Biomedical subjects

D S Ward

Publications and source records attributed to D S Ward.

At least 73 records · Page 4Linked to original sources

PubMed1989

Recursive identification of lung parameters.

Determination of lung capacity (FRC) using insoluble gas washout or equilibrium methods is a common procedure in respiratory tests. The lung model can be extended to include multiple compartments with differing volumes and ventilation fractions. A discrete-time mathematical model of a multi-compartment lung was developed based on mass conservation laws of the gas exchange. To estimate the unknown parameters in the model from experimental data, a recursive prediction error algorithm was implemented. The design of the algorithm provides the capability to track time-varying parameters, such that the system can be monitored on-line. Determination of the model order may be as important as estimation of the parameters, especially in biological systems where little may be known about the structure. Two new criteria to distinguish between models of varying complexity, the 'minimum description length principle' and the 'accumulated prediction error', are illustrated. Theoretical studies show that these criteria yield consistent order estimates of the process. Simulations and experimental data confirm the feasibility of this approach for the estimation of lung parameters.

Algorithms↗

PubMed1989

A study of factors associated with weight change in women who attempt smoking cessation.

This study investigated behavioral and attitudinal relationships over a 12-week time period in 48 women enrolled in a commercial smoking cessation program who were categorized as non-recidivists (NR), early recidivists (ER) and late recidivists (LR) to cigarette smoking. NR had significantly higher weight gains (F = 6.70), significantly higher levels of physical activity (F = 6.42), and significantly less concern of postsmoking cessation weight gain (F = 5.08) than either two groups of recidivists, (p less than or equal to .05). Other findings, although not significant, were that NR exhibited lower caloric intake and more frequent snacking behaviors than either ER or LR. These results indicate an overall stronger commitment to more positive health behaviors in the NR than those who returned to cigarette smoking.

Adult↗

PubMed1989

An extended soluble gas exchange model for estimating pulmonary perfusion--I: Derivation and implementation.

A dynamic model for respiratory exchange of blood soluble gas is described. This model includes a general treatment of tidal breathing, an inhomogeneous lung comprising multiple distensible compartments, and nonlinearities due to multiple-gas effects. The motivation for this new model is the continuing interest in estimating pulmonary perfusion from measurements of respiratory soluble gas exchange. Numerical simulation can be employed to investigate the errors that result from simplifications made in the derivations of simpler models used for this purpose. Examples of such simplifications are the assumptions that ventilation is constant and unidirectional, and that multiple soluble gases can be independently modeled. These results can delimit the boundaries within which perfusion estimates can be considered reliable. An example demonstrating the model and its numerical solution is presented.

Models, Biological↗

PubMed1989

An extended soluble gas exchange model for estimating pulmonary perfusion--II: Simulation results.

The assumptions made in deriving models of soluble gas exchange used for continuous estimation of pulmonary perfusion are critically examined. Comparisons are made between estimation algorithms based on simple and more complex models. The more complex model includes a general treatment of tidal breathing, an inhomogeneous lung comprising multiple distensible compartments, and nonlinearities due to multiple-gas effects. The results show that sensitivity of perfusion estimates to errors inherent in simple linear models. These errors can invalidate the estimates under realistic physiological conditions. Concentration and multiple-gas effects, for example, can cause substantial estimation errors. Large ventilations relative to lung volume can also lead to errors. These simulations can be used to delimit the conditions under which the estimates can be considered reliable. A further set of simulations is used to assess the sensitivity of perfusion estimates to errors in the assumed values of unknown or approximately known model parameters. Inadequate specification of the compartmental structure of the lung (distributions of ventilation/perfusion and ventilation/volume) can cause large estimate errors. Precise estimates of lung tissue volume do not appear to be necessary. These results are important for the practical application of soluble gas methods for pulmonary perfusion determination. In both sets of simulations, it is shown that parameter estimate accuracy must be confirmed independently of goodness-of-fit criteria. Close agreement between predicted and observed end-tidal concentrations does not ensure accurate perfusion estimates.

Computer Simulation↗

PubMed1989

Dynamics of ventilatory response to step changes in PCO2 of blood perfusing the brain stem.

