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Biomedical subjects

L Frank

Publications and source records attributed to L Frank.

At least 145 records · Page 8Linked to original sources
PubMed1981

[The Bonn Cooperative Tumor Aftercare Model. A contribution to the amelioration of tumor patient care in the practitioner's office (author's transl)].

Problems of aftercare of tumor patients are so involved that one doctor cannot cope with them single-handed. Every doctor who has care of tumor patients is dependent on the cooperation of doctors of various faculties as with scarcely any other disease. The experience of a specialized multidisciplinary medical team is as indispensable in aftercare as the general medical supervision of the family doctor. In an action financed by the Federal Minister of Health a cooperative model was worked out intended to enable a qualitatively high level of aftercare for tumor patients over a wide field, making full use of the existing medical welfare structure.

Aftercare↗
PubMed1981

Endotoxin reverses the decreased tolerance of rats to greater than 95% O2 after preexposure to lower O2.

Bacterial endotoxin has a marked protective effect against pulmonary O2 toxicity in rats placed directly in atmospheres of greater than 95% O2. To determine whether endotoxin treatment during exposure to relatively low levels of hyperoxia would protect rats from the accelerated O2 toxicity that normally occurs when these rats are transferred to greater than 95% O2, we gave endotoxin or saline 1) during exposure to 40% O2 (5 days), or 2) during exposure to 40%-60%-85% O2 (2 days at each level). Saline-treated rats showed significantly decreased tolerance on transfer to greater than 95% O2 [LT50 = 47.5 h (exposure 1) and 48.5 h (exposure 2)] compared with normal nonpreexposed rats (LT50 = 66 h). In contrast, endotoxin-treated rats showed a marked tolerance on transfer to greater than 95% O2 [% of rats surviving 72 h = 14/16 (88%) endotoxin-treated vs. 2/16 (13%) saline-treated]. The endotoxin-treated rats, unlike the saline-treated rats, showed significant elevations in lung superoxide dismutase, catalase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase levels after the O2 preexposure periods; this may account for their significantly improved tolerance when challenged with greater than 95% O2 exposure.

Animals↗
PubMed1980

A hypothesis relating breathing pattern to some forms of the "adult respiratory distress syndrome".

Quantitative deficiency of surfactant in neonates results in hyaline membrane disease. Although surfactant is also required for normal gas exchange in adults, no disorders have been clearly attributable to a deficient amount of surfactant. Based on studies in our laboratories as well as on information and ideas in the literature, we suggest that a physical alteration in surfactant may lead to, or contribute to, the development of some forms of "adult" respiratory distress syndrome." In particular, we suggest that an altered breathing pattern contributes to the alveolar collapse and liver-like appearance of the lung found in certain clinical entities, i.e., pulmonary embolism and oxygen toxicity. We hypothesize that in these conditions shallow breathing leads to the aggregation of surfactant into a less functional form resulting in increased alveolar surface tension and atelectasis. The increase in surface tension would also contribute to the edema found in these conditions.

Humans↗
PubMed1980

Oxygen toxicity.

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Animals↗
PubMed1980

Effect of prenatal isoxsuprine on pulmonary oxygen toxicity in the newborn rat.

Isoxsuprine, a beta-sympathomimetic agent used clinically to delay premature parturition and to possibly accelerate fetal lung maturation, was administered to pregnant rats at 48 and 24 h prior to delivery. Newborn rats were placed in 96-98% O2 (or room air) to determine if the prenatal isoxsuprine treatment compromised their tolerance to prolonged hyperoxic exposure. (Exogenous catecholamines are known to exacerbate O2 toxicity in adult animals). Survival of the isoxsuprine-treated pups in O2 (52%) was no different than for control neonates exposed to hyperoxia for 7 days (57%) (P = 0.22). Body weight, lung weight, lung protein, and DNA content of the newborns were also not altered by the prenatal isoxsuprine treatment. Lung antioxidant enzyme activities for superoxide dismutase, catalase, and glutathione peroxidase were the same at birth in the isoxsuprine-treated and control rat pups, and the enzyme activities increased in response to hyperoxic exposure in each group to an equivalent degree. Thus, in utero treatment with isoxsuprine had no apparent adverse effect on newborn rats exposed to a prolonged O2 challenge.

