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Biomedical subjects

S Buckley

Publications and source records attributed to S Buckley.

82 records · Page 5Linked to original sources
PubMed1987

Beta-receptors and surface active material flux in fetal lamb lung: female advantage.

We correlated the ontogeny of pulmonary beta-adrenergic receptors with the onset of surface active material (SAM) flux into tracheal fluid of male and female chronically catheterized fetal lambs. SAM flux began between 0.82 and 0.85 gestation in the females and between 0.85 and 0.89 gestation in the males and matured more rapidly thereafter in the females than in the males (P less than 0.01). beta-Adrenergic receptor binding, using [3H]dihydroalprenolol as the ligand, was saturable, linear, and stereospecific. The order of potency of competitive beta-agonists was isoproterenol greater than norepinephrine greater than epinephrine. The maximal binding capacity (Bmax) of pulmonary beta-receptors approximately doubled between 0.84 and 0.89 gestation, coinciding with the onset of SAM flux. Bmax matured as a third degree polynomial function of gestational age in females (r = 0.9, P less than 0.001) but as a linear function in males (r = 0.8, P less than 0.005). Between 0.86 and 0.93 gestation, Bmax was 1.45-fold greater in females than males (P less than 0.001). The dissociation constant of beta-receptors was not influenced significantly by gender or gestation. We conclude that maturation of pulmonary beta-receptors coincides with the onset of SAM flux in fetal lambs and that both mature more rapidly in females. We speculate that pulmonary beta-receptor maturation and SAM flux are coregulated by hormonal factors. More rapid maturation of pulmonary beta-receptors and SAM flux in females may be a factor in the female advantage with regard to pulmonary surfactant maturation and the survival of premature neonates.

Animals↗
PubMed1987

Effects of glucose infusion on surfactant and glycogen regulation in fetal lamb lung.

To investigate the increased incidence of respiratory distress syndrome (RDS) that occurs in infants of diabetic mothers (IDM) with poor maternal glucose homeostasis, we infused glucose intravenously at a rate of 14 +/- 2 (SD) mg.kg-1.min-1 into eight twin and four singleton chronically catheterized fetal lambs from 112 days (0.77) gestation onward. Twelve catheterized and seven uncatheterized fetuses served as controls, including the eight twins of the glucose-treated fetuses. Glucose infusion resulted in a twofold elevation in fetal serum glucose levels and a 2.2-fold elevation in fetal serum insulin levels. Before 113 days (0.9) gestation, pulmonary disaturated phosphatidylcholine (DSPC) content was 1.5-fold higher in the glucose-infused fetuses than in the controls. However, after 0.9 gestation, pulmonary DSPC content increased 2.2-fold in the controls but did not increase significantly in the glucose-infused fetuses. In addition, the DSPC content of lung lavage was 5.0-fold higher in the controls and lung stability to air inflation was 2.0-fold greater and to deflation was 2.2-fold greater than in the glucose-infused fetuses. Pulmonary adenosine 3',5'-cyclic monophosphate-dependent protein kinase activity was also 1.5-fold higher, and pulmonary protein kinase C activity was 1.3-fold higher in the controls than in the glucose-infused fetuses. In contrast, glucose infusion was associated with a 1.8-fold increase in pulmonary glycogen content and with increased activities of glycogen phosphorylase kinase and glycogen phosphorylase. We conclude that the effects of chronic glucose infusion on fetal lamb lung DSPC and lung stability are compatible with a predisposition of the fetus to develop RDS.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Effects of beta-2 agonist on metabolic regulation in the fetal lamb lung.

To study the effects of beta-2 agonist on metabolic regulation in fetal lamb lung, ritodrine hydrochloride, a preferential beta-2 agonist, was infused i.v. at a rate of 1.3 +/- 0.4 micrograms/kg/min (mean +/- S.D.) for 24 hr into six twin chronically catheterized fetal lambs starting between 0.86 and 0.91 gestation. Lung glycogen was depleted 56% in the ritodrine-infused twins and glycogen phosphorylase a activity was increased 1.8-fold whereas glycogen synthase activity remained unchanged. Cyclic AMP-dependent protein kinase activity increased 1.7-fold, calcium-calmodulin-dependent protein kinase (phosphorylase kinase) activity increased 1.4-fold and calcium-phospholipid-dependent protein kinase (protein kinase C) activity increased 1.6-fold. In addition, the maximal binding capacity of pulmonary beta receptors decreased 49% in the ritodrine-infused twins. However, lung cyclic AMP content was unchanged after 24 hr of ritodrine infusion. We conclude that beta-2 agonist activates protein kinases, depletes glycogen and reduces the binding capacity of beta receptors in the fetal lamb lung. We speculate that these adrenergic mechanisms are involved in regulating the effects of beta-2 agonist on fetal lung liquid and surfactant production.

