Search PubMed⌕ Search

Biomedical subjects

E D Robin

Publications and source records attributed to E D Robin.

At least 109 records · Page 6Linked to original sources
PubMed1977

Special report: dysoxia. Abnormal tissue oxygen utilization.

The ultimate cause of the clinical abnormalities associated with changes in oxygen supply and oxygen utilization is the development of abnormal tissue oxygen metabolism. Until now, there has been no satisfactory term to describe abnormal tissue oxygen metabolism. We propose the term "dysoxia" to fill this gap. There are a number of causes of dysoxia. One of the most interesting is that form of dysoxia related to abnormal mitochondrial structure and function. In this group of disorders, there is abnormal tissue oxygen metabolism, although oxygen supply is normal. Another interesting cause of dysoxia is exposure to high oxygen concentrations. High oxygen concentrations are involved in producing abnormal tissue oxygen metabolism under a number of different circumstances. The concept underlying dysoxia provides a unified approach to a large and important group of disorders involving most branches of clinical medicine.

Child↗
PubMed1977

Some comparative aspects of the organ distribution of superoxide dismutase activity in the freshwater turtle, Pseudemys scripta elegans.

1. Superoxide dismutase activities in five tissues of the relatively anaerobic freshwater turtle were compared with SOD activities in the same tissues of two mammalian species (mouse and rabbit) with a more usual pattern of dependence on O2 availability. 2. SOD activities in brain, lung and skeletal muscle, but not liver or cardiac muscle, are significantly lower in the turtle. The turtle also shows differences in the pattern of relative SOD activities in various tissues as compared to the two mammalian species. 3. The data indicate that a relationship does exist between SOD activities and O2 exposure in intact vertebrate systems, and is consistent with a physiological role for SOD in tissue O2 metabolism.

Animals↗
PubMed1977

Superoxide dismutase (SOD) activity in hypoxic mammalian systems.

Superoxide Dismutase (SOD) activity was compared in rabbit peritoneal macrophages (ambient PO2 approximately 15 Torr) and alveolar macrophages (ambient PO2 approximately 100 Torr) and in brain, lung, cardiac muscle, and skeletal muscle of chromically hypoxic mice(ambient PO2 approximately 50 Torr) and normoxic mice (ambient PO2 approximately 150 Torr). Peritoneal macrophages (PM) have significantly less SOD activity than alveolar macrophages (AM) (PM: 2.94 +/- 0.49 (mean +/- SD); AM:6.03 +/- 1.60 units-mg protein -1 (P less than 0.01)). SOD activity of lung and brain homogenates from the hypoxic mice was significantly less than from the normoxic controls. Heart and skeletal muscle SOD activities were not significantly different. These studies show that limitations of O2 supply are associated with reductions in SOD and are consistent with the thesis that SOD plays an important role in protection against oxygen toxicity in mammalian systems.

Animals↗
PubMed1977

Effect of hyperoxia, hypoxia, and maturation on superoxide dismutase activity in isolated alveolar macrophages.

The influence of ambient O2 tensions and of cell maturation on superoxide dismutase activity were studied in tissue culture--maintained mouse alveolar macrophages. Cultivation under hyperoxic conditions (PO2 about 640 mmHg) for 24 hours was associated with a significant increase in superoxide dismutase activity as compared with normoxic conditions (PO2 approximately 150 mmHg). (Hyperoxia: superoxide dismutase = 7.9 +/- 4.0 (SD); normoxia: superoxide dismutase = 4.4 +/- 1.7 units X mg cell protein-1 P less than 0.05). Hypoxic exposure (PO2 approximately 15 mmHg) was associated with a significant decrease in superoxide dismutase compared to normoxic controls (hypoxia: 2.2 +/- 0.6; normoxic: 3.8 +/- 0.6 units X mg protein-1 P less than 0.01). This decrease was found only after 168 hours of in vitro hypoxia. The in vitro maturation of alveolar macrophages cultivated in air was associated with a progressive increase in superoxide dismutase activity per 10(6) cells, although superoxide dismutase activity per unit protein remained constant. Molecular O2 may modify cell superoxide dismutase activity by altering intrinsic enzyme regulation. The increase in superoxide dismutase activity with hyperoxia and the decrease with hypoxia are consistent with but not unequivocally establish an important role for superoxide dismutase in protecting against cellular O2 toxicity.

Animals↗
PubMed1977

Enzymatic basis for bioenergetic differences of alveolar versus peritoneal macrophages and enzyme regulation by molecular O2.

Alveolar macrophages (AM) and peritoneal macrophages (PM) originate from common precursor cells, but function in different O2 environments. In the present studies, the impact of different O2 tensions on cell metabolism has been quantitatively determined, an enzymatic basis for these differences established, and a mechanism which regulates enzymatic differences demonstrated. O2 consumption and lactate production were compared in rabbit AM and PM in air and nitrogen. In air, AM demonstrate significantly greater O2 utilization. In nitrogen, (where glycolysis is the major source of energy provision) lactate production is two- to threefold greater in the PM. A comparison of several enzymes of energy metabolism in AM and PM indicate that one basis for the differences in cell energetics is a difference in activity of key enzymes of both the oxidative phosphorlyative and the glycolytic sequences. Exposure of cultivated AM to hypoxic conditions results in changes in the activity of these enzymes such that the AM closely resembles the PM. A key enzyme in oxidative phosphorylation (cytochrome oxidase) shows decreased activity and reaches values similar to those found in the PM. A key enzyme in glycolysis (pyruvate kinase) shows increased activity to values resembling those found in the PM. These alterations in enzyme pattern occur in isolated cell systems, suggesting that molecular O2 modifies the intrinsic cellular regulation of some enzymes of energy metabolism. Alterations in O2 tension may lead to alterations of the rate of biosynthesis and (or) the rate of biodegradation of key enzymes involved in oxidative phosphorylation and glycolysis. In turn, the alteration of enzyme patterns leads to a more suitable bioenergetic pattern as a function of O2 availability.

