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G H Gurtner

Publications and source records attributed to G H Gurtner.

54 records · Page 3Linked to original sources
PubMed1977

The Wien effect in compensated metabolic acidosis.

CSF and blood acid-base values were measured in compensated metabolic acidosis, induced in anesthetized dogs by infusion of dilute HCl during hyperventilation. We observed cerebral blood flow-related steady-state differences in PCO2 between CSF and arterial venous blood from the brain. The steady-state values of CSF-blood PCO2 differences and blood H+ activity were intermediate to those observed by us previously during uncompensated acidosis and alkalosis (J. Appl. Physiol. 34: 249-254, 1973). These results are consistent with predictions of the "charged membrane hypothesis" proposed by us to explain CSF and blood acid-base relationship during uncompensated acid-base derangements (J. Appl. Physiol. 34: 243-248, 1973).

Acidosis↗
PubMed1977

Can alveolar pCO2 exceed pulmonary end-capillary CO2? Yes.

In 1891 Christian Bohr observed that alveolar PCO2 could exceed arterial PCO2 when high levels of CO2 were present in the inspired air. He proposed that CO2 could be secreted by the lung. His hypothesis was dismissed as being due to experimental error; however, recently the same phenomenon was rediscovered using modern techniques. A possible explanation for the phenomenon may involve coupling between diffusion and chemical reaction of H+, HCO3-, and CO2 in the vicinity of a negatively charged capillary wall, causing the PCO2 to be higher near the wall that in the bulk phase of capillary blood. Alveolar PCO2 is related to the PCO2 near the wall rather than the bulk phase PCO2. The Charged Membrane Hypotheses can explain the phenomenon of CO2 secretion not by a cellular mechanism, but a physical chemical disequilibrium within the capillary which is maintained by blood flow through the capillary.

Animals↗
PubMed1975

Letter: Wien effect.

Explore the source record for details and available documents.

Acid-Base Equilibrium↗
PubMed1972

Nonequilibrium steady-state differences in partial pressure of CO 2 and in concentration of weak acids and bases between blood and tissue.

Several investigators have demonstrated that under conditions where little or no gas exchange occurs across the alveolar capillary membrane the PCO(2) is higher in the alveolus than in the mixed venous blood, whereas there are no PO(2) differences. Gurtner et al. have explained the DeltaPCO(2) by a model in which H(+) dissociation of proteins due to an electrical field caused by a negatively charged capillary wall (Wien effect) sets up an intracapillary PCO(2) difference between wall and bulk phase which is maintained by blood flow. The model is not specific for CO(2) and predicts that weak acids should be concentrated in a manner similar to CO(2) whereas weak bases should be relatively excluded from the alveolar space. Measurements of the steady-state distribution of the uncharged forms of the weak acids 5,5-dimethyloxyazoladinedione (DMO) and barbital and of the weak base tris(hydroxymethyl)aminomethane (THAM) between mixed venous blood and a fluid-filled lobe of lung were made in living dogs. The results agree fairly well with the predicted values.

Acid-Base Equilibrium↗
PubMedDate not supplied

Post-exposure treatment with isoproterenol attenuates pulmonary edema in phosgene-exposed rabbits.