The technique of artificial brain stem perfusion was used to assess the ventilatory response to step changes in PCO2 of the blood perfusing the brain stem of the cat. A two-channel roller pump and a four-way valve allow switching the gas exchanger into and out of the extracorporeal circuit, which controlled the perfusion to the brain stem. Seven alpha-chloralose-urethan-anesthetized cats were studied, and 25 steps of increasing and 23 steps of decreasing PCO2 were analyzed. A model consisting of a single-exponential function with time delay best described the ventilatory response. The time delays 11.7 +/- 8.1 and 6.4 +/- 6.8 (SD) s (obtained from mean values per cat) for the step into and out of hypercapnia, respectively, were not significantly different (P = 0.10) and were of the order of the transit time of the tubing from valve to brain stem. The steady-state CO2 sensitivities obtained from the on- and off-responses were also not significantly different (P = 0.10). The time constants 87 +/- 25 and 150 +/- 51 s, respectively, were significantly different (P = 0.0002). We conclude that the central chemoreflex is adequately modeled by a single component with a different time constant for on- and off-responses.

Animals↗

PubMed1989

Ventilatory and cardiovascular responses to sufentanil infusion in dogs anesthetized with isoflurane.

The ventilatory and hemodynamic responses to hypoxia, hyperoxia, and hypercapnia before and during sufentanil infusion were studied in 16 chronically tracheostomized dogs anesthetized with two concentrations, 1 and 0.5 minimal alveolar concentration (MAC) of isoflurane. Sufentanil was infused at a rate to obtain a constant end-tidal carbon dioxide (PETCO2) of approximately 50 mm Hg for each isoflurane level. Before the sufentanil infusion, the PETCO2 was increased to 50 mm Hg by adding CO2 to the inspired gas, to allow comparisons at isocapnic conditions. Sufentanil caused only minor hemodynamic changes but significantly reduced ventilation during both levels of isoflurane. The ventilatory response to hypercapnia decreased substantially, but there were no significant alterations in the ventilatory response to hypoxia. After sufentanil infusion, hyperoxia caused a larger decrease in minute ventilation and caused apnea in four dogs. These results suggest that administering sufentanil during isoflurane anesthesia causes a reduction in the contribution of the central chemoreflexes to ventilatory drive and, consequently, a relative increase in the contribution from the peripheral chemoreflexes.

Adjuvants, Anesthesia↗

PubMed1989

The effects of medetomidine, an alpha 2-adrenergic agonist, on ventilatory drive in the dog.

alpha 2-Adrenergic agonists have been used as potent adjuncts to anesthesia and have anesthetic properties themselves. For this reason, we studied the effects of medetomidine, and isoflurane (1 MAC) on ventilatory drive in dogs. Six chronically tracheotomized mongrel dogs were studied during spontaneous ventilation. Arterial blood samples were analyzed for pH, PaCO2, and PaO2. Airway O2, CO2, N2, and isoflurane were continuously monitored using a mass spectrometer; respiratory rate was determined. The hypercapnic ventilatory response was assessed using the Read rebreathing technique. Control measurements were made under isoflurane anesthesia. Fifteen minutes after the medetomidine (20 ug/kg) was given and the isoflurane discontinued, all measurements were repeated. Isoflurane levels were 1.38 volume % during the isoflurane test period and had declined to 0.3 volume % by the time the medetomidine measurements were obtained. The slope of the CO2 response curve was significantly steeper after medetomidine (0.582 vs 0.269 1.min-1.mmHg), suggesting less respiratory depression when compared to the measurements under isoflurane. PaCO2 and endtidal CO2 were significantly lower in the medetomidine group. No other significant differences were found. Under these conditions, medetomidine (20 ug/kg) resulted in normal blood gas values with less depression of the hypercapnic response curve than under isoflurane anesthesia.

Adrenergic alpha-Agonists↗

PubMed1988

Dynamic response of peripheral chemoreflex loop to changes in end-tidal CO2.

The dynamic ventilatory response of the peripheral chemoreflex loop after isoxic step changes in end-tidal PCO2 (PETCO2) (range 5-30 Torr) was studied in 12 alpha-chloralose-urethan-anesthetized cats. The technique of artificial brain stem perfusion allowed the response to be observed in isolation from the central chemoreflex loop. The data were fitted by an exponential with time delay. During normoxia the mean time constant and time delay (with SD) were 8.6 +/- 7.3 and 3.3 +/- 0.9 s, respectively (9 cats, 56 runs). During hypoxia [arterial PO2 (PaO2) approximately 60 Torr] these values were 6.0 +/- 4.5 and 2.9 +/- 0.9 s (6 cats, 38 runs). In 17 of the 94 runs an augmented breath occurred in the first three breaths after the stepwise increase in PETCO2. For these augmented breaths, tidal volume, inspiratory time, and expiratory time were not different from the next augmented breath occurring in the same run in the steady state. Neither a rate-sensitive component nor a central neural mechanism (central afterdischarge), with the property of maintaining an increased but slowly declining respiratory activity for some minutes after cessation of the PETCO2 challenge, was found. We conclude that the description of the ventilatory response of the peripheral chemoreflex loop to step changes in PETCO2 with a single exponential and time delay is adequate.

