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Biomedical subjects

E D Haak

Publications and source records attributed to E D Haak.

7 recordsLinked to original sources
PubMed1983

Effects of 0.1 ppm nitrogen dioxide on airways of normal and asthmatic subjects.

It has been reported (J. Clin. Invest. 57: 301-307, 1976) that inhalation of nitrogen dioxide (NO2) will enhance the bronchial reactivity of asthmatics. This study was designed to evaluate the respiratory effect of a 1-h exposure of normal subjects and of atopic asthmatics to 0.1 parts per million (ppm) NO2. Fifteen normal and 15 asthmatic subjects were exposed to air and to NO2 in a randomized double-blind crossover design. Exposure to either atmosphere was bracketed by bronchial inhalation challenge using aerosolized metacholine chloride solutions. Plethysmographic measurements of specific airway resistance (sRaw) and the forced random noise impedance spectrum (5-30 Hz) were obtained immediately after each methacholine dose. Following acute exposure to NO2, there was a slight but not significant increase in mean base-line sRaw in both normals and asthmatics. The overall base-line resistive properties of the respiratory system determined by forced random noise excitation were not significantly affected by NO2 inhalation either. Finally, there was no change in bronchial response to methacholine challenge in either group. These findings indicate that 0.1 ppm NO2 exposure for 1 h without exercise had no demonstrable airways effects in either young atopic asthmatics with mild disease or young normal subjects.

Adolescent↗
PubMed1983

Pulmonary effects of ozone exposure during exercise: dose-response characteristics.

Because minimal data are available regarding the pulmonary effects of ozone (O3) at levels less than 0.27 ppm, six groups of healthy young males were exposed for 2.5 h to one of the following O3 concentrations: 0.0, 0.12, 0.18, 0.24, 0.30, or 0.40 ppm. Fifteen-minute periods of rest and exercise (65 l/min minute ventilation) were alternated during the first 2 h of exposure. Coughing was observed at all levels of O3 exposure. Small changes in forced-expiratory spirometric variables [forced vital capacity (FVC), forced expiratory volume in 1 s, and mean expiratory flow rate between 25 and 75% FVC] were observed at 0.12 and 0.18 ppm O3, and larger changes were found at O3 levels greater than or equal to 0.24 ppm. Changes in tidal volume and respiratory frequency during exercise, specific airway resistance, the presence of pain on deep inspiration, and shortness of breath occurred at O3 levels greater than or equal to 0.24 ppm. In conclusion, pulmonary effects of O3 were observed at levels much lower than that for which these effects have been previously described. Stimulation of airway receptors is probably the mechanism responsible for the majority of observed changes; however, the existence of a second mechanism of action is postulated.

Adolescent↗
PubMed1981

Correlation of airway resistance with forced random noise resistance parameters.

The correlation between airway resistance (Raw) measured in a plethysmograph and three respiratory resistance parameters measured by forced random noise was evaluated. Forced random noise resistance parameters were the average resistance between 5 and 9 hz (R5-9), the average resistance between 20 and 24 Hz (R20-24), and the extrapolated resistance at 1 Hz (R1). We studied 22 healthy, nonsmoking subjects, 10 of whom had a history suggesting childhood asthma. Serial measurements were made after inhalation of aerosols containing increasing concentrations of methacholine of aerosols containing increasing concentrations of methacholine to obtain data in various stages of bronchoconstriction. There was a broad range of responsiveness to methacholine; the ratio of the peak to base-line values of Raw ranged from 1.1 to 6.3. R1, R5-9, and R20-24 were related to Raw by linear regression analysis. R1 and R5-9 showed excellent correlation with Raw (r = 093 and 4=0.91, respectively); R20-24 showed much poorer correlation (r = 0.62). The slopes of the regression equations for R1 and R5-9 were 1.56 and 0.51, respectively; thus neither provided an exact measure of Raw. The data appear to be consistent with a model in which most of the methacholine-induced increase in resistance occurred in the peripheral airways and only a small fraction in the central airway.

Adolescent↗
PubMed1980

A comprehensive cardiac exercise stress processor for environmental health effects studies.

We have shown that an interactive microcomputer system using noninvasive cardiovascular measurements during exercise is both possible and practical. Experimental use of the system has verified our choice of variables as appropriate for automatic generation of a cardiovascular data base, but additional studies are required to determine the system's sensitivity for assessing health-effect decrements.

Air Pollutants↗
PubMed1979

An analogue echogram range gate tracker for clinical echocardiography.

The fundamental purpose of this paper is to present the results of a feasibility study for an on-line, real-time automatic range gate tracker (ARGT) for clinical echocardiography, specifically for the purpose of determining cardiac output noninvasively and in real time. The basic ARGT design represents an implementation of specific algorithms and a system controller that permit user interaction and interpretation of clinical echocardiograms. In its analytical mode, the ARGT automatically tracks cardiac echoes as visually perceived and selected by the user. While tracking specific cardiac echoes, the ARGT converts the complex ultrasonic echogram into a pair of meaningful analogue signals (corresponding to the motion of the anterior and posterior left ventricular walls) from which dimensional information corresponding to dynamic geometric changes of the heart are derived. From the information, the cardiac output is computed in real time.

Cardiac Output↗
PubMedDate not supplied

Augmentation of myocardial ischemia by low level carbon monoxide exposure in dogs.

This study was conducted to determine whether low level exposure to carbon monoxide would increase myocardial ischemia associated with acute myocardial infarction. An hour after coronary artery ligation, eleven anesthetized dogs underwent five sequential respiratory exposures to 5,000 ppm carbon monoxide, producing mean blood carboxyhemoglobin levels of 4.9% to 17.0%. Ischemia, as indicated by the amount of S-T segment elevation in epicardial electrocardiograms, increased significantly at the lowest carboxyhemoglobin level and increased further with increasing carbon monoxide exposure. These changes occurred in the absence of altered heart rate, blood pressure, left atrial pressure, cardiac output, or blood flow to ischemic myocardium. Flow to non-ischemic myocardium increased with carbon monoxide exposure, the percentage increase being approximately double the increase in carboxyhemoglobin level. Thus, low level exposure to carbon monoxide can significantly augment ischemia in acute myocardial infarction, apparently through a reduction in oxygen supplied to ischemic tissue. The data suggest that hypoxia induced by carbon monoxide exposure is more severe than can be accounted for by a simple reduction in oxygenated hemoglobin.

Animals↗