Animals↗
PubMed1980

Potection from oxygen toxicity with endotoxin. Role of the endogenous antioxidant enzymes of the lung.

Endotoxin treatment of adult rats before hyperoxic exposure significantly increases their survival rate in >95% O(2) (J. Clin. Invest.61: 269, 1978). In this study, we wished to determine: (a) whether endotoxin would protect against O(2) toxicity if it were administered after the animals were already in >95% O(2) for 12-48 h; and (b) the relationship between the endogenous antioxidant enzymes of the lung and the protective effect of endotoxin treatment. Our results showed that adult rats given a single 500 mug/kg dose of endotoxin up to 36 h after the onset of O(2) exposure had significantly increased survival rates and decreased lung fluid accumulation compared to untreated animals in O(2) (P < 0.05). (Survival, 16/49 [untreated rats]; 18/20 [endotoxin at 12 h after the start of O(2) exposure]; 25/26 [endotoxin-24 h]; 15/20 [endotoxin-36 h].)Endotoxin-treated animals in O(2) showed increases in pulmonary superoxide dismutase, catalase, and glutathione peroxidase activities before the usual time of onset of measurable pulmonary edema in untreated animals in O(2). When diethyldithiocarbamate was used to block the superoxide dismutase enzyme rise in the endotoxin-treated rats in O(2), the protective action of endotoxin against pulmonary O(2) toxicity was nullified. In endotoxin-treated, O(2)-exposed mice, there were no lung antioxidant enzyme increases, and no protective effect from O(2) toxicity was achieved. We conclude that, in the rat, a single dose of endotoxin given even 36 h after the onset of hyperoxic exposure results in marked protection against O(2)-induced lung damage; and the increased lung antioxidant enzyme activity in the endotoxin-treated rats appears to be an essential component of this protective action.

Animals↗
PubMed1980

The effect of prenatal dexamethasone treatment on oxygen toxicity in the newborn rat.

To determine whether prenatal corticosteroid therapy had adverse effects on the tolerance of the newborn lung to prolonged high O2 exposure, pregnant rats were given injections of dexamethasone (0.2 mg/kg) at 48 and 24 hours prior to parturition, and the newborn pups were placed in 96% to 98% O2 for the first seven days of life. Dexamethasone treatment resulted in significant decreases in body weight (-17%), lung weight (-30%), lung weight/body weight (-22%), and lung DNA (-18%) compared to untreated rat pups. Despite this growth inhibition, the dexamethasone-treated pups had improved survival in hyperoxia (36/48 = 75% vs 29/48 = 60% for untreated rats, P = .055). In addition, substantial "catch-up" lung growth had occurred by seven days and was complete in 28-day-old rats. Dexamethasone did not interfere with normal pulmonary antioxidant enzyme responses to hyperoxia. Thus, prenatal dexamethasone did not compromise the relative tolerance of the newborn to pulmonary O2 toxicity.

Animals↗
PubMed1979

Endotoxin protection against oxygen-induced acute and chronic lung injury.

Small dosages of endotoxin (100--500 micrograms/kg) provide significant protection against the acute manifestations of pulmonary O2 toxicity and lethality. Ninety-seven percent of endotoxin-treated adult rats survived a 72-h exposure to greater than or equal to 95% O2 with mimimal lung changes, compared to 32% of control animals (P less than 0.01). Exposure to greater than or equal to 95% O2 for 7 days resulted in a 20% survival rate in untreated control rats vs. 98% survival in endotoxin-treated rats (P LESS THan 0.01). Histological evaluation of lung from survivors revealed substantially less collagen and reticular fiber deposition in the endotoxin-treated animal lungs. Endotoxin treatment was associated with increased activity of the protectant antioxidant enzyme systems of the lung in an apparent dose-response manner. Endotoxin's protective activity against O2 toxicity does not appear to depend on an initial toxic insult to the lung like with alpha-naphthylthiourea, oleic acid, or alloxan treatment. The data support a protective role for endotoxin against the acute and the more chronic manifestations of O2-induced pulmonary injury.

