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Biomedical subjects

J P Morray

Publications and source records attributed to J P Morray.

10 recordsLinked to original sources
PubMed1991

Amrinone reduces pulmonary vascular resistance elevated by U46619 in isolated perfused lungs.

The effects of amrinone on pulmonary vascular resistance (PVR) were studied in an isolated, perfused rabbit lung model where all the major determinants of PVR were controlled. In this preparation, the alveolar oxygen and carbon dioxide tensions, vascular pH and vascular oxygen and carbon dioxide tensions, and zonal conditions of the lung and phasic variations of pulmonary artery pressures could be precisely measured and controlled. Measurements of PVR were made by a complete determination of the pulmonary pressure-flow curve and determination of the PVR under identical flow conditions for all studies. This approach allowed a more precise determination of the primary effects of amrinone on normal and elevated PVR than has been previously possible. We found that amrinone in final concentrations of either 4 or 8 micrograms/ml had no effect on basal PVR and no effect on lung water weight to dry ratios. When PVR was elevated by the addition of the thromboxane A2 mimetic U46619, amrinone reduced the PVR by 27% at a final concentration of 4 micrograms/ml and by 74% at a final concentration of 8 micrograms/ml. We conclude that in the doses tested, amrinone has no effects on basal PVR but is able to reduce elevated PVR in a dose-dependent manner. These results are the first to demonstrate clearly that amrinone has the ability to reduce elevated pulmonary vascular tone through a direct mechanism and not through secondary effects on other determinants of PVR such as left atrial pressure (Pla), increased cardiac output with resultant vascular recruitment, or increases in mixed venous oxygen tension. The possible implications for the clinical use of amrinone in situations of elevated PVR are discussed.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1990

Oxygen delivery and consumption during hypothermia and rewarming in the dog.

Changes in oxygen consumption (VO2) and oxygen delivery (DO2) were compared in three groups of paralyzed, sedated dogs: 1) a group (n = 5) cooled to 29 degrees C and immediately rewarmed to 37 degrees C; 2) a group (n = 5) cooled to and maintained at 29 degrees C for 24 h, and then rewarmed; and 3) a group (n = 5) maintained at 37 degrees C for 24 h. During the cooling phase, in both the acute and prolonged hypothermia animals, VO2 and DO2 decreased significantly from control values (P less than 0.05). The decrease in DO2 occurred as a result of a similar decrease in cardiac index (CI; P less than 0.05) that was associated with a significant increase in systemic vascular resistance index (SVRI; P less than 0.05). Arteriovenous oxygen content difference (C(a-v)O2), O2 extraction ratio, mixed venous oxygen tension (PVO2), pH, and base deficit (BD) were not different from control values even during prolonged hypothermia. Normothermic control dogs also demonstrated a significant decrease in CI (P less than 0.05) at 24 h. Surface rewarming increased VO2 back to control values in the acute hypothermia group and to values above control (P less than 0.05) in the prolonged hypothermia group. DO2 remained below control in both groups, resulting in a significant increase in O2 extraction (P less than 0.05) and a decrease in PVO2 (P less than 0.05) in the prolonged hypothermia animals. Following rewarming administration of sodium nitroprusside returned DO2, CI, and SVRI to control values but did not increase VO2. All animals survived the study without need for inotropic support.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Short-acting barbiturate sedation: effect on arterial pH and PaCO2 in children.

One hundred and fifteen unpremedicated children, induced with thiamylal, a short-acting thiobarbiturate, administered rectally (25 mg.kg-1 body wt) or intravenously (6 mg.kg-1) had arterial pH of 7.36 +/- 0.03 and PaCO2 of 40 +/- 4 mmHg. In 22 children over two years of age, the use of fentanyl (1.2 +/- 0.7 microgram.kg-1) in addition to the thiamylal did not change blood gas data compared to those children over two years receiving only barbiturates (pH 7.36 vs 7.36, PaCO2 41 vs 40 mmHg). Children with cyanotic congenital heart disease showed similar pH and PaCO2 to acyanotic children following administration of the short-acting barbiturate. Thiobarbiturates, given in a titrated fashion under direct observation, have clinically small effects on arterial pH and PaCO2 in paediatric patients.

Administration, Rectal↗
PubMed1988

Effect of pH and PCO2 on pulmonary and systemic hemodynamics after surgery in children with congenital heart disease and pulmonary hypertension.

Fourteen children with congenital heart disease and associated pulmonary hypertension (preoperative mean pulmonary artery pressure (MPAP) 48 mm Hg +/- 1 SEM were examined to determine the effect of arterial carbon dioxide tension (PaCO2) and pH on pulmonary and systemic hemodynamics after surgical repair. Baseline measurements were obtained with hyperventilation to PaCO2 20 to 30 mm Hg (pH 7.56 +/- 0.01 mm Hg). The addition of carbon dioxide to inspired gas to achieve a PaCO2 40 to 45 mm Hg (pH 7.35 +/- 0.01) resulted in a significant increase in MPAP, from 32 +/- 5 mm Hg to 47 +/- 8 mm Hg (p less than 0.05). An increase in mean cardiac index (CI) from 2.7 +/- 0.3 L/min/m2 to 3.3 +/- 0.3 L/min/m2 (p less than 0.05) explained in part the associated increase in MPAP. For a subgroup of eight patients with postoperative MPAP greater than 30 mm Hg (at pH 7.35 to 7.40), pulmonary vascular resistance index (PVRI) also significantly increased (p less than 0.05) as PaCO2 was increased, implying a direct pulmonary vasodilating effect of alkalosis. Removal of carbon dioxide from inspired gas returned hemodynamic values to baseline. The higher the MPAP at physiologic pH the greater the absolute amount of MPAP reduction and PVRI reduction (p less than 0.05) with alkalosis. No complications from alkalosis were seen. We suggest that a trial of hypocarbic alkalosis in the child with severe residual pulmonary hypertension after surgical repair of congenital heart disease is warranted to reduce right ventricular afterload.

Adolescent↗
PubMed1987

Brain death?

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Brain Death↗
PubMed1985

Isolated deafness following recovery from neurologic injury and adult respiratory distress syndrome. A sequela of intercurrent aminoglycoside and diuretic use.

We report two children who survived neurologic injury (near-drowning and Reye's syndrome) and adult respiratory distress syndrome and who required prolonged ventilatory support. Follow-up examination in both children showed steady neurologic recovery, but five months following discharge from their acute illness, profound hearing loss was diagnosed in both children. A review of the literature is reported and the hypothesis that combined aminoglycoside antibiotic and loop diuretic therapy caused the hearing loss is presented. Recommendation is made for audiologic assessment within six months of recovery from critical illness of pediatric patients in whom therapy has included loop diuretic and aminoglycoside antibiotic therapy.

Aminoglycosides↗