Adrenergic beta-Agonists↗
PubMed1987

Effects of beta-2 agonist on tracheal fluid flow, surfactant and pulmonary mechanics in the fetal lamb.

To study the effects of beta-2 agonist on tracheal fluid, surfactant and pulmonary mechanics in fetal lamb lung, ritodrine hydrochloride, a preferential beta-2 agonist, was infused i.v. at a rate of 1.3 +/- 0.4 micrograms/kg/min (mean +/- S.D.) for 24 hr into six twin chronically catheterized fetal lambs starting between 0.86 and 0.91 gestation. Ritodrine infusion was associated with statistically significant metabolic and pulmonary effects in comparison with twin controls. Fetal serum glucose levels were elevated 1.7-fold, arterial blood pH fell 0.04 U and arterial blood pO2 fell 5.1 torr in the ritodrine-infused twins. Tracheal fluid flow was reduced 6.9-fold and surface active material flux into the tracheal fluid was thereby virtually eliminated. But the surface active material content of tracheal fluid and lung lavage increased 3.0-fold. The surfactant phospholipid content of lung lavage also increased 3.0-fold with no change in its composition. There was a concomitant improvement in pulmonary mechanics on pressure-volume curves: the lungs of the ritodrine-infused twins filled with 1.7-fold more air on inflation to 40 cm of water pressure and also retained 1.7-fold more air on deflation to 10 cm of water pressure. We conclude that beta-2 agonist inhibits tracheal fluid flow, increases surfactant in lung lavage and improves lung stability in the fetal lamb lung. We speculate that preferential beta-2 adrenergic stimulation of the fetal lung with ritodrine could be helpful in the prevention of neonatal respiratory distress syndrome because of enhanced surfactant availability in airways and improved pulmonary mechanics.

Adrenergic beta-Agonists↗
PubMed1986

Pneumomediastinum and subcutaneous cervical emphysema during third molar extraction under general anesthesia.

A case of pneumomediastinum and subcutaneous cervical emphysema during the extraction of third molars under general anesthesia has been presented. The most likely cause was pulmonary barotrauma secondary to a faulty expiratory valve. This emphasizes the need for the proper preoperative check of all anesthetic equipment. Although pneumomediastinum and subcutaneous cervical emphysema are usually self-limiting conditions with rapid recovery, the patient must undergo close observation for the possible development of serious complications.

Adult↗
PubMed1984

The effect of low-density lipoproteins on the synthesis of cyclic nucleotides induced by prostacyclin in isolated platelets.

Isolated platelets are strongly sensitized by the presence of low-density lipoproteins (LDL) so that they aggregate with very low concentrations of other agonists or exhibit spontaneous aggregation. Prostacyclin (PGI2) is a potent inhibitor of aggregation, but its action was reversed by LDL. This effect of LDL was accompanied by a decrease in the synthesis of cyclic AMP induced by PGI2, but its efficacy depended on the relative concentrations of LDL and PGI2. PGI2 also enhanced the synthesis of cyclic GMP, but this was completely reversed by the presence of LDL. LDL did not remove inhibitory prostaglandins, e.g. E1, from their receptor sites. The lipoproteins also decreased cyclic AMP synthesis induced by forskolin, which has its effect on the GTP-sensitive protein or the catalytic unit of the adenylate cyclase enzyme complex. It is proposed that LDL may act on the enzyme catalytic unit via an inhibitory GTP-sensitive protein or by a separate mechanism which indirectly impedes the production of cyclic AMP.

Blood Platelets↗
PubMed1978

Arterial hypertension in immediate postoperative period after valve replacement.

Paroxysmal hypertension occurred during the first 8 hours after cardiac valve replacement in 15 of 186 consecutive patients. The clinical characteristics of this hypertension were similar to those of hypertension after myocardial revascularization, except that this complication occurred much less frequently after valve replacement (8.1%) than after myocardial revascularisation (33%) (P less than 0.001). Hypertension resulting from hypoxia, hypercapnia, shivering, or arousal from anaesthesia was excluded from consideration. The rise in systemic arterial pressure (average 34/35 mmHg +/- 4.9/4.3 SE) was usually associated with a reduction in central venous pressure (12/15 patients) and a mild increase (2 to 4 cm saline) in left atrial pressure. The incidence of hypertension was not related to the valve replaced (aortic or mitral), type of lesion (stenosis or regurgitation), preoperative level of blood pressure, or use of hypothermia during operation. However, none of the 18 patients who had double valve replacement showed significant rise in blood pressure after operation. It is suggested that these hypertensive episodes may be related to pressor reflexes from the heart and/or great vessels.

Aortic Valve↗