal Decline of Pulmonary Vascular Resistance Shortly after Birth through Lung Parenchymal Injury

Meconium Aspiration Delays Normal Decline of Pulmonary Vascular Resistance Shortly after Birth through Lung Parenchymal Injury

Inflammation in Meconium Aspiration Syndrome: Targets for Pharmacological Modulation

Endothelin-1 andL-Arginine in Preterm Infants with Respiratory Distress

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