Animals↗
PubMed1977

Overdiagnosis and overtreatment of pulmonary embolism: the emperor may have no clothes.

Pulmonary embolism is being overdiagnosed and overtreated, especially in previously normal women using oral contraceptives, with undesirable consequences in heparin treatment. This is in part a consequences of high estimates of its occurrence based on postmortem data and in part of technologic developments in diagnostic methods. Blood gas data are not diagnostically very helpful. Perfusion scans should be used, largely to exclude the diagnosis. Ventilation scans are only occasionally helpful and are expensive. Pulmonary angiography is the most accurate diagnostic means currently available. Further studies are needed to elucidate the prevalence and natural life history of pulmonary embolism in the previously healthy person.

Angiography↗
PubMed1977

Acute cyanide poisoning complicated by lactic acidosis and pulmonary edema.

Massive cyanide poisoning occurred in a 21-year-old man who had ingested 600 mg of potassium cyanide. The clinical course was marked by acute pulmonary edema and lactic acidosis. Because the poison was unidentified until nine hours after ingestion, the patient received only supported treatment which included diuresis, oxygen, bicarbonate, and assisted ventilation. A review of the literature shows that many case reports are poorly documented and do not provide a firm basis for evaluating therapy. To our knowledge, only four patients, including ours, have had blood levels of cyanide measured. In the absence of a suitable history, diagnosis of cyanide poisoning is difficult. A simple chemical test which can be performed on gastric aspirate is available. Hydroxocobalamin may be used as a nontoxic specific antidote. Nonspecific supportive therapy is of great importance.

Acidosis↗
PubMed1976

Intracellular edema and dehydration: effects on energy metabolism in alveolar macrophages.

The effects of intracellular edema and dehydration on energy metabolism in alveolar macrophages were studied. Intracellular edema increased lactate production and reversibly decreased oxygen consumption. Dehydration caused no significant change in lactate production but irreversibly decreased oxygen consumption. These phenomena may be applicable to a wide variety of clinical problems including lung and brain edema.

Animals↗
PubMed1976

Intracellular and subcellular oedema and dehydration.

Changes in intracellular water content appear to be common abnormalities induced by a wide variety of pathogenic mechanisms. Such changes in cell water produce changes in the water in various subcellular organelles bound by semipermeable membranes. Cell and subcell functions then alter in their turn. In isolated alveolar macrophages (rabbit), intracellular and intramitochondrial oedema reduces mitochondrial O2 utilization. Metabolic control is maintained because lactate production reverses (Pasteur effect). On reconstitution, O2 utilization and lactate production return towards normal, indicating reversibility. Cellular and intramitochondrial dehydration also reduces mitochondrial O2 utilization but metabolic control is lost because lactate production also decreases. Osmotic reconstitution does not reverse the abnormality. Exposure to hypotonic media leads to release of lysosomal enzymes (beta-glucuronidase, EC 3.2.1.31) to the extracellular phase of isolated alveolar macrophages. Some of this release is caused by exocytosis although, at low osmotic concentrations, intralysosomal oedema ultimately ruptures lysosomes, with extensive discharge of enzyme. In turn, lysosomal enzymes may injure more normal cells. Impairment of energy metabolism caused by hypoxia leads to intracellular oedema, because Na+ accumulates in the cells when ATP is no longer available for the sodium pump. Continued studies of the disorders in cell physiology caused by changes in cell and subcell water should provide important new insights into a wide variety of disease states (including pulmonary oedema).

Adenosine Triphosphate↗
PubMed1976

Chronic thromboembolic occlusion of main pulmonary artery or primary branches. Case report and review of the literature.

Chronic thromboembolic occlusion of the left pulmonary artery in a 36 year old woman is described, and similar cases reported in the past 15 years are discussed. On review, this disease remains a rare entity. In the majority of cases, the etiology is thrombophlebitis and acute pulmonary embolism. Associated cardiopulmonary disease is uncommon. The most common presenting symptom is unexplained dyspnea, and the majority of patients have past histories of hemoptysis. Acute cardiovascular collapse is distinctly rare. Most physical signs and laboratory tests are normal or nonspecific. The perfusion lung scan, although nonspecific, is the best screening test. Antemortem diagnosis, with rare exception, is established by pulmonary angiography. Eleven patients have been operated on: thromboembolectomy in nine, saphenous vein graft in one and pneumonectomy in one. Operative mortality was 36 per cent (four of 11), definite improvement was seen in 46 per cent (five of 11), and 18 per cent (two of 11) survived the operation with no improvement. The role of medical therapy in this disease is considered.

Adult↗
PubMed1976

Speculations on neurogenic pulmonary edema (NPE).

Evidence suggests the following pathogenesis for neurogenic pulmonary edema. The initial phase results from a centrally mediated, massive, sympathetic discharge. This produces intense, generalized, but transient, vasoconstriction with a resultant shift of blood from the high-resistance systemic circulation to the lowresistance pulmonary circulation. Marked increases in pulmonary vascular pressures and marked increases in pulmonary blood volume then produce pulmonary edema because of the hydrostatic effect of increased pulmonary capillary pressure. In addition, pulmonary hypertension and hypervolemia injure pulmonary blood vessels, altering pulmonary capillary permeability and producing lung hemorrhage. After the transient systemic and pulmonary vascular hypertension subside, the patient is left with abnormal pulmonary capillary permeability, so that pulmonary edema persists in the face of normal hemodynamics and normal cardia function.

Animals↗