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Biomedical subjects

M H Gewitz

Publications and source records attributed to M H Gewitz.

49 records · Page 3Linked to original sources
PubMed1983

Echocardiographic characteristics of premature infants with patient ductus arteriosus.

As part of a multicenter collaborative study, M-mode echocardiograms were obtained shortly after birth on 3,559 premature infants with birth weight less than or equal to 1,750 g. Of these infants, 1,496 did not develop a cardiac murmur or other signs of a "hemodynamically significant" patent ductus arteriosus (PDA). Echocardiographic parameters from this "normal" group were compared with results obtained from 415 infants in whom PDA was diagnosed on the basis of clinical findings alone, irrespective of the echocardiogram (PDA group). The best discrimination between the two groups, when considering a single parameter, was provided by a left atrial to aortic root ratio (LA/AO) of 1.40, a left ventricular to aortic root ratio (LV/AO) of 2.10, or a left ventricular systolic time interval ratio (LPEP/LVET) of 0.27. Multivariate analysis demonstrated that better separation between the two groups occurred when the left atrial to aortic root ratio and the left ventricular systolic time interval ratio were considered jointly. Because of a large degree of overlap of all echocardiographic variables between the normal group and the group with PDA, the echocardiogram alone was not a good indicator of PDA. However, when used in conjunction with a priori estimates of the probability of PDA (based, for example, on birth weight and degree of respiratory disease), use of echocardiographic data was found to improve the detection of hemodynamically significant patent ductus arteriosus in premature infants.

Age Factors↗
PubMed1982

Changes in pulmonary function during the diuretic phase of respiratory distress syndrome.

To evaluate the relationship between improvement in pulmonary function and spontaneous diuresis in respiratory distress syndrome, nine premature infants requiring mechanical ventilation for RDS were studied at a mean age of 11.9 hours prior to the onset of diuresis, at onset of diuresis, at maximum urine output (mean age 44.9 hours), and at 24 hours after maximum urine output. Prior to diuresis functional residual capacity decreased from mean +/- SEM of 16.2 +/- 2 to 13.3 +/- 1.2 ml/kg, and dynamic lung compliance decreased from 2.5 +/- 0.3 to 1.8 +/- 0.3 ml/cm H2O (P less than 0.05), indicating that the respiratory disease was worsening. There was no significant change in alveolar-arterial oxygen gradient, peak inflating pressure, or rate of intermittent mandatory ventilation over this period. At the time of maximum urine output, however, FRC had increased 36% (P less than 0.05). CL had increased by 60% to 2.8 +/- 0.4 ml/cm H2O (P less than 0.025), AaDO2 had decreased from 246 +/- 27 to 184 +/- 30 torr (P less than 0.005), and PIP had decreased from 14.9 +/- 2.2 to 11.3 +/- 2.1 cm/H2O (P less than 0.05). On follow-up study 24 hours after maximum urine output, there was no further significant improvement in FRC, CL or PIP, but IMV rate and AaDO2 continued to decrease. These data show that the pulmonary function in RDS deteriorates until the onset of diuresis, after which it rapidly improves. This diuresis may represent the removal of excess lung liquid and seems necessary for improvement in RDS.

Diuresis↗
PubMed1982

Reversible changes in norepinephrine extraction by the lungs in children with pulmonary hypertension.

Extraction of circulating vasoactive hormones by the lung may influence systemic vasomotor tone. Since this process occurs in the pulmonary microcirculation, we evaluated the effects of pulmonary artery hypertension (PAH) secondary to congenital heart disease (CHD) on this metabolic function of lung. Eleven patients with varying congenital cardiac lesions were studied preoperatively and postoperatively. Five had normal pulmonary artery pressure (PAP) (group I), and six had PAH with peak systolic PAP greater than 40 mm Hg (group II). PA and postpulmonary arterial blood samples were collected before and after surgery at the time of pressure measurements. Norepinephrine (NE) and epinephrine (EPI) levels were determined by radioenzymatic assay. Preoperatively, circulating NE levels were higher (P less than 0.05) and NE extraction measured was lower (P less than 0.01) in group II patients as compared with group I. Extraction increased in group II postoperatively after PA pressures were reduced, becoming equivalent to group I postoperative values. EPI extraction was negligible in either group at any time. These data demonstrate that lungs of children are capable of selective catecholamine uptake and that elevated PAP occuring with CHD is associated with a decrease in this capability and an increase in circulating NE levels. Additionally, the decrease in NE extraction observed with PAH is reversible once PAP is reduced by surgical repair of the cardiac defect.

