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Biomedical subjects

R Dueck

Publications and source records attributed to R Dueck.

24 records · Page 2Linked to original sources
PubMed1980

Is childhood schizophrenia a cholinergic disease? I. Muscle morphology.

Four hypotonic boys (aged 4 years and 11 months, 6 years and 9 months, 7 years and 4 months, and 8 years and 10 months, respectively), all of whom demonstrated a formal thought disorder, had been psychotic for more than six months, and met the DSM-III criteria for chronic undifferentiated schizophrenia, were studied with respect to skeletal muscle morphology. A significant difference between the mean fiber diameters of type I and type II muscle fibers was observed in the three boys with the most severe thought disorder, type II muscle fibers being consistently smaller. No significant difference in the mean fiber diameter between the two fiber types were seen in the fourth boy, who was also the only one who demonstrated any secondary thought process. The boys differed in their activity levels, but there was no correlation between type II muscle fiber atrophy and hypoactivity. It is hypothesized that a depressed cholinergic system is implicated in the pathogenesis of both the muscle fiber atrophy and the formal thought disorder.

Adenosine Triphosphatases↗
PubMed1978

Chromatographic analysis of multiple tracer inert gases in the presence of anesthetic gases.

A gas chromatographic method for simultaneous analysis of multiple tracer inert gases in blood and expired gas samples is described. The method enables determination of the distribution of ventilation-perfusion ratios in the lungs during anesthesia with nitrous oxide and halothane. In addition, simultaneous analysis of anesthetic gas concentration in blood permits calculation of the amount of uptake or elimination of anesthetic gases from the Fick principle.

Anesthesia, Inhalation↗
PubMed1977

Effects of positive end-expiratory pressure on gas exchange in dogs with normal and edematous lungs.

The effects of positive end-expiratory pressure (PEEP) at 5, 10, 15, and 20 cm H2O on the distribution of ventilation-perfusion (VA/Q) ratios was determined in four normal dogs and in ten with oleic acid-induced acute hemorrhagic pulmonary edema. Tidal volume and frequency were held constant at all times with mechanical ventilation during intravenous pentobarbital and gallamine anesthesia. Normal dogs had little or no shunt, and no areas of low (less than 0.1) or high VA/Q (greater than 10.0) at zero end-expiratory pressure (intermittent positive-pressure breathing). In these animals increasing PEEP caused progressive depression of cardiac output, associated with an increase in ventilation to both high VA/Q and unperfused regions. PEEP greater than or equal to 10 cm H2O resulted in a reduction in Pao2 and an increase in PaCO2. In dogs with pulmonary edema, PEEP's of 5 and 10 cm H2O resulted in dramatic reductions in shunt, virtual obliteration of low VA/Q regions, and market improvement in Pao2. However, at 15 and 20 cm H2O PEEP's high VA/Q and dead space ventilation with CO2 retention again developed in all but the most severely affected (shunt greater than 40%) dogs.

Acute Disease↗
PubMed1977

Ventilation-perfusion inequality in chronic obstructive pulmonary disease.

A multiple inert gas elimination method was used to study the mechanism of impaired gas exchange in 23 patients with advanced chronic obstructive pulmonary disease (COPD). Three patterns of ventilation-perfusion (Va/Q) inequality were found: (a) A pattern with considerable regions of high (greater than 3) VA/Q, none of low (less than 0.1) VA/Q, and essentially no shunt. Almost all patients with type A COPD showed this pattern, and it was also seen in some patients with type B. (b) A pattern with large amounts of low but almost none of high VA/Q, and essentially no shunt. This pattern was found in 4 of 12 type B patients and 1 of type A. (c) A pattern with both low and high VA/Q areas was found in the remaining 6 patients. Distributions with high VA/Q areas occurred mostly in patients with greatly increased compliance and may represent loss of blood-glow due to alveolar wall destruction. Similarly, well-defined modes of low VA/Q areas were seen mostly in patients with severe cough and sputum and may be due to reduced ventilation secondary to mechanical airways obstruction or distortion. There was little change in the VA/Q distributions on exercise or on breathing 100% O2. The observed patterns of VA/Q inequality and shunt accounted for all of the hypoxemia at rest and during exercise. There was therefore no evidence for hypoxemia caused by diffusion impairment. Patients with similar arterial blood gases often had dissimilar VA/Q patterns. As a consequence the pattern of VA/Q inequality could not necessarily be inferred from the arterial PO2 and PCO2.

Bronchitis↗