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F J Accurso

Publications and source records attributed to F J Accurso.

49 records · Page 3Linked to original sources
PubMed1988

Fetal pulmonary vasodilation and vasoreactivity during metabolic acidaemia.

We studied the pulmonary vascular response to progressive metabolic acidaemia and to an abrupt increase in oxygen tension during metabolic acidaemia in 8 chronically-prepared fetal sheep. Left pulmonary artery blood flow was measured by electromagnetic flow transducer. Two and a half hour infusion of NH4Cl into the fetal inferior vena cava caused pH to fall to 6.94 +/- 0.01 from 7.37 +/- 0.01 (P less than 0.001). During this period of progressive metabolic acidaemia, left pulmonary artery blood flow increased from a baseline value of 60 +/- 8 to 105 +/- 14 ml.min-1 (P less than 0.002). Pulmonary artery pressure did not change significantly and calculated pulmonary vascular resistance fell indicating fetal pulmonary vasodilation. PO2 rose significantly (19.8 +/- 0.7 to 24.1 +/- 1.8 torr; P less than 0.03) and oxygen saturation fell (54.6 +/- 2.8% to 38.9 +/- 3.5%; P less than 0.001) confirming a rightward shift of the oxyhaemoglobin dissociation curve. During acidaemia, administration of 100% oxygen to the ewe further increased fetal PO2 to 37.9 +/- 2.3 torr within 10 min (P less than 0.001) and this increase in PO2 was accompanied by an increase in left pulmonary artery blood flow (P less than 0.001), a fall in pulmonary artery pressure (P less than 0.03) and a decrease in pulmonary vascular resistance (P less than 0.001) indicating further vasodilation. The response of the fetal pulmonary circulation to a 2-h period of increased oxygen tension was qualitatively similar in acidaemic and non-acidaemic fetuses. We conclude that the progressive metabolic acidaemia imposed by these experimental conditions increases pulmonary blood flow likely through an increase in fetal PO2 and that metabolic acidaemia does not block the normal vasodilatory response to an increase in oxygen tension.

Acidosis↗
PubMed1987

Persistent fetal pulmonary hypoperfusion after acute hypoxia.

To determine the effects of duration of hypoxia on fetal pulmonary blood flow and vasoreactivity, we studied the response of the fetal pulmonary vascular bed before, during, and after prolonged (2-h) and more brief (30-min) exposures to acute hypoxia in 19 chronically instrumented unanesthetized fetal lambs. Left pulmonary arterial blood flow was measured by an electromagnetic flow transducer. Fetal PO2 was lowered by delivering 10-12% O2 to the ewe. During 2-h periods of hypoxia left pulmonary arterial blood flow decreased, and main pulmonary arterial and pulmonary vascular resistance increased. The increase in pulmonary vascular resistance was sustained throughout the 2-h period of hypoxia. After the return of the ewe to room air breathing, pulmonary vascular resistance remained elevated for at least 1 h despite the rapid correction of hypoxemia and in the absence of acidemia. In contrast, after 30 min of hypoxia, left pulmonary arterial blood flow, pulmonary arterial pressure, and pulmonary vascular resistance returned to base-line values rapidly with the termination of hypoxia. The persistent pulmonary hypoperfusion after 2 h of hypoxia was attenuated by alpha-adrenergic blockade and was characterized by a blunted vasodilatory response to increases in fetal PO2. When fetal PO2 was elevated during the posthypoxia period in the presence of alpha-blockade, pulmonary blood flow still remained unresponsive to increases in fetal PO2. We conclude that 2-h periods of acute hypoxia can decrease fetal pulmonary vasoreactivity, and we speculate that related mechanisms may contribute to the failure of the normal adaptation of the pulmonary circulation at birth.

Adrenergic alpha-Antagonists↗
PubMed1986

Time-dependent response of fetal pulmonary blood flow to an increase in fetal oxygen tension.

We describe the temporal characteristics of the response of the fetal pulmonary circulation to the vasodilatory stimulus of a sustained increase in fetal PO2 (5.1 +/- 0.7 Torr) in 13 chronically prepared fetal sheep. Left pulmonary artery blood flow was measured by electromagnetic flow transducer. Fetal PO2 was increased by delivery of 100% oxygen to the ewe and did not significantly change during the 2 h period of oxygen administration. Fetal left pulmonary artery blood flow slowly increased to a peak approximately 2.7 times the control value 40-50 min after the onset of increased PO2. It then steadily declined toward baseline over the next hour of increased PO2. Maximal pulmonary blood flow in response to the increase in PO2 increased with gestational age. Pulmonary arterial, aortic, and left atrial blood pressures did not change significantly in the animals in which measurements were made. We conclude that the changes in fetal pulmonary blood flow with increased fetal PO2 depend upon the time after the PO2 is increased. The adaptation seen during the second hour suggests the existence of mechanisms that tend to keep the fetal pulmonary circulation chronically constricted at any PO2 likely to be encountered in fetal life.

