Influence of an antagonist of slow-reacting substance of anaphylaxis on the cardiovascular manifestations of hypoxia in piglets.

Leukotrienes have been implicated in the pathogenesis of hypoxic pulmonary hypertension in adult animals and in persistent pulmonary hypertension with accompanying hypoxemia in the neonate. In order to elucidate the role of leukotrienes in hypoxic pulmonary hypertension in a young animal model, the effects of a leukotriene antagonist, FPL 57231, were evaluated in anesthetized piglets. Cardiac output and vascular pressures were measured and pulmonary and systemic vascular resistances calculated prior to and during hypoxia. These measurements were compared during continued hypoxia between a control and treatment group which received FPL 57231. FPL 57231 infusion resulted in significant decreases in mean pulmonary artery pressure (p less than 0.04), pulmonary vascular resistance (p less than 0.01) and the ratio of pulmonary/systemic vascular resistance (p less than 0.01). Systemic vascular resistance fell approximately 25% from hypoxic baseline (p less than 0.01) while PVR decreased 54%. There were no differences between groups in mean systemic arterial pressure, cardiac output, pH, or PaCO2. In addition, pretreatment with FPL 57231 attenuated the hemodynamic response to hypoxia. These data suggest that leukotrienes may, in part, mediate hypoxic pulmonary vasoconstriction in piglets.

Physiologic and biochemical effects of ritodrine therapy on the mother and perinate.

The materno-fetal and neonatal effects of ritodrine were studied in 37 women treated for premature labor with intravenous (i.v.) ritodrine. Marked cardiovascular, respiratory, and biochemical side effects of therapy were seen in the mothers and tachycardia was noted in the fetuses. The neonates of 18 women in whom ritodrine successfully postponed delivery were delivered with good Apgar scores and their admission vital signs and nursery courses were benign. Ritodrine failed to delay delivery more than a week in 19 mothers. There were no differences between their newborns and 20 control neonates in admission vital signs, blood gases, blood chemistries, complete blood counts, platelet counts, peak bilirubin, or duration of oxygen therapy. This study revealed no deleterious effects on neonates delivered after maternal ritodrine therapy despite significant maternal and fetal effects.

Cardiovascular changes in group B streptococcal sepsis in the piglet: response to indomethacin and relationship to prostacyclin and thromboxane A2.

Seventeen piglets were infected with a continuous intravenous infusion of live group B beta-hemolytic streptococci (GBS). Hemodynamic changes were recorded, and blood samples were drawn for measurement of thromboxane B2 (TxB2) (stable metabolite of thromboxane A2) and 6-keto-PGF1 alpha (stable metabolite of prostacyclin). Control animals (n = 9) received only bacteria, while treatment animals (n = 8) received indomethacin, 3 mg/kg IV, 15 min after the start of the bacterial infusion. Control animals responded to the bacteria within 15 min with marked elevation in mean pulmonary artery pressure (Ppa) from 15 +/- 8 to 39 +/- 6 mm Hg and decline in PaO2 from 80 +/- 11 to 51 +/- 6 mm Hg and cardiac output (CO) from 0.24 +/- 0.07 to 0.13 +/- 0.07 liters/min/kg. Mean arterial blood pressure (AoP) significantly decreased from baseline value of 95 +/- 13 to 51 +/- 32 mm Hg by 180 min. In animals treated with indomethacin, these changes were reversed or significantly attenuated. The hemodynamic changes were associated temporally with elevations in plasma concentrations of TxB2 or 6-keto-PGF1 alpha. In the first 60 min, TxB2 levels in both groups correlated with Ppa (r = 0.72, p less than 0.001) and PaO2 (r = -0.60, p less than 0.001). A strong negative correlation between TxB2 and CO was observed over the first 180 min (r = -0.73, p less than 0.001). There was a statistically significant correlation between AoP and 6-keto-PGF1 alpha concentration between 60 and 180 min (r = -0.54, p less than 0.002). Indomethacin improved the hemodynamic function in this model of GBS sepsis.(ABSTRACT TRUNCATED AT 250 WORDS)

Intrauterine positional deformations masquerading as multiple congenital malformations.

A 1,340-g male neonate was delivered by emergency cesarean section at 28 weeks' gestation following failed therapy with isoxsuprine hydrochloride and fetal distress. Transverse-lie presentation with the posterior side of the thorax wedged into the maternal pelvis and the head flexed firmly against the anterior side of the thorax led to a severe deformation sequence initially interpreted as multiple congenital malformations. This case illustrates the difficulty in distinguishing between pure deformations and malformations with and without subsequent deformations. It also emphasizes the clinician's need for a definitive diagnosis to guide the management of suspected malformations that are potentially lethal or portend a poor neurodevelopmental outcome.

The occipital horn of the lateral ventricles in premature infants. An ultrasonographic study.