Alloxan↗
PubMed1979

Effects of low-dose prenatal corticosteroid administration on the premature rat.

Administration of dexamethasone (0.2 mg/kg/day) to the pregnant rat on days 19 and 20 of gestation has been found to have marked effects on the body and organ weight of fetuses delivered 1 day prematurely on day 21 of gestation. Longer-term dexamethasone treatment earlier in gestation (days 14-18) had even more pronounced effects on body and organ weights in rat fetuses delivered three days prematurely. Dexamethasone treatment for 2 days prior to delivery had no effect on the survival of 1-, 2- and 3-day premature rats. The marked inhibitory effect on organ and body weight observed in the premature rats resulted from prenatal steroid therapy approximating that used in human pregnancies (dexamethasone 0.2 mg/kg/day for 48 h prior to premature delivery).

Animals↗
PubMed1978

Oxygen toxicity in neonatal and adult animals of various species.

Neonatal and adult animals of five species were exposed to 95+% O2. Survival time and changes in lung antioxidant enzyme activity (superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GP)) in response to hyperoxia were determined. Adult animals succumbed to O2 lung toxicity in 3--5 days. Neonatal rats, mice and rabbits showed minimal lung changes after 7 days of hyperoxic exposure and these same neonatal animals showed rapid and significant increases in lung antioxidant enzyme activities. In contrast, neonatal guinea pigs and hamsters had no lung antioxidant enzyme response to hyperoxia and these neonates died in 95+% O2 as readily as their respective parent animals. Results from an in vitro hyperoxic exposure system suggest that the lack of enzymic response of the guinea pig (and hamster) neonates to O2 challenge is due to an inherent pulmonary biochemical unresponsiveness rather than to a deficiency of a necessary "serum factor." The results of this species and age study support the important role of the lung antioxidant enzyme defense system in protection of the lung from O2-induced injury.

Animals↗
PubMed1978

The role of endotoxin in protection of adult rats from oxygen-induced lung toxicity.

Adult rats show evidence of severe lung damage after 72h of continuous exposure to hyperoxia (96-98% O2). Treatment of adult rats with a solution of Plasmanate, inadvertently contaminated with endotoxin-producing organisms, or with purified endotoxin itself markedly altered the lung toxicity associated with hyperoxic exposure (survival in treated animals = 110/113 [97%] versus survival in untreated animals = 56/172 [33%]). After 72h of hyperoxic exposure, the endotoxin-treated rats demonstrated significant increases in lung superoxide dismutase, catalase, and glutathione peroxidase activity, a protectant enzyme response not seen in untreated adult rats. The basis for endotoxin's protective effect from hyperoxic lung damage is believed to be related to the stimulated increase in activity of the pulmonary antioxidant enzyme defense system. Some previously known actions of endotoxin are speculated to also serve a protective function by opposing some of the usual detrimental effects of high concentrations of O2 on the lung.

Animals↗
PubMed1978

Oxygen toxicity: comparison of lung biochemical responses in neonatal and adult rats.

Neonatal rats (4--7 days old) and adult rats (approximately 80 days old) were continuously exposed to either 96--98% oxygen or air. Examination of the lungs of neonatal rats, who survived 5 days of oxygen exposure with no evidence of respiratory distress, showed significant increases in the pulmonary superoxide dismutase (SOD) activity (peak value: 144% of air-exposed controls), glutathione peroxidase (GP) activity (126%), glutathione reductase (GR) activity (122%), reduced glutathione (GSH) level (176%), and glucose-6-phosphate dehydrogenase activity (151%). Adult rats, most of whom succumbed within 3 days of oxygen exposure, did not show any significant increase in the activities of pulmonary SOD, GP, GR, and the level of GSH as compared to the air-exposed adult animals. Glucose-6-phosphate dehydrogenase was significantly elevated in the 72-hr oxygen-exposed adult rats. It is concluded that increases in the lung complement of SOD, GR, GP, and GSH in the neonatal rat during oxygen challenge may provide the mechanism(s) for their increased tolerance to hyperoxia-induced lung injury as compared to the adults.

Aging↗