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Biomedical subjects

D K Das

Publications and source records attributed to D K Das.

At least 307 records · Page 17Linked to original sources
PubMed1984

Effect of starvation and diabetes on glucose transport in the lung.

Transport of glucose by the isolated and perfused rat lung was studied using 2-deoxy-D-(1-14C)-glucose, 2-(1-14C)-DG, and 3-O-methyl-(U-14C)-glucose, 3-(U-14C)-MG. Uptake of 3-(U-14C)-MG was reduced by 20% in the lungs of fasting and diabetic rats, the uptake was restored by refeeding and insulin treatment, respectively. Although the intracellular accumulation of unphosphorylated 2-(1-14C)-DG in lungs was altered by a small amount in diabetes and fasting, the intracellular accumulation of phosphorylated 2-(1-14C)-DG was significantly reduced and restored by insulin treatment and refeeding, suggesting that phosphorylation was inhibited in these conditions. The reduction of glucose utilization in fasting or diabetic state was shown to be due to the inactivation of hexokinase II enzyme. Thus, a specific glucose-carrier system is present in the rat lung which appears to be insulin-sensitive and is under the nutritional and hormonal control.

Animals↗
PubMed1983

Effect of ischemia on fatty acid metabolism in fetal lung.

The effects of ischemia on in vivo fatty acid metabolism in fetal lung were studied using rabbit fetuses of 25 to 28 gestational age. Ischemia was produced by inflating the aortic balloon thereby reducing the uterine blood flow. Ischemic insult resulted significant increase in lactate/pyruvate and NADH/NAD ratios and decrease in ATP/ADP ratio in fetal lung. Levels of CoA, acetyl CoA, carnitine and acetyl carnitine decreased while those of long chain acyl CoA and long chain acyl carnitine enhanced. Tissue content of these metabolites returned to normal after 2 hr stabilization following 20 min of ischemic insult. Ischemia also caused small increase in lipogenesis and neutral lipid content of fetal lungs. Our results thus suggest that beta-oxidation in fetal lung is inhibited and becomes rate-limiting for fatty acid oxidation during ischemia. Sudden occurrence of hypoxia or ischemia in the fetus is a typical challenge for the obstetricians. The patients occasionally suffer from neurological injury following cerebral hypoxemia. The hypoxic insult may also affect the respiratory activity significantly. For example, acute alveolar hypoxia causes pulmonary vasoconstriction by damaging pulmonary vascular smooth muscle (1) and results in reduction of fatty acid oxidation by limiting the ATP supply required for metabolic processes (2). Hypoxia has also been shown to decrease the rate of palmitate incorporation into phospholipids (3), inhibit rate of fatty acid synthesis (3) and depress rate of incorporation of fatty acid and phosphatidic acid into lipids (4). Despite the fact that fatty acids represent a major substrate for energy metabolism in lung, no work has been done on the fatty acid metabolism in fetal lung. The present study was designed to determine the fate of fatty acid oxidation in fetal lung during ischemic challenge. The levels of acyl CoA and acylcarnitine intermediates were also measured in order to determine the rate-controlling steps of fatty acid metabolism in the fetal lung.

Adenosine Diphosphate↗
PubMed1983

Hormonal control of pulmonary surfactant synthesis.

