Search PubMed⌕ Search

Biomedical subjects

L Storme

Publications and source records attributed to L Storme.

At least 37 records · Page 2Linked to original sources
PubMed1999

K+-channel blockade inhibits shear stress-induced pulmonary vasodilation in the ovine fetus.

To determine whether K+-channel activation mediates shear stress-induced pulmonary vasodilation in the fetus, we studied the hemodynamic effects of K+-channel blockers on basal pulmonary vascular resistance and on the pulmonary vascular response to partial compression of the ductus arteriosus (DA) in chronically prepared late-gestation fetal lambs (128-132 days gestation). Study drugs included tetraethylammonium (TEA; Ca2+-dependent K+-channel blocker), glibenclamide (Glib; ATP-dependent K+-channel blocker), charybdotoxin (CTX; preferential high-conductance Ca2+-dependent K+-channel blocker), apamin (Apa; low-conductance Ca2+-dependent K+-channel blocker), and 4-aminopyridine (4-AP; voltage-dependent K+-channel blocker). Catheters were inserted in the left pulmonary artery (LPA) for selective drug infusion and in the main pulmonary artery, aorta, and left atrium to measure pressure. An inflatable vascular occluder was placed around the DA. LPA flow was measured with an ultrasonic flow transducer. Animals were treated with saline, high- or low-dose TEA, Glib, Apa, CTX, CTX plus Apa, or 4-AP injected into the LPA. DA compression caused a time-related decrease in pulmonary vascular resistance in the control, Glib, Apa, CTX, CTX plus Apa, and low-dose TEA groups but not in the high-dose TEA and 4-AP groups. These data suggest that pharmacological blockade of Ca2+- and voltage-dependent K+-channel activity but not of low-conductance Ca2+- and ATP-dependent K+-channel activity attenuates shear stress-induced fetal pulmonary vasodilation.

4-Aminopyridine↗
PubMed1999

Inducible NO synthase inhibition attenuates shear stress-induced pulmonary vasodilation in the ovine fetus.

Recent studies have suggested that type II (inducible) nitric oxide (NO) synthase (NOS II) is present in the fetal lung, but its physiological roles are uncertain. Whether NOS II activity contributes to the NO-mediated fall in pulmonary vascular resistance (PVR) during shear stress-induced pulmonary vasodilation is unknown. We studied the hemodynamic effects of two selective NOS II antagonists [aminoguanidine (AG) and S-ethylisothiourea (EIT)], a nonselective NOS antagonist [nitro-L-arginine (L-NNA)], and a nonselective vasoconstrictor (U-46619) on PVR during partial compression of the ductus arteriosus (DA) in 20 chronically prepared fetal lambs (mean age 132 +/- 2 days, term 147 days). At surgery, catheters were placed in the left pulmonary artery (LPA) for selective drug infusion, an ultrasonic flow transducer was placed on the LPA to measure blood flow, and an inflatable vascular occluder was placed loosely around the DA for compression. On alternate days, a brief intrapulmonary infusion of normal saline (control), AG, EIT, L-NNA, or U-46619 was infused in random order into the LPA. The DA was compressed to increase mean pulmonary arterial pressure (MPAP) 12-15 mmHg above baseline values and held constant for 30 min. In control studies, DA compression reduced PVR by 42% from baseline values (P < 0.01). L-NNA treatment completely blocked the fall in PVR during DA compression. AG and EIT attenuated the decrease in PVR by 30 and 19%, respectively (P < 0.05). Nonspecific elevation in PVR by U-46619 did not affect the fall in PVR during DA compression. Immunostaining for NOS II identified this isoform in airway epithelium and vascular smooth muscle in the late-gestation ovine fetal lung. We conclude that selective NOS II antagonists attenuate but do not block shear stress-induced vasodilation in the fetal lung. We speculate that stimulation of NOS II activity, perhaps from smooth muscle cells, contributes in part to the NO-mediated fall in PVR during shear stress-induced pulmonary vasodilation.

Animals↗
PubMed1999

In vivo evidence for a myogenic response in the fetal pulmonary circulation.

