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Biomedical subjects

E L Stevens

Publications and source records attributed to E L Stevens.

9 recordsLinked to original sources
PubMed1994

The effects of reversing distending pressure sequences in the neonatal piglet.

We studied different sequences of lung inflation in ventilated newborn piglets with normal lungs in order to determine the effects of sequence, magnitude and duration of distending pressure on pulmonary function, and/or hemodynamics. End-expiratory pressure was varied using a continuous negative extrathoracic pressure (CNEP) device. Three groups of ventilated piglets with normal lungs were exposed to 2 cmH2O increments of CNEP from -2 to -12 cmH2O, and to decrements from -12 to -2 cmH2O, or to only -6 cmH2O. Lung inflation sequence, magnitude of inflation pressure, and duration of inflation had significant effects on end-expiratory lung volume and lung compliance at numerically equivalent pressure levels. End-expiratory lung volume and lung compliance varied (at four and five of six inflation pressures studied) by as much as 68% and 104%, respectively. Hemodynamic effects of the lung inflation sequence were more variable; those found to be different at numerically equivalent pressure levels were associated with changes in lung compliance and ventilation. Differences in pulmonary mechanics can best be explained by the effects of lung inflation on alveolar recruitment versus overinflation.

Animals↗
PubMed1994

Effect of baseline lung compliance on the subsequent response to positive end-expiratory pressure in ventilated piglets with normal lungs.

OBJECTIVE: To determine the pulmonary function and hemodynamic effects of incremental positive end-expiratory pressure in two groups of normal ventilated newborn piglets with different baseline dynamic lung compliance. DESIGN: Prospective, controlled, intervention study. SETTING: Animal laboratory. INTERVENTIONS: One group of piglets (inflation group) was prepared with 3 cm H2O (0.29 kPa) positive end-expiratory pressure and a maximal lung inflation to increase baseline lung compliance as compared with the other group (no-inflation group), prepared by 3 hrs of ventilation at zero end-expiratory pressure. Both groups were then subjected to a sequence of incremental positive end-expiratory pressures from 0 to 12 cm H2O (0 to 1.18 kPa) in 2-cm increments for 15-min periods at each level followed by a 60-min recovery period at zero end-expiratory pressure. MEASUREMENTS AND MAIN RESULTS: Pulmonary function, hemodynamic and blood gas data were collected at each positive end-expiratory pressure value and at 15-min intervals during recovery. Baseline dynamic lung compliance was 5.2 +/- 0.3 mL/cm H2O (53.04 +/- 3.06 mL/kPa) in the inflation group and 2.5 +/- 0.1 mL/cm H2O (25.5 +/- 1.02 mL/kPa) in the no-inflation group. No differences were found in any other pulmonary function, hemodynamic or blood gas value at baseline. Incremental positive end-expiratory pressure resulted in a decrease in dynamic lung compliance and an increase in end-expiratory lung volume in both groups of piglets; dynamic lung compliance was greater in the inflation group at all times. No differences were found in end-expiratory lung volume between groups. Hemodynamic changes in both groups of piglets included: decreased cardiac output and increased pulmonary vascular resistance and systemic vascular resistance. The changes in cardiac output (-23% vs. -32%), pulmonary vascular resistance (+53% vs. +95%), and systemic vascular resistance (17% vs. 51%) were less in the inflation group as compared with the no-inflation group. CONCLUSIONS: Baseline dynamic lung compliance is an important determinant of the subsequent effect of positive end-expiratory pressure on pulmonary function and hemodynamics in the ventilated piglet with normal lungs.

Animals↗
PubMed1993

Ontogeny of epithelial modulation of airway smooth muscle function in the guinea pig.

The purpose of this study was to investigate the ontogeny of guinea pig airway smooth muscle (ASM) responses and the epithelial modulation of these responses. Paired tracheal rings from fetal, newborn, and adult guinea pigs were studied. One of each pair was denuded of airway epithelium (AE) by gentle rubbing. Isometric tension was measured in rings mounted in organ baths filled with Krebs' solution. Cumulative dose-response curves were generated by adding either acetylcholine (ACh) or histamine over a concentration range of 10(-8)-10(-4) M. Significant agent-specific, age-related differences in maximal contraction were seen for both ACh and histamine in intact tissues (Ach: for fetus 66.7 +/- 6.2 x 10(-2) g/mg wet wt, for newborn 51.4 +/- 6.2, for adult 29.3 +/- 2.6; histamine: for fetus 46.1 +/- 5.1, for newborn 72.9 +/- 6.0, for adult 25.3 +/- 3.2). Similar differences in sensitivity to both agents were observed (EC50 with ACh: for fetus 0.80 +/- 0.11 x 10(-6) M; for newborn 0.85 +/- 0.26 x 10(-6) M; for adult 1.7 +/- 0.20 x 10(-6) M; EC50 with histamine; for fetus 1.88 +/- 0.50 x 10(-6) M; for newborn 1.34 +/- 0.16 x 10(-6) M; for adult 3.78 +/- 0.75 x 10(-6) M). Removal of AE caused a significant decrease in maximal responses to ACh in fetal tissue, a smaller, insignificant one for newborn and a nonsignificant alteration for adult tissues. Age-related sensitivity difference was abolished with removal of AE to ACh but not to histamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1993

Pancuronium does not alter the hemodynamic status of piglets after normoxia or hypoxia.