The size of the occipital horn of the lateral ventricles was determined on parasagittal ultrasound scans in premature infants. In 52 neonates without evidence of intracranial haemorrhage, the pulvinar-posterior horn wall distance measured an average of 11.6 mm +/- 2 mm. In infants with intracranial pathology, the average length of the occipital horn varied from 16.3 mm +/- 2.5 mm to 31.8 mm +/- 7.4 mm. An occipital horn measurement greater than 16 mm indicated ventricular enlargement. Occipital horn asymmetry also indicated ventricular dilatation. In normal neonates the side-to-side difference averaged 0.6 mm while in neonates with ventriculomegaly the mean difference was 2.6 mm. The occipital horn frequently represents the first and may represent the only portion of the lateral ventricle to enlarge. Precise measurement of the occipital horn dimension, therefore, represents an excellent method for the identification and follow-up of ventriculomegaly in premature neonates.

Temporal comparative analysis of computed tomography with ultrasound for intracranial hemorrhage in premature infants.

This study focuses on comparison of computed tomography and ultrasound in premature infants with intracranial hemorrhage and its complications. It was determined that close correlation (95%) exists between CT and ultrasound for evaluation of ventriculomegaly. Although there is reasonable correlation for the identification and localization of periventricular, intraventricular and choroidal hemorrhages, ultrasound defined such lesions at higher rates. Subarachnoid blood and periventricular edema were diagnosed better or exclusively by CT.

Choroid plexus hemorrhage in premature neonates: recognition by sonography.

In 34 consecutive infants admitted to the neonatal intensive care unit with birth weight of less than 1,500 g, 80 cranial real-time sonograms were obtained to determine the incidence of choroid plexus hemorrhage. Choroid plexus hemorrhage was diagnosed only in the absence of germinal matrix hemorrhage. Diagnostic criteria included choroid plexus nodularity, enlargement (greater than 12 mm in anteroposterior diameter), or asymmetry between right and left (greater than 5 mm). Ipsilateral intraventricular clots or occipital horn dilatation supported the diagnosis of choroid plexus hemorrhage in most cases. Choroid plexus hemorrhage appeared to be the sole bleeding site in 10 (59%) of the 17 patients with intracranial hemorrhage. Hemorrhage in the region of the caudate nucleus was seen in the other seven cases (41%). Ventricular dilatation and/or intraventricular hemorrhage accompanied nine (90%) of the 10 cases of choroid plexus hemorrhage. This study suggests that in very low-birth-weight premature neonates, the choroid plexus may be a more frequent site of intracranial hemorrhage than previously believed.

Ultrasonographic detection of perinatal intracerebellar hemorrhage.

Intracerebellar hemorrhage in premature infants represents a life-threatening event. Prompt diagnosis of this form of intracranial hemorrhage is crucial, as surgical intervention may dramatically improve the prognosis. Whereas clinical signs associated with posterior fossa pathology in infants remain nonspecific, ultrasound provides a rapid, noninvasive means of identifying this potentially treatable abnormality. A case is presented.

Cranial real-time ultrasound in premature neonates.

Two hundred and seventy-three ultrasound examinations in 140 premature infants were performed with a transportable real-time scanner. Evidence for intracranial pathology was found in 86 (61%) of infants. In 66 infants (47%) a hemorrhage and in 79 infants (56%) ventricular dilatation was present. Choroid plexus larger than 12 mm was suggestive for either a bleeding into or onto the plexus. Cavum septi pellucidi was present in 72% of examined infants.

Platelet dysfunction and coagulopathy in intraventricular hemorrhage in the premature infant.

We investigated platelet count, bleeding time, platelet aggregation, prothrombin time, activated partial thromboplastin time, and fibrinogen level in 58 very low-birth-weight infants during the first postnatal day to determine the relationship between hemostatic disorders and intraventricular hemorrhage. Thirty-two of the 58 infants (55%) were found to have periventricular-intraventricular hemorrhage by computerized tomography or autopsy. Nine patients (16%) had subarachnoid hemorrhage only and 17 (29%) had no evidence of intracranial hemorrhage. Infants with IVH had a significantly lower mean platelet count than did infants with no SAH/IVH. However, only five patients with IVH had initial thrombocytopenia. The IVH group had a mean bleeding time which was significantly prolonged compared to that of the group without SAH/IVH. Similarly, patients with IVH had a mean platelet aggregation response which was significantly diminished in comparison to that of patients with no SAH/IVH. Infants with IVH had a significantly longer mean PT than did infants with no SAH/IVH. In addition, babies with IVH had a significantly longer mean APTT compared to that of babies without SAH/IVH. The groups did not differ significantly with respect to fibrinogen levels. Three infants with IVH had disseminated intravascular coagulation in the early neonatal period. These data suggest that disorders of platelet-capillary interaction and defects in the intrinsic and extrinsic coagulation pathways may play important roles in intraventricular hemorrhage in the premature infant.