In vitro studies have suggested that pulmonary arteries can exhibit a myogenic response and that this myogenic response may be potent during the perinatal period. However, whether a myogenic response can be demonstrated to exist in vivo and the potential role of the myogenic response on the regulation of pulmonary blood flow during fetal life is unknown. We hypothesized that an acute increase in pulmonary artery pressure resulting from partial compression of the ductus arteriosus (DA) in the fetus may simultaneously activate two opposing responses: 1) blood flow-induced vasodilation (owing to shear stress); and 2) pressure-induced vasoconstriction (owing to the myogenic response). To test this hypothesis, we studied the hemodynamic response to partial DA compression with and without inhibition of shear stress-induced vasodilation by nitric oxide synthase blockade in chronically prepared late-gestation fetal lambs. Without inhibition of nitric oxide synthase, pulmonary vascular resistance progressively decreased by 39 +/- 5% during the DA compression period (p < 0.05). In contrast, DA compression after nitric oxide synthase inhibition caused left pulmonary artery blood flow to initially increase and then steadily decrease toward a plateau value, and caused pulmonary vascular resistance to progressively increase by 28 +/- 4% above baseline (p < 0.05). The plateau value of pulmonary vascular resistance was reached in less than 5 min after the onset of DA compression. Left pulmonary artery blood flow after 10 min of partial DA compression did not change with the rise in pulmonary artery pressure; plateau values of pulmonary vascular resistance increased linearly with the increase in pulmonary artery pressure. These results support the hypothesis that the perinatal lung circulation has a potent myogenic response, and that this response may be masked in vivo under physiologic conditions by nitric oxide synthase activity. We speculate that the myogenic response may become a predominant regulatory mechanism of pulmonary vascular resistance when endothelium-dependent vasoreactivity is impaired, such as in persistent pulmonary hypertension of the newborn.

Animals↗
PubMed1999

Acute intrauterine pulmonary hypertension impairs endothelium-dependent vasodilation in the ovine fetus.

To determine whether acute pulmonary hypertension in utero alters fetal pulmonary vascular reactivity, we compared pulmonary vasodilation with an endothelium-dependent agonist, acetylcholine, with that of an endothelium-independent agonist, 8-bromo-guanosine 3',5'-cylic monophosphate. Acute pulmonary hypertension was produced in chronically prepared, late-gestation fetal lambs by 3 repeated 30-minute partial occlusions of the ductus arteriosus (DA). The first DA compression increased LPA blood flow from 80 +/- 10 to 180 +/- 21 mL/min (p < 0.01) and decreased pulmonary vascular resistance. In contrast, LPA blood flow did not change and pulmonary vascular resistance increased by 25% during the third period of DA compression. Pulmonary vasodilation during acetylcholine infusion after serial DA compressions was decreased in comparison with the acetylcholine-induced vasodilator response achieved during the baseline period (fall in pulmonary vascular resistance = -49 +/- 7% (baseline) versus -25 +/- 5% after repeated DA compressions; p < 0.05). In contrast, the vasodilator response to 8-bromo-guanosine 3',5'-cylic monophosphate remained intact. To determine whether decreased nitric oxide (NO) production may contribute to altered vasoreactivity after acute pulmonary hypertension, repeated DA compressions were performed after treatment with a nonspecific NO synthase inhibitor (nitro-L-arginine). NO synthase inhibition blocked the pulmonary vasodilation during the first DA compression period, and repeated DA compressions after NO synthase inhibition did not further alter the hemodynamic response to DA compression. These findings support the hypothesis that brief hypertension due to DA compression impairs endothelium-dependent pulmonary vasodilation in the fetus, and that this may be due to decreased NO production.

Acetylcholine↗
PubMed1998

Measurement of respiratory mechanics in paediatric intensive care: in vitro assessment of a pulmonary function device.

OBJECTIVE: To evaluate a recently developed and manufactured device for monitoring respiratory parameters in mechanically ventilated children. DESIGN: In vitro study using a lung model. SETTING: University paediatric intensive care unit. MATERIAL AND INTERVENTIONS: Evaluation of the accuracy of volume and pressure measurements, of the determination of respiratory system compliance (10 to 30 ml/cmH2O) and of resistance (20 and 50 cmH2O/l per s) by the inflation technique (volume- and pressure-controlled mode of ventilation); assessment of interobserver agreement for compliance (10, 15 ml/cmH2O) and resistance (20, 50 cmH2O/l per s) determinations (ANOVA, intraclass correlation coefficient). MEASUREMENTS AND RESULTS: The accuracy of volume measurements (No.1 Fleisch pneumotachograph) was < or = 5 % of true volumes up to 11 (Flow: 30 l/min) even after the introduction of an endotracheal tube. The accuracy of pressure measurements up to 70 cmH2O was < or = 2.5% of the true values. Coefficients of variation of volume and pressure measurements were < 2%. The accuracy of compliance and resistance determinations was, respectively, < or = 17 and 25% of the true values. No significant observer effect was found on compliance and resistance determinations. Indeed, mean differences in compliance and resistance determinations by pairs of observers were < 1%. Intraclass correlation coefficients were > 0.98. CONCLUSIONS: The measuring error of volume, pressure, compliance and resistance determined using this monitoring system seems acceptable for monitoring purpose. Moreover, use of this system by members of the medical team can be recommended since results obtained by observers, even untrained ones, were similar. In vivo evaluation is now needed.