Adolescent↗
PubMed1981

Oral hydralazine in patients with pulmonary vascular disease secondary to congenital heart disease.

Two patients with pulmonary vascular obstructive disease secondary to congenital heart disease were evaluated hemodynamically before and during oral hydralazine therapy. Both patients were assessed postoperatively and had no significant residual shunts. Pulmonary vascular resistance failed to decrease, and an increase in pulmonary arterial pressure occurred because of increased cardiac output secondary to systemic arteriolar dilatation. These responses were sufficiently consistent to warrant a warning against the use of oral hydralazine except under controlled conditions in patients with secondary pulmonary vascular obstructive disease.

Administration, Oral↗
PubMed1981

Uptake and metabolism of biogenic amines in the developing rabbit lung.

Uptake and metabolism of biogenic amines in developing lung were studied in a total of 62 New Zealand White rabbits aged 28 days of gestation to 28 days postnatal. Lungs were perfused in vitro with 5-[14C]hydroxytryptamine (5-HT) or [14C]phenylethylamine (PEA) and coperfused with high-molecular-weight [3H]dextran to assess the vascular space perfused. Patterns of uptake and metabolism of PEA and 5-HT as functions of age were markedly different. PEA uptake and metabolism gradually increased with advancing age. No differences were observed in 5-HT uptake or metabolism within the postnatal age range studied, but the magnitude of each process for 5-HT was significantly lower in premature animals. Functional maturity for both uptake and metabolism of PEA was observed by 14-21 days of age. Inhibition of intrapulmonary monoamine oxidase by semicarbazide and pargyline showed that PEA metabolism was unaffected by the former and moderately reduced by the latter agent only in animals older than 1 wk. Thus the lung of the newborn rabbit effectively takes up and metabolizes PEA and 5-HT, but age-related differences are evident in the development of specific monoamine oxidase subtypes. Reduced 5-HT metabolism in lung of premature animals paralleled changes in the measured vascular space, possibly reflecting difficulty in perfusing premature lungs as well as immature functional status. This study emphasizes the importance of determining functional vascular perfusion (by coperfusion with intravascular markers) when studying the developing lung.

Animals↗
PubMed1977

Pulmonary hypertension in the perinatal aspiration syndromes.

Ten patients clinically diagnosed as having perinatal aspiration syndromes were found to have pulmonary hypertension. These infants were either term or postmature babies and had the following characteristics: (1) systemic or suprasystemic levels of pulmonary artery pressure (range, 50 to 117 mm Hg); (2) a degree of pulmonary hypertension not related to the degree of aspiration evident on chest roentgenograms; (3) evidence of right-to-left shunting at the ductal or foramen ovale level; and (4) sustained severe hypoxemia despite 100% inspired oxygen concentration. The overall mortality for the group was 50%. Since these patients had marked clinical and physiologic similarities to patients previously reported as having the persistent fetal circulation syndrome (PFC), they were classified as having "PFC with aspiration." The existence of pulmonary hypertension should be suspected despite roentgenographic evidence of aspiration in any patient who also manifests the clinical characteristics of PFC because its treatment may alter the prognosis of such patients.

Birth Weight↗
PubMedDate not supplied

Effect of early furosemide administration in neonates with respiratory distress syndrome.

The effect of early furosemide-induced diuresis was prospectively evaluated in 39 neonates less than 24 hr of age with clinical respiratory distress syndrome (RDS) who received either four doses of furosemide (1 mg/kg) or no diuretic. Measurements of FiO2 alveolar-arterial oxygen gradient (P[A-a]O2), peak inspiratory pressure (PIP), and urine output as a fraction of intake (O/I) were averaged for every 8 hr. The furosemide group overall showed a significant decrease (P less than 0.01) in FiO2, P[A-a]O2, and PIP with an earlier (32 hr vs 52 hr) and more pronounced diuresis (35% greater O/I) when compared to the controls. This effect was accentuated in the subgroup with 1,000-1,500 g birth weight (significantly lower FiO2 and P(A-a)O2 from 16 to 48 hours), while no increase in urine output was observed for the infants weighing less than 1,000 g. A significant reduction in supplemental oxygen and need for ventilatory support at 96 hr of age was observed in the furosemide-treated, less than 1,500-g infants. The incidence of patent ductus arteriosus was not increased following furosemide therapy, and no significant difference in echocardiographic parameters was observed in 21 infants from both groups, who were followed daily during the first week of life. This study suggests that early furosemide-induced diuresis, particularly in infants weighing 1,000-1,500 g at birth, promotes improvement in pulmonary functions in RDS and leads to faster reduction in oxygen and ventilatory support.