Animals↗

PubMed1988

The effects of sufentanil on the hemodynamic and respiratory response to exercise.

The effects of the potent opioid, sufentanil, were studied in 11 athletes. Sufentanil was administered intravenously (up to 0.5 microgram.kg-1 over 10 min) to the subjects while they ran at 14 km.hr-1 on a level treadmill. Prior to, and after, the drug infusion, the treadmill was inclined by 6% for 4 min and CO2 was inhaled for 4 min. Two groups were studied: group 1 (six subjects) breathed room air and group 2 (five subjects) breathed O2 enriched air. During level running the ventilation (liters.min-1) of the group 1 subjects was reduced (65.3 +/- 8.6 to 55.9 +/- 4.9, P = 0.09, mean +/- standard error) and PaCO2 (mm Hg) increased from 37.6 +/- 0.7 to 44.0 +/- 0.5 (P less than 0.05). PaO2 (mm Hg) was substantially reduced from 92.0 +/- 2.0 to 70.0 +/- 2.0 (P less than 0.05). In group 2, where hypoxia did not occur, ventilation was reduced from 62.5 +/- 1.5 to 47.6 +/- 1.0 (P less than 0.05). The ventilatory response to the CO2 was shifted to the right but the slope was unchanged by sufentanil. The 6% grade did not cause any significant change in the PaCO2 in either group 1 (0.1 +/- 0.4 prior and 0.8 +/- 0.5 mm Hg increase after sufentanil) or group 2 (1.0 +/- 1.5 prior and 0.4 +/- 0.9 mm Hg increase after sufentanil). The heart rate response was unaffected by sufentanil but the blood pressure increase in response to the 6% grade was blocked with the drug.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1987

Cardiorespiratory and metabolic effects of dopamine and dobutamine infusions in dogs.

The effects of iv dobutamine and dopamine infusions were studied at six incremental doses (range 5 to 160 micrograms/kg.min) in two groups of five dogs. Dobutamine decreased the systemic vascular resistance (SVR), without significant changes in mean arterial pressure (MAP), or pulmonary vascular resistance (PVR). Dopamine increased MAP, SVR, and PVR, except for a decrease at 10 micrograms/kg.min. Both drugs produced dose-related increases in cardiac output and venous admixture; however, with dopamine the dose-response curve reached a plateau at doses greater than 40 micrograms/kg.min. While the oxygen consumption (VO2) increased progressively in both groups, the oxygen availability ratio (DO2/VO2) and arteriovenous oxygen content difference (CaO2 - CvO2) were maintained mainly by increased cardiac output in the dobutamine group and hemoglobin concentration in the dopamine group. Thirty minutes after termination of drug infusions, the DO2/VO2 dropped, and CaO2 - CvO2 increased significantly in both groups. These changes were mainly due to sustained high VO2; however, in the dopamine group, a larger imbalance resulted from further decreases in cardiac output to levels below the control value.

Animals↗

PubMed1987

Equine endotoxemia: cardiovascular, eicosanoid, hematologic, blood chemical, and plasma enzyme alterations.

Ponies with electromagnetic blood flow transducers implanted around the main pulmonary and left main coronary arteries, were used to evaluate effects of chronic sublethal endotoxin on cardiac output (CO), stroke volume, and left coronary blood flow (LCBF). Plasma thromboxane (TX), as indicated by TXB2, prostacyclin as indicated by 6-keto-prostaglandin (PG) F1 alpha, and hematologic and blood chemical values also were evaluated. Over 24 hours, 2 groups of ponies were given progressively increasing IV and intraperitoneal doses of Escherichia coli lipopolysaccharide (LPS) at 0, 6, 12, and 18 hours. Group 1 was not treated and group 2 was treated with flunixin meglumine, before each LPS insult. Initial LPS inoculation in group 1 led to 10-fold increases in TXB2 and 6-keto-PGF1 alpha values by 30 and 90 minutes, respectively. These eicosanoid values returned to base line by 6 hours after each insult. Although repeated LPS injections stimulated recurring high plasma concentrations of 6-keto-PGF1 alpha, TXB2 production became less with each successive LPS insult. Cardiac output decreased to 55% to 60% of base-line values in association with increased 6-keto-PGF1 alpha values. Left coronary blood flow could not be evaluated accurately. Severe lactic acidosis developed in group 1. Group-2 ponies remained clinically normal, indicating protection of cardiovascular function and peripheral perfusion with flunixin meglumine. Seemingly, flunixin meglumine helped to maintain acceptable cardiovascular function and tissue perfusion during endotoxemia. Flunixin meglumine given to healthy ponies had no effect on cardiovascular function.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗

PubMed1987

Effect of dopamine on hypoxic-hypercapnic interaction in humans.

To investigate the effect of intravenous dopamine on the chemical regulation of ventilation, we studied the ventilatory responses to hypercapnic hypoxia during dopamine infusion. Intravenous dopamine (3 micrograms X kg-1 X min-1) was administered to six healthy human subjects. Two hypoxic challenges (PETO2 = 52.5 +/- 2.5 mm Hg, SaO2 = 88.8 +/- 2.2%; mean +/- SD) were administered at three CO2 levels (PETCO2 = 40.8 +/- 0.5, 45.6 +/- 0.2, 49.8 +/- 0.3 mm Hg) to each subject. The ventilatory responses were quantified by calculation of slopes and intercepts of the relationship between minute exhaled ventilation (VE) and arterial hemoglobin saturation (SaO2), and by the relationship between this slope (delta VE/delta SaO2) and carbon dioxide tension. Dopamine caused a 77% reduction in delta VE/delta SaO2 (hypoxic sensitivity) during eucapnia, a 39.5% reduction in hypoxic sensitivity at PETCO2 = 46 mm Hg, and 38% reduction at PETCO2 = 50 mm Hg (P less than 0.05). Dopamine also reduced normoxic ventilation at all carbon dioxide levels. There was a greater depression in VE during hypercapnia (25.7% reduction) than during eucapnia (12% reduction). This indicates that dopamine depresses the normoxic ventilatory response to carbon dioxide. Intravenous dopamine reduces the ventilatory response to both hypoxia and hypercapnia but preserves the augmentation of hypoxic ventilatory drive by hypercapnia.

Dopamine↗

PubMed1987

In vitro calibration and surgical implantation of electromagnetic blood flow transducers for measurement of left coronary blood flow and cardiac output in the pony.

Electromagnetic flow transducers were implanted via left thoracotomy in 8 ponies (122.7 to 263.6 kg) around the main pulmonary and left main coronary arteries for continuous measurement of mean and pulsatile blood flow. Flow transducers were calibrated in vitro with a gravity flow system. The mean +/- SE pulmonary flow was 73.1 +/- 5.1 ml/kg of body weight/min. Left coronary flow was 0.95 +/- 0.07 ml/kg/min (1.3% of cardiac output) and was not believed to be an accurate measurement. This was caused by the inability to implant a zero-flow occluder, requiring the use of minimum flow during systole as zero-flow base line. However, relative changes in left coronary flow were measured. Ponies were maintained up to 5 weeks with no adverse effects. Measurement of mean pulmonary flow with chronically implanted electromagnetic flow transducers provided an accurate continuous measurement of cardiac output with a minimum of restraint.

Animals↗

PubMed1986

Effect of exogenous dopamine on the hypercapnic ventilatory response in cats during normoxia.

The effects of exogenous dopamine on the normoxic hypercapnic ventilatory response were assessed in nine chloralose-urethane anesthetized cats using the technique of dynamic end-tidal forcing. The ventilatory responses to step changes in end-tidal PCO2 (PETCO2) were measured before (control), during and after intravenous infusion of dopamine (420 micrograms X kg-1 X h-1). Each response was separated into a slow central and a fast peripheral chemoreflex loop by fitting two exponential functions to the measured ventilation. Both loops were described by a CO2 sensitivity, time constant, time delay and a single off-set B (extrapolated PETCO2 of the steady-state response curve at zero ventilation). Dopamine infusion only caused a significant increase of B (mean 0.3 kPa, P less than 0.0001) compared to control; the other model parameters were not significantly affected. After dopamine infusion B returned to significantly lower values (mean 0.2 kPa, P = 0.006) than in control. In two additional cats the dopamine administered to the blood which was artificially perfusing the brainstem, did not affect ventilation. We conclude that in normoxic cats the effect of exogenous dopamine on the ventilatory response to CO2 is due to a CO2 independent inhibition of the ventilatory drive which originates outside the brainstem.