The specific activities of palmitoyl-CoA synthetase, phospholipase A2, and lysophosphatidylcholine acyltransferase enzymes were low in the lungs of diabetic and hypophysectomized rats as compared to those found in the normal controls. Administration of triiodothyronine (T3), to the diabetic and hypophysectomized rats restored the normal activities of these enzymes. Stimulation of the enzyme activities were also observed when normal rats were injected with the above hormone. The enhancement of the enzyme activities was also found to be dependent on the dose and duration of the hormonal treatment. Optimum levels were achieved at a dose of about 100 micrograms/100 g body weight of T3, 3-4 days after the administration of this hormone. Actinomycin D or cycloheximide abolished the hormone-mediated stimulation of these enzymes in diabetic and hypophysectomized rats. Reduced rate of in vivo palmitoyl-CoA synthetase synthesis was observed in the lungs of diabetic and hypophysectomized animals. Administration of T3 stimulated the rate of synthesis of this enzyme indicating increasing synthesis of this enzyme and not of activation of the pre-existing inactive species. Reduced phospholipid contents, specially decreased amount of lecithin and dipalmitoyl lecithin (DPL) were observed in the lungs of the diabetic and hypophysectomized animals as compared to those in the normal animals. T3 also increased the lecithin and DPL content of the normal rat lungs. These results provide evidence for the involvement of the thyroid hormones in the control of the pulmonary surfactant. The results further suggest that T3 was capable of inducing the enzymes of the "deacylation-reacylation" pathway involved in palmitate incorporation into phosphatidylcholine thereby contributing to the stimulation of dipalmitoyl phosphatidylcholine biosynthesis.

1-Acylglycerophosphocholine O-Acyltransferase↗
PubMed1983

The effect of oxygen adaptation on oxyradical injury to pulmonary endothelium.

Rats exposed to 85% O2 for 7 days develop an increase in pulmonary tissue levels of antioxidant enzymes and are able to survive subsequent exposure to 100% O2. In order to examine endothelial cell function in O2-adapted rats, we chemically generated oxygen radicals within the pulmonary circulation of lungs isolated from 85% O2-exposed rats and used [14C]5-hydroxytryptamine (5-HT) uptake as an indicator of endothelial cell function. The [14C]5-HT uptake in lungs of O2-exposed rats was similar to that in air-exposed rats and was reduced by cyanide, anoxia, and by imipramine. After generation of O2-derived free radicals within the pulmonary circulation, there was a progressive decline in [14C]5-HT uptake in both groups, with a more rapid decline seen in the lungs of air-exposed rats. These data suggest that pulmonary endothelial cells that survive 85% O2 exposure for 7 days are capable of normal function and are more resistant to further oxyradical injury.

Adaptation, Physiological↗
PubMed1982

The effect of oxygen-derived free radicals on pulmonary endothelial cell function in the isolated perfused rat lung.

Oxygen-derived free radicals have been shown to damage endothelial cells in tissue culture. We have extended these observations to demonstrate a direct toxic action of oxy radicals on endothelial cell function in the isolated perfused rat lung model. Using an enzymatic system of hypoxanthine and xanthine oxidase, we generated a superoxide flux of 5-7 nmol/min within the pulmonary circulation. This resulted in alteration of endothelial cell function, including a progressive fall in the cellular transport of (14C) 5-hydroxytryptamine, edema formation manifested by a falling dry weight ratio and increasing mean transit times appearance of thiobarbituric acid reactive material in the perfusate indicating lipid peroxidation, and histologic evidence of edema formation with disruption of the endothelial cell plasma membrane. Inhibitor studies confirmed that the observed effects were due to superoxide radical generation. Oxygen derived free radicals may play a role in the pulmonary endothelial cell damages seen in inflammatory disorders and oxidant lung injury.

Animals↗
PubMed1981

Effect of dexamethasone on the synthesis of dipalmitoyl phosphatidylcholine.

Glucocorticoids are known to enhance surfactant production by stimulating the formation of phosphatidylcholine. This study was performed to determine the effect of steroids on one of the pathways involved in the incorporation of palmitic acid into phosphatidylcholine--the 'deacylation-reacylation pathway'. Palmitoyl CoA synthetase, lysopalmitoyl cholineacyltransferase and phospholipase A2 were enhanced significantly as a result of direct administration of dexamethasone into 27-day fetal rabbits. Cycloheximide inhibited the steroid induced enhancement of activity. Immunologic studies demonstrated an accelerated rate of synthesis of palmitoyl CoA as a result of the dexamethasone treatment. The data suggest that steroids are capable of inducing enzymes of the 'deacylation-reacylation pathway' involved in palmitate incorporation into phosphatidylcholine thereby contributing to the acceleration of dipalmitoyl phosphatidylcholine biosynthesis.

