Reduction In Oxygen Requirements Research Articles

Investigation of Reduction in Oxygen Requirements of Biological Phosphorus Removal Systems

The introduction of an anaerobic zone before the aerobic zone of a conventional activated sludge system was previously found to result in less-than-theoretical oxygen use. The difference between actual and theoretical oxygen use was termed Anaerobic Stabilization (AnS). In this study, an improved method was developed for the determination of AnS, and was applied to a lab-scale Anaerobic/Oxic (A/O) system in which nitrification was chemically inhibited. 15-20 percent of the theoretical oxygen requirement was eliminated by AnS. Oxygen, COD, and sulfate were found to be the major species involved in redox reactions in the system, and therefore major components of AnS. Production of hydrogen, methane, or carbon monoxide, and limitations of the COD test were eliminated as possible explanations for AnS. Aeration-induced stripping of reduced volatile species produced in the anaerobic zone was identified as a possible mechanism requiring further investigation.

Review article

Natural surfactant (Surfactant TA, Survanta, CLSE, SF-RI 1, Curosurf and human surfactant obtained from amniotic fluid) therapy for RDS in very premature infants has been evaluated in 17 controlled clinical trials. Uniformly intratracheal surfactant administration caused a decreased intensity of mechanical ventilation during the first hours (reduced inspiratory pressure, reduced oxygen requirements) as an immediate effect of surfactant administration. Metanalysis reveals barotraumatic pulmonary complications mainly, pneumothorax and pulmonary interstitial emphysema to occur less frequently in surfactant-treated infants in virtually all trials; an increased incidence of survival without bronchopulmonary dysplasia following surfactant treatment was observed in 10 controlled clinical trials. The incidence of other complications of prematurity (intracranial hemorrhage, patent ductus arteriosus and necrotizing enterocolitis) was unchanged following natural surfactant treatment. Dosing of natural surfactant is still under investigation, however recent data indicate that the initial dose should not be less than 100 mg/kg b.w. and retreatment should be given to infants with unsatisfactory response (i.e. fraction of inspired oxygen (FiO2) > 40%). Timing of surfactant treatment still remains controversial. Prophylactic treatment shortly following birth has been compared with rescue-treatment, i.e. surfactant administration to infants suffering from manifest RDS in most studies 4-8 h after birth. Conflicting data from 5 controlled trials may be interpreted as follows: prophylactic treatment seems to be favourable for extremely premature infants (GA < or = 26 weeks) and rescue treatment seems to be adequate for infants of 27-30 weeks of gestation. Intratracheal surfactant instillation in very premature infants did not result in an improved lung function for 24 h to 48 h in all patients. Ten--25% of study infants were reported to be "non-responders", i.e. infants without sustained decrease in oxygen requirements (i.e. FiO2 > 40%). Various factors may be operative including congenital bacterial infections (sepsis or pneumonia), lung hypoplasia and cardiac failure. Inactivation of surface properties of natural surfactant caused by a leakage of proteins across the alveolar-capillary membrane was observed in experimental and clinical studies. Current investigations focus on a combination of postnatal steroids and surfactant treatment to improve lung function and outcome in "non-responders". As long as any controlled clinical studies are being published, this approach remains experimental. Up to now, any controlled clinical trials have been performed to assess different modes of artificial ventilation (e.g. high frequency oscillating ventilation versus conventional ventilation) combined with surfactant therapy. Data obtained from premature animals given natural surfactant indicate any advantage with respect to gas exchange and lung histology to result from high frequency ventilation.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of TA-3090, a new calcium channel blocker, on myocardial substrate utilization in ischemic and nonischemic isolated working fatty acid-perfused rat hearts.

Experimental studies have shown that calcium channel blockade has a protective effect on the ischemic myocardium. Although these agents may act by decreasing intracellular Ca2+ accumulation during reperfusion or to reduce oxygen requirements by decreasing myocardial work load, recent evidence suggests that calcium blockers may also favorably alter energy substrate metabolism in ischemic and reperfused myocardium. In this study, TA-3090, a new calcium channel blocker with minimal effect on myocardial work load, was used to study the effect of calcium channel blockade on both myocardial substrate utilization and reperfusion recovery of ischemic hearts. Isolated working rat hearts were perfused at an 11.5 mm Hg preload and an 80 mm Hg afterload with Krebs-Henseleit buffer containing 11 mM glucose, 1.2 mM palmitate, and 500 microunits/ml insulin. In aerobically perfused spontaneously beating hearts, a 0.5 microM dose of TA-3090 had a mild depressant effect on heart rate but no effect on peak systolic pressure development. In paced hearts (250 beats/min), 0.5 microM TA-3090 had no effect on either peak systolic pressure development or contractility. Fatty acid and glucose oxidation was determined by measuring 14CO2 production in hearts perfused with either [14C]palmitate or [14C]glucose, respectively, whereas glycolysis was determined by measuring 3H2O production from [3H]glucose. Under aerobic conditions, fatty acid oxidation was not altered by TA-3090, but a significant decrease in glucose oxidation and glycolytic rates was observed. If hearts were subjected to a 30-minute period of no-flow ischemia, the addition of 0.5 microM TA-3090 to the perfusate before ischemia significantly improved reperfusion recovery of mechanical function. The protective effects of TA-3090 were not observed if TA-3090 was added at the time of reperfusion and were not related to a depression of function before ischemia. TA-3090, added before ischemia, significantly reduced glycogen and ATP depletion during no-flow ischemia and also significantly decreased glycolytic rates in hearts subjected to low-flow ischemia (coronary flow = 0.5 ml/min). Combined, our data suggest that the beneficial effects of calcium channel blockade on the ischemic myocardium are not related solely to a decrease in myocardial work load or metabolic demand before ischemia, but rather may in part be related to a decrease in myocardial energy demand during ischemia itself, resulting in preservation of ATP and a decrease in glycolysis. The decrease in glycolytic rates during ischemia may also result in a reduction of glycolytic product accumulation during ischemia.

