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Biomedical subjects

H J Wiseman

Publications and source records attributed to H J Wiseman.

10 recordsLinked to original sources
PubMed1986

Prostaglandin synthetase inhibition in group B streptococcal shock: hematologic and hemodynamic effects.

A rabbit model of group B Streptococcal (GBS) shock was used to study the effects of prostaglandin synthetase inhibition on the hemodynamic and hematologic response to GBS shock. The infusion of heat-killed GBS in groups I and II produced significant decreases in mean arterial pressure, neutrophil counts, and platelet counts (p less than 0.05), and significant rises in concentrations of thromboxane B2 and 6-Keto-PGF1 alpha, the stable metabolites of thromboxane A2 and prostacyclin (p less than 0.05). Administration of indomethacin (4 mg/kg) after GBS infusion (group II) was associated with a significant rise in mean arterial pressure and a significant decline in thromboxane B2 and 6-Keto-PGF1 alpha concentrations (p less than 0.05) but had no effect on GBS-induced hematologic alterations. Indomethacin administration before GBS infusion (group III) prevented alterations in mean arterial pressure and was associated with a decrease in thromboxane B2 and 6-Keto-PGF1 alpha concentrations. Indomethacin in group III did not prevent neutropenia and thrombocytopenia and may have exacerbated neutropenia. Alteration of experimental GBS shock with prostaglandin synthetase inhibition produces disparate hemodynamic and hematologic response.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Myocardial dysfunction in group B streptococcal shock.

A rabbit model of group B Streptococcal (GBS) shock was used to determine if myocardial dysfunction contributes to GBS shock and, if so, to ascertain if prostaglandins modulate this dysfunction. The infusion of heat-killed GBS (group I) produced a dramatic decrease in the first derivative of left ventricular pressure with respect to time (LVdP/dt) from baseline values (p less than 0.05). LVdP/dt remained stable in rabbits pretreated with indomethacin (group II) and in saline-infused control rabbits (group III), and was significantly different at 30 min from LVdP/dt in group I (p less than 0.05). Values for group I mean arterial pressure, cardiac output, pulmonary vascular resistance, and heart rate and for pH and pO2 after GBS infusion were all significantly different from baseline values and from postinfusion values for groups II and III (p less than 0.05). Systemic vascular resistance and left ventricular end diastolic pressure did not change significantly in any group at any time interval. These results indicate a primary role for myocardial dysfunction in the pathogenesis of GBS shock, and suggest strongly that prostaglandins modulate GBS-induced myocardial dysfunction.

Animals↗
PubMed1983

Sonographic determination of renal volumes in normal neonates.

Renal diseases that affect renal size without altering renal architecture require a quantitative means of detection. A prospective study was undertaken to establish normal values for renal volumes in healthy neonates using sonography. Volumes were determined by two methods; (1) the serial area-volume method using parallel transverse images; and (2) the prolate ellipsoid model of the kidney using orthogonal diameters taken from ultrasound images. Renal volumes for both the right and left kidneys in both sexes were found to be approximately 10 ml. There was no significant difference between the results obtained by either method, nor were there significant differences between the volumes of the right and left kidneys within either sex. No difference in renal volume was noted between sexes. The mean greatest renal length was also computed for right and left kidneys in both sexes. Knowledge of normal renal volumes may aid in the diagnosis of urinary system disorders in neonates.

Female↗
PubMed1982

Gallbladder distension in septic neonates.

Eight cases of neonatal gallbladder distension are described. Group B streptococcal sepsis (5 infants) of suspected sepsis (3 infants) was present and probably played an aetiological role in the development of a distended gallbladder. Two infants required surgery because of persistent gallbladder enlargement and rising levels of bilirubin. Five responded to vigorous medical management and one died from sepsis and pneumonia. The need for conservative early management is stressed.

Gallbladder Diseases↗
PubMed1978

ABO hemolytic disease of the newborn: evaluation of management and identification of racial and antigenic factors.

Data from 16,320 deliveries from two time periods were examined to compare the incidence of positive direct Coombs' tests and the number of exchange transfusions performed, using different methods of screening and treatment in each time period. Early routine screening revealed an eightfold increase in the number of Coombs-positive infants, while the combined effect of instituting early screening and the change from white light to special blue light phototherapy greatly diminihsed the number of exchange transfusions. In addition, data concerning racial and blood antigen factors in ABO hemolytic disease of the newborn (HDN) are compared, showing an increase in incidence but no increase in severity for black infants and infants with blood type B. Also, use of cord blood parameters in management of ABO HDN is discussed.

ABO Blood-Group System↗
PubMed1977

Cholecystitis and hydrops of the gallbladder in the newborn.

Inflammatory gallbladder disease is not usually considered in the evaluation of septic newborn infants. When present, the radiographic findings are thought to be sparse. Three instances were recently encountered with radiographic evidence to indicate right upper quadrant abdominal disease. In one, a negative defect on the bodygram phase film of a high volume contrast study demonstrated gallbladder hydrops. Cholecystitis extended to obstruct the pyloroduodenal area with inflammatory reaction in 2 other patients. In all instances, the radiographic changes prompted surgical intervention at an early age.

Acute Disease↗
PubMedDate not supplied

Neonatal gallbladder enlargement and alpha 1-antitrypsin deficiency.

Patients with clinical signs of alpha 1-antitrypsin deficiency in the neonatal period usually present with prolonged obstructive jaundice. We report a patient with alpha 1-antitrypsin deficiency who presented with gallbladder enlargement in the neonatal period. This gallbladder enlargement may be due to cystic duct hypoplasia or atresia, which has been reported in association with alpha 1-antitrypsin deficiency. The diagnosis of alpha 1-antitrypsin deficiency should be considered in neonates with gallbladder enlargement and prolonged obstructive jaundice.

Gallbladder Diseases↗