This study investigated the post-treatment effect of isoproterenol (ISO) on pulmonary parameters in rabbits whole-body-exposed to a lethal dose of the toxic gas phosgene. Phosgene is widely used in industry as a chemical intermediate for the production of plastics, drugs and polyurethane products. The results of this study are from five study groups: 10-min perfused baseline; uninjured controls exposed to air; phosgene-exposed; phosgene-exposed isoproterenol-treated intravascularly and intratracheally (ISO i.v.+i.t.); and phosgene-exposed isoproterenol-treated intratracheally (ISO i.t.). Treatment with ISO was administered as either a continuous intravascular infusion (24 microg min(-1)) from the beginning to end of perfusion (i.v.) and a 24-microg intratracheal bolus (i.t.) or just an i.t. bolus immediately prior to the start of perfusion. Rabbits of 2.5-3 kg were exposed to a cumulative dose of phosgene to attain a concentration x time exposure-effect of 1500 ppm x min. Lungs were isolated in situ and perfused 50-60 min after the start of exposure with Krebs-Henseleit buffer at 40 ml min(-1). Pulmonary artery pressure (Ppa), tracheal pressure (Pt) and lung weight gain (lwg) were continuously measured. Leukotrienes (LT) C4/D4/E4 were measured in the perfusate every 20 min during perfusion. At the immediate conclusion of the experiment, lung tissue was frozen in liquid N2 and analyzed for glutathione (GSH) and cyclic 3',5'-adenosine monophosphate (cAMP). Post-treatment with ISO by either i.v.+i.t. or i.t. routes 50+ min after phosgene exposure significantly lowered Ppa, Pt and lwg. Phosgene-exposed rabbits post-treated with ISO i.t. had significantly higher levels of reduced GSH (3 +/- 0.4 nmol mg(-1) protein), GSH/GSSG ratios (3.3 +/- 0.6 nmol mg(-1) protein) and percentage of total as reduced GSH (75 +/- 2.5%) compared with phosgene-exposed rabbits: 1.9 +/- 0.3, 2 +/- 0.3 and 58 +/- 6.3%, respectively. The ISO (i.v.+i.t.) post-treatment route significantly increased reduced GSH (6.2 +/- 1.7 nmol mg(-1) protein), GSH/GSSG ratio (5.9 +/- 0.8 nmol mg(-1) protein) and percentage of total as reduced GSH (85 +/- 1.7%) when compared to the phosgene-only group. The ISO i.t. and ISO i.v.+i.t. treatments significantly reduced perfusate LTC4/D4/E4 150 min after the start of exposure by 90% and 48%, respectively. These data suggest that protective mechanisms for ISO involve reduced vascular pressure, decreased LTC4/D4/E4-mediated pulmonary capillary permeability and a favorable lung tissue redox state compared with untreated phosgene-exposed rabbits.

Animals↗
PubMedDate not supplied

Postexposure treatment with aminophylline protects against phosgene-induced acute lung injury.

Pretreatment with aminophylline has been shown to protect against various types of acute lung injury. Mechanisms responsible for protection are multifactorial but are thought to involve upregulation of cAMP. While previous studies focused on pretreatment, the present investigation examined post-treatment in rabbits following exposure to a lethal dose of the oxidant gas phosgene. Rabbits, 2-3 kg, were exposed to a cumulative dose of phosgene to attain a c x t exposure effect of 1500 ppm.min. Lungs were isolated in situ and perfused for 90-100 min after exposure with Krebs-Henseleit buffer at 40 mL/min. Pulmonary artery pressure (Ppa), tracheal pressure (Pt), and lung weight gain (lwg) were measured continuously. Leukotrienes C4/D4/E4 were measured in the perfusate every 20 min during perfusion. At the immediate conclusion of the experiment, lung tissue was frozen in liquid N2 and analyzed for reduced GSH, GSSG, cAMP, and lipid peroxidation (TBARS). Post-treatment with aminophylline 80-90 min after exposure significantly lowered Ppa, Pt, and lwg. Aminophylline significantly reduced TBARS and perfusate LTC4/D4/E4, and prevented phosgene-induced decreases in lung tissue cAMP. These data suggest that protective mechanisms observed with aminophylline involve decreased LTC4/D4/E4-mediated pulmonary capillary permeability and attenuated lipid peroxidation. Direct antipermeability effects of cAMP on cellular contraction may also be important in protection against phosgene-induced lung injury.

Administration, Inhalation↗
PubMedDate not supplied

Interaction of carbon monoxide and cyanide on cerebral circulation and metabolism.

Significant elevations of carboxyhemoglobin and blood cyanide have been found in fire victims. The nature of the interaction of acute exposures to these agents is unclear. This study was undertaken to describe the of cyanide and carbon monoxide--alone and in combination--on the circulation and metabolism of the brain in anesthetized dogs. Cerebral blood flow increased to 130 and 200% of control with elevations in carboxyhemoglobin to 30 and 51% or with elevations in blood cyanide to 1.0 and 1.5 microgram/ml, respectively. Cerebral oxygen consumption remained unchanged until the higher level of carbon monoxide or cyanide was reached. When carbon monoxide and cyanide were administered simultaneously, cerebral blood flow increased in an additive manner, but significant decreases in cerebral oxygen consumption occurred at the combination of the lower concentrations. These data suggest that carbon monoxide and cyanide are physiologically additive on producing changes in cerebral blood flow, but may act synergistically on cerebral metabolism.

Animals↗