Long term transtracheal oxygen delivery through microcatheter in patients with hypoxaemia due to chronic obstructive airways disease.

Transtracheal administration of oxygen is a new technique for long term treatment. Twenty patients with hypoxaemia due to chronic obstructive airways disease were studied while receiving oxygen through a microcatheter inserted percutaneously into the trachea. By bypassing most of the dead space and avoiding oxygen wastage at the face this method of delivery reduced oxygen requirements by roughly half compared with delivery through nasal cannulas, thus reducing costs and facilitating portable treatment. Twelve of these patients continued to use the system for up to 13 months in preference to using nasal cannulas. Two important complications were a staphylococcal infection and a fractured catheter. Transtracheal oxygen reduced breathlessness and helped patients with routine daily activities. Transtracheal administration of oxygen is a practical method of treatment which may have an important role in rehabilitating patients with chronic lung disease.

Oxygen transport, consumption and utilization during barbiturate intoxication.

Factors related to oxygen availability and requirements were measured on 51 occasions in 14 patients intoxicated with short-acting barbiturates. Patients had no clinical signs of circulatory shock. The cardiac index was normal (3.4 +/- 1.1 1/min/m2) but there was a slight decrease of the mean arterial oxygen content (17.2 +/- 3.0 ml/100 ml). Oxygen transport was normal (571 +/- 199 ml/min/m2). However, the arteriovenous oxygen differences were decreased (3.4 +/- 1.0 ml/100 ml). Oxygen consumption was reduced (110 +/- 42 ml/min/m2) and the oxygen extraction ratio (oxygen consumption/oxygen transport) was decreased (0.20 +/- 0.05), thus confirming a decreased oxygen utilization. Arterial concentration of lactate was normal. Accordingly the observed decrease in oxygen consumption was related to a reduction in oxygen requirements during barbiturate intoxication rather than due to an imbalance between availability and metabolic requirements for oxygen.

Pulmonary rehabilitation of the patient with COPD.

The basic aims in managing COPD are to minimize hypoxia and to improve the ventilation-perfusion relationship. A progressive daily walking exercise program together with pulmonary physiotherapy, creative or occupational therapy, and respiratory therapy to improve bronchial hygiene is advocated. The main benefits of this program, in addition to improved emotional and sociologic status, are increased exercise tolerance, reduced dyspnea (work of breathing), and reduced oxygen requirements.

Effects of prindolol on isoproterenol-induced subendocardial ischaemia in dogs with multiple chronic coronary artery occlusion.

Multiple chronic coronary artery occlusions were produced in dogs by implantation of ameroid rings on the circumflex branches of the left and right coronary artery. Sixty-five per cent of the animals survived. Seventy-seven per cent of the remaining animals had no detectable myocardial infarction. Myocardial blood flow distribution was studied 4 weeks after operation using the tracer microsphere technique. During control conditions myocardial blood flow was homogeneously distributed within the left ventricle. In one group of dogs, regional dilatory capacity was tested by intravenous infusion of dipyridamole. Four compartments of myocardial blood flow were found. The collateral dependent subendocardium with 114 ml/min-100 g-1 was the lowest perfusion rate. In another group of dogs myocardial blood flow distribution was examined during isoproterenol infusion and after beta-blockade with prindolol during continuous isoproterenol infusion. During isoproterenol infusion, a nonhomogeneous blood flow pattern was found when the heart rate increased to 200/min together with a slight fall in diastolic perfusion pressure. Under these conditions, the flow to the collateral dependent subendocardium was severely diminished, while the flow to the areas perfused by normal coronary arteries increased, reflecting compensatory vasodilation. After beta-blockade with prindolol 0.1 mg/kg, the myocardial blood flow distribution was also nonhomogeneous but in the opposite direction: the collateral dependent subendocardium was now the best perfused compartment. The flow to the areas perfused by normal coronary arteries decreased due to the reduced oxygen requirements, while the collateral dependent subendocardium remained maximally dilated. This phenomenon was explained as a postischaemic reactive hyperaemic response to the isoproterenol-induced ischaemia in the collateral dependent subendocardium.