Airway Resistance↗
PubMed1998

Disease-related response to inhaled nitric oxide in newborns with severe hypoxaemic respiratory failure. French Paediatric Study Group of Inhaled NO.

Inhaled nitric oxide (iNO) has been shown to improve oxygenation in severe persistent pulmonary hypertension of the newborn (PPHN). However, PPHN is often associated with various lung diseases. Thus, response to iNO may depend upon the aetiology of neonatal acute respiratory failure. A total of 150 (29 preterm and 121 term) newborns with PPHN were prospectively enrolled on the basis of oxygenation index (OI) higher than 30 and 40, respectively. NO dosage was stepwise increased (10-80 ppm) during conventional mechanical or high-frequency oscillatory ventilation while monitoring the oxygenation. Effective dosages ranged from 5 to 20 ppm in the responders, whereas iNO levels were unsuccessfully increased up to 80 ppm in the nonresponders. Within 30 min of iNO therapy, OI was significantly reduced in either preterm neonates (51+/-21 vs 23+/-17, P < .0001) or term infants with idiopathic or acute respiratory distress syndrome (45+/-20 vs 20+/-17, P < .0001), 'idiopathic' PPHN (39+/-14 vs 14+/-9, P < .0001), and sepsis (55+/-25 vs 26+/-20, P < .0001) provided there was no associated refractory shock. Improvement in oxygenation was less significant and sustained (OI=41+/-16 vs 28+/-18, P < .001) in term neonates with meconium aspiration syndrome and much less (OI=58+/-25 vs 46+/-32, P < .01) in those with congenital diaphragmatic hernia. Only 21 of the 129 term newborns (16%) required extracorporeal membrane oxygenation (57% survival). Survival was significantly associated with the magnitude in the reduction in OI at 30 min of iNO therapy, a gestational age > or =34 weeks, and associated diagnosis other than congenital diaphragmatic hernia. Conclusion, iNO improves the oxygenation in most newborns with severe hypoxaemic respiratory failure including preterm neonates. However, response to iNO is disease-specific. Furthermore, iNO when combined with adequate alveolar recruitment and limited barotrauma using exogenous surfactant and HFOV may obviate the need for extracorporeal membrane oxygenation in many term infants.

Administration, Inhalation↗
PubMed1998

[Exhale nitric oxide (NO) and respiratory function measured with body plethysmography in children].

BACKGROUND: Exhaled nitric oxide (NO) may be a marker of airway inflammation. Previous studies in adults have shown that the level of NO in exhaled air is influenced by several factors (breath holding, exercise, etc), or by several disease (asthma, congestive heart failure, diseases of the upper respiratory tract, cystic fibrosis, etc). However, few studies have been performed in children less than 3 years of age. The aim of this study was to determine endogenous NO levels in children with various diseases during lung volume measurements. PATIENTS AND METHODS: Fifty-two children aged 18.3 +/- 9.5 months were studied. The population was divided in two groups, according to the underlying disease: a group of 39 children with cystic fibrosis (n = 7), bronchopulmonary dysplasia (n = 17), asthma (n = 7) or recurrent respiratory tract infections (n = 8) and a second group of 13 children without respiratory disease. Lung function was measured by whole body plethysmography and several respiratory parameters were calculated (functional residual capacity [FRC], compliance and resistances of the respiratory system, trapped volume). NO production was measured on a chemiluminescence analyzer from mixed exhaled air collected into a bag, over a period of 5 minutes. RESULTS: NO production was related to disease: exhaled NO levels were three times higher in bronchopulmonary dysplasia and cystic fibrosis, compared to NO levels in children without respiratory disease. They were higher in asthma. They were not altered in recurrent respiratory tract infections. No correlation was found between respiratory parameters and NO production. However, exhaled NO levels were correlated to trapped volume, which defined dynamic part of pulmonary hyperinflation. CONCLUSION: Levels of endogenous NO in infants were similar to those measured in adults with and without inflammatory respiratory disease. Lung distention influenced exhaled NO production.