1-Acylglycerophosphocholine O-Acyltransferase↗
PubMed1981

Diabetes, hypophysectomy, or thyroidectomy reduces nuclear L-triiodothyronine-binding capacity of rat lung.

L-T3 (T3) receptors of the lungs of rats were found to be under hormonal control. The apparent binding capacity of T3 receptors of lungs of diabetic, hypophysectomized, and thyroidectomized rats were 0.224 +/- 0.009, 0.195 +/- 0.007, and 0.102 +/- 0.008 pmol/mg DNA, as compared to 0.0321 +/- 0.014 pmol/mg DNA for normal animals. The binding affinities for T3 in normal, diabetic, hypophysectomized, and thyroidectomized rats were 256 +/- 3.24, 270 +/- 3.81, 249 +/- 4.03, and 260 +/- 8.2 pM, respectively. The magnitude of the maximum binding capacity in these cases was apparently not due to the loss of either T3 receptors or DNA during the incubation. Serum T3 and T4 concentrations in normal rats were 120.0 +/- 7.2 ng/dl and 5.9 +/- 0.5 micrograms/dl, respectively. Diabetes, hypophysectomy, and thyroidectomy lowered these values to 79 +/- 5.4, 60 +/- 5.8, and 30 +/- 1.6 ng/dl for T3 and 3.5 +/- 0.3, 2.7 +/- 0.4, and 1.9 +/- 0.2 micrograms/dl for T4, respectively.

Animals↗
PubMed1981

Effect of aminophylline on the synthesis of dipalmitoyl phosphatidyl choline in fetal rabbit lung.

Aminophylline (A) administration to pregnant rabbits resulted in accelerated formation of phospholipids, the known important components of pulmonary surfactant [1]. The present study was undertaken to determine the effect of A on one of the pathways involved in the incorporation of palmitic acid into phosphatidyl choline (PC)--the "deacylation-reacylation pathway." A was injected intraperitoneally into rabbit fetuses at 27 days of gestation and its effect on palmitoyl CoA synthetase (PCS) and lysopalmitoyl choline acyl transferase (LPC-AT) were studied. Only LPC-AT was enhanced significantly (P less than 0.05) as a result of direct administration of A. This study supports the suggestions by previous investigators that antenatal administration of aminophylline may prove to be an effective means of enhancing lung maturation by stimulating the formation of pulmonary surfactant production before premature delivery. However, the dose that was used in this experimental study was far more than the usual clinical dose that had been suggested previously.

1-Acylglycerophosphocholine O-Acyltransferase↗
PubMed1980

Competition between platelets and lung for 5-hydroxytryptamine uptake.

The pulmonary endothelial cell removes 5-5-hydroxytryptamine (5-HT) from the circulation by a process of uptake and metabolism. The platelet, the major source of 5-HT in the circulation, represents another potential site of uptake for this amine. Platelet uptake of 5-HT infused into the pulmonary circulation was evaluated using isolated ventilated rat lungs. Lungs were perfused with buffer, platelet-poor, platelet-rich, or thrombin-treated platelet-rich plasma followed by an infusion of (14C) 5-HT. Platelet counts, aggregation response to adenosine diphosphate, and in vitro uptake of 55-HT were unchanged after circulation through the lung. In the presence of buffer or platelet-poor plasma, the lung removed 65.5 +/- 1.4% and 67.8 +/- 0.8%, respectively, of the infused (14C) 5-HT. In the presence of platelet-rich plasma, the lung removed 51.3 +/- 3.0 and platelet fraction 30.1 +/- 1.4% of the infused (14C) 5-HT. Recently aggregated platelets removed 24.4 +/- 1.8%, whereas platelets exposed to low oxyygen tensions removed 14.7+/- 0.6% of the (14C) 5-HT. These results indicate that 5-HT released inot the pulmonary circulation is either taken up by the endothelium and metabolized or taken back up by the platelet and stored.

Animals↗