Erythropoiesis and Erythropoietin in Hypo- and Hyperthyroidism*

Qualitative and quantitative studies of erythropoiesis in 23 patients with hypothyroidism and 21 patients with hyperthryoidism included routine hematologic evaluation, bone marrow morphology, status of serum iron, B12 and folate red blood cell mass and plasma volume by radioisotope methods, erythrokinetics and radiobioassay of plasma erythropoietin. A majority of patients with the hypothyroid state had significant reduction in red blood cell mas per kg of body weight. The presence of anemia in many of these patients was not evident from hemoglobin and hematocrit values due to concomitant reduction of plasma volume. The erythrokinetic data in hypothyroid patients provided evidence of significant decline of the erythropoietic activity of the bone marrow. Erythroid cells in the marrow were depleted and also showed reduced proliferative activity as indicated by lower 3H-thymidine labeling index. Plasma erythropoietin levels were reduced, often being immeasurable by the polycythemic mouse bioassay technique. These changes in erythropoiesis in the hypothyroid state appear to be a part of physiological adjustment to the reduced oxygen requirement of the tissues due to diminished basal metabolic rate. Similar investigations revealed mild erythrocytosis in a significant proportion of patients with hyperthyroidism. Failure of erythrocytosis to occur in other patients of this group was associated with impaired erythropoiesis due to a deficiency of hemopoietic nutrients such as iron, vitamin B12 and folate. The mean plasma erythropoietin level of these patients was significantly elevated; in 4 patients the levels were in the upper normal range whereas in the rest, the values were above the normal range. The bone marrow showed erythyroid hyperplasia in all patients with hyperthyroidism. The mean 3H-thymidine labeling index of the erythroblasts was also significantly higher than normal in hyperthyroidism; in 8 patients the index was within the normal range whereas in the remaining 13 it was above the normal range. Erythrokinetic studies also provided evidences of increased erythropoietic activity in the bone marrow. It is postulated that thyroid hormones stimulate erythropoiesis, sometimes leading to erythrocytosis provided there is no deficiency of hemopoietic nutrients. Stimulation of erythropoiesis by thryoid hormones appears to be mediated through erythropoietin.

Effect of nitrate infusions on the systemic and coronary circulations following acute experimental myocardial infarction in the intact dog

To determine the systemic and the coronary effects of nitrates in acute myocardial infarction, 3 groups of anesthetized closed chest dogs were studied. In a group of normal dogs an hour-long intravenous infusion of isosorbide dinitrate was administered. In a second group a small infarct of the myocardium was produced by catheter wedging in a small coronary side branch. In the third group occlusion of a branch of the main left coronary artery was produced by a thrombus-forming catheter electrode. Isosorbide dinitrate infusion in normal dogs caused reductions in aortic pressure, left ventricular end-diastolic pressure and cardiac output and work. Coronary resistance was reduced only at 5 minutes of infusion. Systemic effects of isosorbide dinitrate were similar in the 2 groups with infarction. Mild hypotension (average 10 mm Hg) did not provoke ventricular arrhythmias. Unlike the cardiac output in normal dogs, this value tended to rise rather than fall and left ventricular work was unchanged. The dogs with catheter wedging showed a significant increase in coronary collateral flow and a decrease in resistance. Narrowing of the coronary arteriovenous oxygen difference occurred in the dogs with wedging and thrombus formation. In the absence of cardiogenic shock nitrates may be safely administered to dogs with acute experimental myocardial infarction and may result in enhanced collateral coronary flow and reduction in oxygen requirements of the heart.

Pathologic and histochemical observations in experimental hypothermia.

The potential value of hypothermia for surgical procedures necessitating extracorporeal exclusion of the heart, as well as other conditions in which reduced oxygen requirement of tissues would be advantageous, is well recognized. Unfortunately, accounts concerning the application of this procedure in both humans and the experimental animal indicate that it is hazardous and unpredictable, resulting in death in an alarming number of instances. Despite numerous investigations related to physiologic processes during the hypothermic state, little information has been disclosed which might be conclusively interpreted as responsible for such failures. Anatomical investigations, similarly, have failed to reveal alterations which might be directly related to the fatalities encountered. In addition, results of morphologic studies have been largely contradictory. Early investigators were impressed with the lack of overt morphologic change associated with hypothermia. Sano and Smith 1 observed focal pancreatic necrosis in 10% of patients subjected to this procedure in the treatment of