Birth Weight↗
PubMedDate not supplied

Ventricular arrhythmia in the X-linked cardiomyopathy Barth syndrome.

Barth syndrome is an X-linked disorder characterized by dilated cardiomyopathy, cyclic neutropenia, skeletal myopathy, abnormal mitochondria, and growth deficiency. The primary defect is a mutation in the TAZ gene on the X chromosome at Xq28, resulting in abnormal phospholipid biosynthesis and cardiolipin deficiency. To date, there has been no systematic evaluation of the cardiac phenotype. We report five cases of cardiac arrest and/or placement of an internal cardiac defibrillator with documented ventricular arrhythmia. We suggest that ventricular arrhythmia is part of the primary phenotype of the disorder and that patients should be screened accordingly.

Acyltransferases↗
PubMedDate not supplied

The PaO2 response to changes in end expiratory pressure in the newborn respiratory distress syndrome.

To quantitate the effect of changes in end-expiratory pressure (EEP) upon PaO2 in infants with the respiratory distress syndrome, arterial blood gas (ABG) data was reviewed in 28 neonates. A total of 94 ABG specimen pairs were analyzed (specimen I taken before EEP adjustment; specimen II taken after EEP change). An overall change in PaO2 of 15 torr was noted per cm H2O change in EEP. Patients in whom the level of EEP was low (0-3 cm H2O) at the time of Sample I had a greater change in PaO2 (p less than 0.01) than infants whose Sample I ABG was taken at mid-range of EEP (4-6 cm H2O) or at high ranges (7-12 cm H2O). At the high ranges of EEP a minimal and variable PaO2 response was observed. The PaO2 response was not statistically different between neonates on controlled ventilation and those breathing spontaneously. Survivors had a greater PaO2 response than did nonsurvivors, but because of the variables affecting respiratory distress syndrome (RDS) patients, it could not be determined if this PaO2 response had a prognostic value. From this data, the clinician is provided with a guide to the expected PaO2 response when a change in EEP is made.

Humans↗
PubMedDate not supplied

Monocrotaline induces interleukin-6 mRNA expression in rat lungs.

Monocrotaline-induced pulmonary hypertension (PH) in rats is preceded by an inflammatory response in the lungs, and interleukin-6 (IL-6) is expressed in response to inflammation. To evaluate the role of IL-6 in monocrotaline-induced PH, rats received a single subcutaneous injection of monocrotaline (60 mg/kg) or an equivalent amount of normal saline. Pulmonary artery pressure (Ppa), right ventricular hypertrophy (RVH), expression of IL-6 mRNA, and bioactivity of IL-6 in the lungs of these rats were examined 48 hours and 1 and 2 weeks after administration of monocrotaline. The effects of dexamethasone treatment on monocrotaline-induced PH also were evaluated. Two weeks after administration of monocrotaline, significant PH and RVH developed in these rats. Reverse transcription-polymerase chain reaction (RT-PCR) revealed expression of IL-6 mRNA in the lungs 48 hours and 1 and 2 weeks after administration of monocrotaline. This was confirmed using ribonuclease protection assay. The bioactivity of IL-6 in lung extracts progressively increased. Dexamethasone markedly inhibited expression of IL-6 mRNA and IL-6 bioactivity in the lungs, with concomitant attenuation of monocrotaline-induced PH and RVH. Our data show that monocrotaline induces expression of IL-6 mRNA in rat lungs and that inhibition of IL-6 results in attenuation of PH. These findings indicate that IL-6 may play a role in the pathogenesis of PH.

Analysis of Variance↗
PubMedDate not supplied

Pulmonary hypertension in infancy and childhood.

Abnormalities of pulmonary artery pressure and resistance continue to complicate many varieties of cardiovascular problems in childhood. Much recent effort has been devoted to understanding the cellular mechanisms underlying the pathophysiology of pulmonary hypertension, centering on endothelial cell dysfunction as a principal factor. Defects in the vasodilation machinery of the endothelial cell, such as overexpression of vasoconstrictor elements, have been implicated in various forms of pulmonary hypertension. This includes pulmonary hypertension that is secondary to congenital heart disease, and the primary forms that occur in older children and in neonates. In addition, experimental methods assessing cyclic adenosine monophosphate-mediated and cyclic guanosine monophosphate-mediated vasoreactivity suggest a possible genetic basis in the responses of the pulmonary microvasculature. This article reviews some of the current information that has been developed along these lines, and explores the implications of these data for therapeutic strategies to treat this complex problem.

Child↗