Pancuronium is a neuromuscular blocking agent commonly used to eliminate agitation in sick newborn infants requiring mechanical ventilation. Experimental data supporting this method of intervention are controversial, and hemodynamic studies in newborn infants report conflicting results. This study was designed to determine the hemodynamic effects of pancuronium administered under conditions of normoxia, hypoxia, and preexposure to hypoxia in neonatal piglets with normal lungs. After baseline hemodynamic and blood gas measurements were obtained, pancuronium was administered in two i.v. bolus injections of 0.1 mg/kg. Tidal volume and minute ventilation were maintained constant during the experimental procedure by adjusting ventilator settings. Twenty min after pancuronium, no changes from baseline values were found in arterial blood gases, heart rate, cardiac output, mean arterial pressure, systemic vascular resistance, pulmonary artery pressure, pulmonary vascular resistance, central venous pressure, or pulmonary capillary wedge pressure in any of the three conditions studied. In conclusion, pancuronium administered during normoxia, hypoxia, or after preexposure to hypoxia while controlled ventilation is maintained does not alter systemic or pulmonary hemodynamic status of the newborn piglet.

Animals↗
PubMed1992

Furosemide differentially relaxes airway and vascular smooth muscle in fetal, newborn, and adult guinea pigs.

Furosemide, an inhibitor of Cl-dependent Na+,K+ cotransport, is the most frequently used diuretic in newborns. Recently, furosemide was also demonstrated to decrease bronchial hyper-responsiveness in adults, although little is known about the direct effect of furosemide on smooth muscle of immature animals. This in vitro study was designed to determine the action of furosemide on airway and vascular smooth muscle during ontogeny. Extrathoracic trachea (ET), main stem bronchi, main pulmonary artery, and thoracic aorta ring segments from fetal, newborn, and adult Hartley albino guinea pigs were suspended in HEPES solution for measurement of isometric tension. Furosemide (30 or 300 microM) was administered after preconstriction with an ED35-70 concentration of histamine or acetylcholine for airway and ED40-100 concentration of norepinephrine for vessels. Furosemide (30 microM) caused significant relaxation of airway smooth muscle at all ages. After histamine-induced preconstriction, fetal airway segments exhibited greatest relaxation (183 +/- 28%), with newborn airway demonstrating 123 +/- 15% relaxation and modest relaxation seen in adults (40 +/- 4%). This pattern was similar for both ET and bronchus and appeared greater for histamine compared with ACh preconstriction. Epithelial removal slightly enhanced relaxation. Furosemide also relaxed pulmonary artery segments, but at a 10-fold higher concentration. In striking contrast to the pattern seen in airway, adult pulmonary artery relaxed more than newborn and newborn, more than fetus. Cyclooxygenase blockade and endothelium removal did not change pulmonary artery relaxation. Furosemide did not significantly relax aorta after NE preconstriction. Taken together, these results suggest that furosemide may be more effective in relaxing airway compared with vascular smooth muscle, and the ontogeny of these responses indicates a greater efficacy and selectivity in airways of immature animals.

Acetylcholine↗
PubMed1989

Mucopolysaccharidosis I presenting with endocardial fibroelastosis of infancy.

We describe two female infants with Hurler syndrome (mucopolysaccharidosis I) whose deaths are attributed to cardiac failure with associated, autopsy-confirmed endocardial fibroelastosis. One infant had confirmed alpha-L-iduronidase deficiency in cultured dermal fibroblasts, and the other infant had histologic evidence of tissue mucopolysaccharide accumulation at autopsy and a sibling with confirmed alpha-L-iduronidase deficiency and the Hurler syndrome phenotype. Clear cells ("Hurler" cells) were identified within the myocardium and endocardium of both infants. We propose that the ventricular mural accumulation of mucopolysaccharides induced extensive proliferation of elastic or collagen fibers within the endocardium. Cardiac failure may precede recognition of clinical and roentgenographic features of Hurler syndrome. Our findings and a literature review suggest that certain heritable storage disorders, including mucopolysaccharidosis I, should be considered when infants have clinical electrocardiographic and echocardiographic findings consistent with endocardial fibroelastosis or have autopsy-documented endocardial fibroelastosis.

Endocardial Fibroelastosis↗