Publications by authors named "EK Stabenau"

The present study exposed frogs to the PAH pyrene and measured exercise performance, muscle contractile ability, mitochondrial O(2) consumption, and membrane potential. Leopard frogs, Rana pipiens, were exposed for seven days in control or pyrene saturated water aquaria. Frogs were randomly placed into one of four groups: (i) pyrene-exposed exercised, (ii) control, exercised, (iii) pyrene-exposed, non-exercised, and (iv) control, non-exercised.

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The effects of a 0-12-hour naphthalene exposure on pulmonary CO(2) excretion and bioaccumulation in the leopard frog, Rana pipiens, were investigated. The data showed that naphthalene transport occurred from the aqueous phase into the frog tissue. The first-order rate constant (k in day-1) for the entry of naphthalene from the water into the frog was 0.

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Carbonic anhydrase (CA) catalyzes the interconversion of CO(2) and HCO(3)(-). Intracellular (extravascular) and intravascular (extracellular) CA has been identified and localized in the lungs of reptiles and mammals. Less information is known, however, on the presence of intravascular CA in the lungs of amphibians and avians.

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This study examined whether the snake lung possesses intravascular carbonic anhydrase (CA). Lungs were perfused with control salines and with salines containing CA inhibitors. Perfusion with control salines resulted in a stable CO(2) excretion, whereas CA inhibitors significantly reduced pulmonary CO(2) excretion.

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Turtles possess a significant postcapillary CO2 partial pressure (PCO2) disequilibrium between arterial blood and alveolar gas. There are several possible explanations for this blood disequilibrium including a slow rate of erythrocyte physiological anion shift (Cl-/HCO3- exchange) or inaccessibility of plasma HCO3- to red blood cell or pulmonary carbonic anhydrase. The present study characterized the contribution of erythrocyte anion exchange and pulmonary and erythrocyte carbonic anhydrase to CO2 excretion and, hence, to postcapillary CO2-HCO3--H+ equilibration in blood-perfused turtle (Pseudemys scripta) lungs.

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1. Hypothermia is a documented response to hypoxia but little is known about possible gender differences. Because female rats have a greater hypoxic ventilatory response than males, we hypothesized that females would be more tolerant of hypoxia.

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Direct measurements have found that ectothermic vertebrates possess a significant postcapillary PCO2 disequilibrium between arterial blood and alveolar gas, indicating that the CO2-HCO3(-)-H+ system does not reach equilibrium during pulmonary capillary transit. One plausible explanation for the blood disequilibrium is that turtle lungs lack vascular carbonic anhydrase (CA) to enhance the conversion of blood HCO3- to CO2. The present study characterized the contribution of pulmonary vascular CA to CO2 excretion and postcapillary CO2-HCO3(-)-H+ equilibration in the turtle.

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Objective: To examine the physiologic effects of inhalation anesthesia in aquatic turtles to improve anesthetic techniques and postanesthetic monitoring.

Design: Retrospective case series.

Animals: 9 Kemp's ridley sea turtles.

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Alveolar-capillary CO2 equilibration involves diffusive equilibration of CO2 across the blood-gas barrier and chemical equilibration of perfusate CO2-HCO-3-H+ reactions. These processes are governed by different, but related, driving forces and conductances. The present study examined the importance of pulmonary carbonic anhydrase (CA) for diffusive and reactive CO2 equilibration in isolated rat lungs.

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The inhibitor sensitivity of pulmonary vascular carbonic anhydrase (CA) was examined in situ to identify the specific isozyme responsible for vascular activity and to study its distribution in the lung. Vascular CA activity was monitored in isolated rat lungs by measuring the rate of CO2 excretion and the magnitude of postcapillary CO2-HCO(3-)-H+ disequilibria. Lungs were perfused with isotonic salines containing gluconate, sulfate, Cl-, or I-, with or without sulfonamide derivatives.

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Erythrocytes of Kemp's ridley sea turtle (Lepidochelys kempi) contain a 100- to 105-kDa protein that is reactive with a monoclonal antibody to the membrane domain of human erythrocyte band 3. Based on inhibition of membrane HCO(3-)-Cl- exchange with 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS), sea turtle erythrocytes were found to contain 4 x 10(6) copies of band 3 per cell. Unidirectional HCO3- transfer, specifically HCO3- out----in-Cl-in----out exchange, where subscript in----out represents transfer from inside to outside and subscript out----in represents transfer from outside to inside, was characterized by a maximal exchange rate of 1.

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