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Biomedical subjects

S A Glantz

Publications and source records attributed to S A Glantz.

At least 19 recordsLinked to original sources
PubMed1992

Philip Morris's failed experiment in Pittsburgh.

The campaign for passage and implementation of Pittsburgh's Smoking Control Ordinance in 1987 illustrates the role controversy plays in tobacco control. Proponents of the ordinance sought at first to keep it noncontroversial, while the tobacco industry tried to defeat the ordinance by generating controversy, claiming that severe economic and social disruption would occur. After the ordinance had been in force for a year, Philip Morris tried to take over its implementation, seeking to redefine the central issue as one of social accommodation rather than health. To succeed, Philip Morris's effort had to be widely accepted and noncontroversial. Proponents of the ordinance countered with controversy to undermine the campaign and expose the company's intentions. The controversy made the established health organizations uncomfortable, causing them to play only a marginal role. Surprisingly, the people who prevailed were the nonsmokers' rights activists, a small group with limited resources.

Health Care Coalitions↗
PubMed1991

The politics of local tobacco control.

Until the nonsmokers' rights movement, tobacco control activity was at the federal or state levels, which is where the tobacco industry dominates. Since the appearance of the nonsmokers' rights movement, progress in tobacco control has occurred primarily at the local level. In response to the success of this movement, the tobacco industry has developed "smokers' rights" groups and other tactics to fight local legislation. Several recent local campaigns in California illustrate these tactics. Tobacco control forces follow many paths, from sitting on the sidelines to making a serious commitment to smoking control legislation. Despite the tobacco industry's superior financial resources, the outcome of proposed local tobacco control legislation appears to depend on how seriously the health advocates mobilize in support of the local legislation. When the health community makes a serious commitment of time and resources, it wins. When it fails to make such a commitment, the tobacco industry prevails, more by default than by its superior financial resources.

California↗
PubMed1991

A new approach to in situ left ventricular volume clamping in dogs.

Major contributing factors modulating left ventricular (LV) diastolic behavior are active relaxation of myocardium and volume change during filling, the interaction of which complicates analysis of diastolic pressure-volume relationship, especially in early diastole. To separate the effect of active relaxation and filling, a method was introduced [E. L. Yellin, M. Hori, C. Yoran, E. H. Sonnenblick, S. Gabbay, R. W. M. Frater, Am. J. Physiol. 250 (Heart Circ. Physiol. 19): H620-H629, 1986] to interrupt mitral inflow and keep LV volume constant throughout diastole. Their preparation requires replacing the mitral valve with an artificial valve using cardiopulmonary bypass, which might cause significant change in cardiac performance or produce detrimental systemic effects. We developed a new volume-clamping method that preserves the native mitral valve and apparatus intact and avoids cardiopulmonary bypass. A modified Bjork-Shiley prosthetic valve (20 mm orifice diam) in a special mounting ring was placed above the native mitral valve through the left atrium and secured from outside the heart. This prosthetic valve was controlled by a cable connected to solenoids outside the dog, triggered by the electrocardiogram or other physiological signal. We compared our method (n = 7) with that of Yellin et al. (n = 2) in nine random source dogs. In our method, no end-diastolic pressure gradient or regurgitant pressure wave was observed, and the prosthetic valve did not disturb movement of the native mitral valve. When the prosthetic valve was forced to a closed position at end systole, LV volume, measured with a conductance catheter, was maintained at or near end-systolic volume throughout diastole.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Passive smoking and heart disease. Epidemiology, physiology, and biochemistry.