Animals↗

PubMed1986

Effect of dopamine on transient ventilatory response to exercise.

The effect of exogenous dopamine on the development of exercise hyperpnea was studied. Using a bicycle ergometer, five subjects performed repetitive square-wave work-load testing from unloaded pedaling to 80% of each subject's estimated anaerobic threshold. The breath-by-breath ventilation (VE), CO2 production (VCO2), and O2 consumption (VO2) responses were analyzed by curve fitting a first-order exponential model. Comparisons were made between control experiments and experiments with a 3-micrograms X kg-1 X min-1 intravenous infusion of dopamine. Steady-state VE, VCO2 and VO2 were unchanged by the dopamine infusion, both during unloaded pedaling and at the heavier work load. The time constants for the increase in VE (tau VE) and VCO2 (tau CO2) were significantly (P less than 0.05) slowed (tau VE = 56.5 +/- 16.4 s for control, and tau VE = 76.4 +/- 26.6 s for dopamine; tau CO2 = 51.5 +/- 10.6 s for control, and tau CO2 = 64.8 +/- 17.4 s for dopamine) (mean +/- SD), but the time constant for VO2 (tau O2) was not significantly affected (tau O2 = 27.5 +/- 11.7 s for control, and tau O2 = 31.0 +/- 10.1 s for dopamine). We conclude that ablation of carotid body chemosensitivity with dopamine slows the transient ventilatory response to exercise while leaving the steady-state response unaffected.

Anaerobiosis↗

PubMed1986

Role of the physician and physical education teacher in the treatment of obesity at school.

Obesity ranks as a leading chronic pediatric disorder, with estimates ranging from 10 to 25% of the childhood and adolescent population. Physical hypoactivity is prevalent among obese youth and may be an etiological factor. Physical training, with or without nutritional intervention, has been found effective for weight and body fat control. The purpose of this paper is to examine the role that the physician and physical education teacher can play in the treatment of obesity at school. Studies of school-based intervention programs utilizing exercise, nutrition and behavior modification are reviewed. Suggestions are outlined for school-based obesity programs.

Adolescent↗

PubMed1985

Ruptured urinary bladder in a heifer.

A yearling Holstein heifer was admitted with abdominal pain and bilateral, ventral abdominal distention. Bladder rupture was diagnosed by abdominocentesis and endoscopy. Correction of metabolic derangements was accomplished by volume diuresis, with maintenance of a urethral catheter before surgical repair of the bladder. The cause of the bladder rupture was believed to be related to adhesions resulting from previous surgery for urachal abscessation. Bladder rupture, which usually occurs in bulls or steers secondary to urolithiasis or in cows after dystocia, also should be considered in prepartum heifers with dehydration, abdominal pain, and abdominal distention.

Animals↗

PubMed1985

Comparison of chemoreflex gains obtained with two different methods in cats.

This study investigates the correspondence between results of the ventilatory response to CO2 obtained using the technique of dynamic end-tidal CO2 forcing (DEF) and results obtained using the technique of artificial brain stem perfusion (ABP). The DEF technique separates the dynamic ventilatory response into a slow and fast component with gains g1 and g2 as well as the extrapolated CO2 tension at zero ventilation (Bk). The ABP technique results in steady-state central (Sc) and peripheral (Sp) chemoreflex gains and extrapolated CO2 tension at zero ventilation (B). Experiments were performed on 14 alpha-chloralose-urethan anesthetized cats. A wide range of relative peripheral chemosensitivities was obtained by subjecting eight cats to normoxic and three cats to hypoxic CO2 challenges and three cats to both conditions. Statistical analysis of the experimental data showed that the vectors (g1, g2, Bk) and (Sc, Sp, B) for each cat did not differ significantly (P = 0.56). This was also the case for the vectors [g2/(g1 + g2), Bk] and [Sp/(Sc + Sp), B] (P = 0.21). We conclude that in the DEF experiments the slow ventilatory response to isoxic changes in end-tidal CO2 can be equated with the central chemoreflex loop and the faster ventilatory response to the peripheral chemoreflex loop. The agreement between the two techniques is good.

Animals↗