Biomarkers↗
PubMed1998

Inhaled nitric oxide neither alters oxidative stress parameters nor induces lung inflammation in premature lambs with moderate hyaline membrane disease.

The purpose of this investigation was to examine whether inhaled nitric oxide (NO) may alter oxidative stress parameters and induce lung inflammation in moderate hyaline membrane disease (HMD). Eighteen moderately premature lambs (130 days gestation, term = 147 days) were randomly assigned to treatment with 20 ppm inhaled NO (n = 8) from the onset of ventilation or used as control (n = 10). Except inhaled NO, treatments were intentionally similar to those applied in clinical situations. The main studied parameters were oxidative stress index measurements on lung parenchyma and in circulating blood, lung parenchyma microscopic examination and bronchoalveolar lavage cell count. We found that 20 ppm of inhaled NO for 5 h did not change significantly either malondialdehyde and total antioxidant status levels in circulating blood, or malondialdehyde, reduced glutathione, glutathione peroxidase and glutathione reductase in lung parenchyma. Amino-imino-propene bond generation, which are lipoperoxidation markers, was similar in both groups. Furthermore, no significant changes in the number of inflammatory cells in lung lavage products and in lung parenchyma microscopic examination could be found. Therefore, these data do not support the hypothesis that short-term NO inhalation increases oxidative stress and lung inflammation in an experimental model of moderate HMD.

Administration, Inhalation↗
PubMed1998

[Twenty practical questions about prenatal corticosteroid therapy].

Since Liggins and Howie first published their work, numerous studies have shown that corticosteroids significantly decrease perinatal mortality and morbidity, without complication for the mothers and child. Corticosteroids should be prescribed in case of threatening premature birth. Imminent delivery premature rupture of the membranes and gestationnal age over 34 weeks are not contraindications to prescription, as corticosteroids can be safely given all in these circumstances. Theoretically, more than half of premature neonates should have been treated with corticosteroids. Actually, only 20% or less are currently treated. The cost-effectiveness ratio of an antenatal corticosteroid policy would be extremely positive: more than 1,500 prenatal deaths could theoretically be avoided in France annually and the overall cost of neonatal care would decrease by 10%.

Anti-Inflammatory Agents↗
PubMed1996

[Is Ambu ventilation of newborn infants a simple question of finger-touch?].

Insufflation pressures were measured during manual ventilation using a neonatal rebreathing bag (Ambu on a manikin. Maximal insufflation pressures were greater than that published or given by the manufacturer, theoretically limited to 30 cm of water at open valve, and that whatever the number of fingers used for the compression of the bag. These results indicate that Ambu ventilation, often mandatory for newborn resuscitation, does not simply rely upon the finger-touch of the operator and that it always has a risk of baro and/or volotraumatism.

Humans↗
PubMed1996

Strecker stent placement in the superior mesenteric artery for recurrent ischemic colitis.

We report on a case of recurrent superior mesenteric artery (SMA) stenosis with symptomatic mesenteric angina after SMA angioplasty. Stent placement of postostial atherosclerotic disease was proposed, with successful result. Moderate aortic protrusion was noted. Feasibility of PTA and stenting of mesenteric stenoses become increasingly obvious, but long term follow-up studies still have to provide sufficient results on clinical outcome and possible complications.

Aged↗
PubMed1996

Aortic coarctation associated with an aberrant right subclavian artery.

We report a case of aortic coarctation associated with an aberrant right subclavian artery in a young male who was investigated for hypertension. Angiography, CT examination with multiplanar reconstruction and MRI were useful in delineating the extension of the coarctation and the exact anatomy of the aberrant right subclavian artery.

Adult↗
PubMed1996

Pulmonary hypertension of the newborn and urogenital anomalies in two male siblings: a new family with misalignment of pulmonary vessels.

The association of pelvi-ureteric junction obstruction (PUJO) and rapidly fatal persistent pulmonary hypertension of the newborn (PPHN) has been observed in two male siblings. PUJO was also observed in a maternal uncle, whose daughter suffered from vesico-ureteral reflux (VUR). In both patients, histopathologic study of the lungs showed misalignment of pulmonary veins (MAPV), which is a rare autosomal recessive condition leading to severe PPHN and death within the neonatal period. It has occasionally been described associated with PUJO. The authors point out that: i: MAPV has to be carefully searched in case of PPHN; ii: PUJO could be an important finding associated with MAPV, and the only prenatal indication of this lethal condition.

Humans↗