Animals↗
PubMed1986

Adaptation of fetal pulmonary blood flow to local infusion of tolazoline.

Although tolazoline is the most commonly used drug in the treatment of neonatal pulmonary hypertension, its mode of action and efficacy remain incompletely understood. In order to study the effects of tolazoline on a high resistance pulmonary circulation and to better understand mechanisms that control pulmonary vascular tone and reactivity in the fetus, we infused tolazoline either continuously or as bolus into the left pulmonary artery of 15 chronically instrumented, normoxic fetal lambs during late gestation. The vasodilatory effects of bolus injections of tolazoline (2.5 mg) were inhibited by the prior administration of the histaminergic receptor blockers, cimetidine (56%), diphenhydramine (56%), or both (100%). During the continuous infusion of tolazoline (4.5 mg/h for 9 min), pulmonary blood flow to the left lung increased from 61 +/- 6 ml/min (mean +/- SE; control) to 100 +/- 10 (peak) at 30 min (p less than 0.001). However, following this initial vasodilatation, pulmonary blood flow steadily decreased toward control values by 90 min, despite the continued infusion of tolazoline (p less than 0.001). Although the calcium channel blocker, verapamil, and the alpha-adrenergic blocker, phentolamine, had little effect on fetal pulmonary blood flow when infused alone, both drugs increased the vasodilatory response to tolazoline (p less than 0.001). We conclude that tolazoline effects pulmonary vasodilatation by a histaminergic mechanism and that subsequent refractoriness to the drug is a calcium-dependent process which may be partially mediated by an alpha-adrenergic mechanism.

Animals↗
PubMed1985

Pulmonary vascular response to oxygen in infants with severe bronchopulmonary dysplasia.

The cardiac catheterization data of six infants with bronchopulmonary dysplasia (BPD) were reviewed to examine the responsiveness of their pulmonary vascular beds to changes in oxygen tension. The infants were studied because of slow recovery from their oxygen requirements and clinical evidence of persistent pulmonary hypertension. All were receiving home oxygen therapy and had abnormal chest radiographs and right ventricular hypertrophy by ECG at the time of catheterization (mean age, 25 months). All infants had mean pulmonary artery pressure greater than 25 mm Hg in room air, with a mean of 48 mm Hg. All decreased mean pulmonary artery pressure by at least 10 mm Hg when placed in high levels of inspired oxygen (FiO2 greater than 80), with a mean pulmonary artery pressure of 25 mm Hg. This represented a significant decrease in mean pulmonary artery pressure from room air pressures (P less than .005). Mean pulmonary artery pressure was also measured in three infants who were breathing supplemental oxygen by nasal cannula at flow rates similar to levels used for outpatient therapy. Most of the reduction in mean pulmonary artery pressure that occurred at high FiO2 occurred at these lower flow rates of supplemental oxygen. It is concluded that infants with bronchopulmonary dysplasia who have pulmonary hypertension generally have reactive pulmonary vascular beds, responsive to supplemental oxygen. Continuous oxygen therapy by nasal cannula may be useful in the treatment of pulmonary hypertension associated with bronchopulmonary dysplasia.

Bronchopulmonary Dysplasia↗
PubMed1984

Unsuspected cardiopulmonary abnormalities complicating bronchopulmonary dysplasia.

Bronchopulmonary dysplasia is a serious chronic lung disease of infancy but despite numerous problems such as poor growth, recurrent lower respiratory tract infections, and cor pulmonale, steady improvement and recovery may generally be expected. We report four infants with bronchopulmonary dysplasia in whom the cardiopulmonary course did not show the usual steady improvement. Each infant was found to have an unsuspected cardiopulmonary lesion in addition to lung disease: two had congenital heart disease and two upper airway obstruction. Three improved after surgical intervention but one patient died immediately after this. Persistent right ventricular hypertrophy in patients with bronchopulmonary dysplasia maintained on supplemental oxygen, and a particularly slow rate of recovery from the need for supplemental oxygen are markers that should lead to evaluation for coexisting cardiopulmonary abnormalities.

Airway Obstruction↗
PubMed1984

Experience with home oxygen in the management of infants with bronchopulmonary dysplasia.

We followed the clinical course of 23 infants with bronchopulmonary dysplasia (BPD) on home oxygen therapy during the first year of life in order to monitor patterns of growth, need for hospital readmission, and improvement in oxygenation. Oxygenation was assessed by serial, resting, awake, and room air transcutaneous PO2 (tcPO2) measurements at clinic visits. Weight gain was poor, with boys growing below the fifth percentile and girls growing at the tenth percentile. Ten of the 23 infants (43%) required rehospitalizations. There were no deaths. Fourteen of the 23 infants (61%) were taken off supplemental oxygen by 12 months corrected age, at a mean age of 7.9 months. Mean rate of improvement in tcPO2 was 3 torr/month, but wide individual variation was found. Infants off of oxygen treatment at 12 months corrected age grew at a significantly greater rate than those still requiring oxygen supplementation (p less than 0.02). Infants with right ventricular hypertrophy (RVH) by electrocardiogram tended to resolve their RVH while on home oxygen therapy. We conclude that infants with BPD on home oxygen therapy generally show steady improvement in oxygenation, but grow poorly and require frequent hospitalizations.

Body Weight↗
PubMed1983

Primary tracheomalacia.

Tracheomalacia is a rare congenital malformation of the tracheobronchial cartilages in which the supporting cartilaginous rings permit expiratory collapse of the airway. The condition is usually mild and self-limited. There is a severe variant, however, that is life-threatening and warrants separate categorization. Four children with severe primary tracheomalacia were treated recently. The clinical symptoms, diagnostic findings, and eventual treatment of these patients were highly distinctive and almost identical in all 4, permitting us to make the following observations: (1) primary severe tracheomalacia must be suspected in infants with unexplained respiratory distress manifested by stridor and cyanosis; (2) symptoms are not present at birth but appear insidiously after the first weeks of life, are markedly aggravated by respiratory tract infections, and are made worse by agitation; (3) bronchoscopy is essential for definitive diagnosis and should be employed early in the diagnostic process; (4) tracheostomy is probably essential in most instances; and (5) resolution, although spontaneous, does not occur until after 2 years of age.

Cartilage Diseases↗
PubMedDate not supplied

Persistent morbidity and mortality of protein calorie malnutrition in young infants with CF.

Young infants with cystic fibrosis (CF) are at risk for developing symptomatic protein-calorie malnutrition (PCM) characterized by hypoalbuminemia, edema, and anemia. We reviewed the hospital charts of all infants less than 12 months of age referred to our CF clinic between 1979 and 1982 and found nine patients with PCM (13%). Their courses were characterized by age less than 7 months (nine patients), frequent use of soy formula (eight patients), presence of gastrointestinal or respiratory symptoms before being diagnosed with CF (eight patients), severe respiratory distress often requiring mechanical ventilation (five patients), significant infections (three patients), and high mortality (five patients). We further noted that eight infants were not on pancreatic enzyme therapy at the onset of PCM. This clinical study extends the findings of earlier reports of PCM in patients with CF by showing that this syndrome persists as a major source of morbidity and mortality in young infants with CF, especially those fed soy formula and not receiving pancreatic enzyme supplements. Because PCM can develop rapidly and may be the presenting sign of CF in young infants, we speculate that early diagnosis of CF with institution of pancreatic supplements may decrease incidence and severity of PCM in young patients with CF.

Anemia↗
PubMedDate not supplied

Physiologic circadian rhythmicity in preterm infants.

This study investigated evidence of a circadian rhythm in the physiologic variables of transcutaneous oxygen (tcPO2) level, pulse rate, respiratory rate, frequency of respiratory pauses, and skin temperature in six 34- to 37-week-preterm infants. A value for each variable was noted every 30 minutes for 24 hours, providing 245 observations for each infant. An adaptation of cosinor analysis, a least squares procedure that determines the cosine curve for a 24-hour period that best fits the observed pattern of values, was applied to the data. Statistically significant circadian rhythmicity was found for five of the six subjects with regard to skin temperature. Significant circadian rhythm was also demonstrated in two or three patients for all other variables. No significant consistent synchrony for individual variables across subjects was found. Actual peak values of respiratory pause frequency and trough values of tcPO2, however, occurred between midnight and 4:30 A.M. for every infant. Preterm infants exhibited evidence of a circadian rhythm in skin temperature, and tcPO2 and respiratory pause frequency exhibited day/night pattern characteristics.

Circadian Rhythm↗