The evidence that ETS increases risk of death from heart disease is similar to that which existed in 1986 when the US Surgeon General concluded that ETS caused lung cancer in healthy nonsmokers. There are 10 epidemiological studies, conducted in a variety of locations, that reflect about a 30% increase in risk of death from ischemic heart disease or myocardial infarction among nonsmokers living with smokers. The larger studies also demonstrate a significant dose-response effect, with greater exposure to ETS associated with greater risk of death from heart disease. These epidemiological studies are complemented by a variety of physiological and biochemical data that show that ETS adversely affects platelet function and damages arterial endothelium in a way that increases the risk of heart disease. Moreover, ETS, in realistic exposures, also exerts significant adverse effects on exercise capability of both healthy people and those with heart disease by reducing the body's ability to deliver and utilize oxygen. In animal experiments, ETS also depresses cellular respiration at the level of mitochondria. The polycyclic aromatic hydrocarbons in ETS also accelerate, and may initiate, the development of atherosclerotic plaque. Of note, the cardiovascular effects of ETS appear to be different in nonsmokers and smokers. Nonsmokers appear to be more sensitive to ETS than do smokers, perhaps because some of the affected physiological systems are sensitive to low doses of the compounds in ETS, then saturate, and also perhaps because of physiological adaptions smokers undergo as a result of long-term exposure to the toxins in cigarette smoke. In any event, these findings indicate that, for cardiovascular disease, it is incorrect to compute "cigarette equivalents" for passive exposure to ETS and then to extrapolate the effects of this exposure on nonsmokers from the effects of direct smoking on smokers. These results suggest that heart disease is an important consequence of exposure to ETS. The combination of epidemiological studies with demonstration of physiological changes with exposure to ETS, together with biochemical evidence that elements of ETS have significant adverse effects on the cardiovascular system, leads to the conclusion that ETS causes heart disease. This increase in risk translates into about 10 times as many deaths from ETS-induced heart disease as lung cancer; these deaths contribute greatly to the estimated 53,000 deaths annually from passive smoking. This toll makes passive smoking the third leading preventable cause of death in the United States today, behind active smoking and alcohol.

China↗
PubMed1990

Two dimensions describe left ventricular volume change during hemodynamic transients.

Left ventricular (LV) volume can be estimated from three orthogonal dimensions measured by sonomicrometry. Often, an index based on fewer than three dimensions has been substituted for volume. We consider whether a consistent relationship between LV cross-sectional area, computed as the product of the minor axes dimensions and LV three-dimensional volume, is maintained throughout the responses to application and release of vena caval, pulmonary artery, and aortic occlusions, which were held for approximately 30 beats. In six dogs, the relationship between area and volume was highly linear, with an average correlation of 0.98 and standard error of the estimate of 0.9 ml. Within each dog, there were small but statistically significant differences in the intercepts in the regression lines among the three interventions. However, the magnitude of these differences averaged only 0.5 ml. There was not a systematic difference between the relationship for vena caval and pulmonary artery occlusions, and the relationship for aortic occlusions shifted upward by an average of only 0.8 ml. We conclude that cross-sectional area can be substituted for the three-dimensional volume during the transient responses to acute alterations in the external load conditions.

Animals↗
PubMed1990

Missing data in two-way analysis of variance.

We previously described a regression approach to analysis of variance computations that permitted analysis of unbalanced designs and experiments with missing data in two-way (or higher) analyses of variance Am. J. Physiol. 255 (Regulatory Integrative Comp. Physiol. 24): R353-R367, 1988. That approach can only be used correctly under a set of narrow, and relatively uninteresting, circumstances. In fact, in the example we worked, we extended that approach beyond its intended scope and incorrectly computed F statistics for testing hypotheses about the main effects of strain of rat and nephron site in a study of renal Na(+)-K(+)-adenosinetriphosphatase. This paper presents the correct approach, which can be generalized to most situations likely to be encountered when two-way, or higher, analyses of variance are used.

Adenosine Triphosphatases↗
PubMed1990

Pulmonary model to predict the effects of series ventricular interaction.

To fully describe the mechanisms of diastolic interaction between the right ventricle and left ventricle, it is necessary to understand how a change in right ventricular output (Qrvo) is transmitted across the pulmonary circulation. This series ventricular interaction is manifest as the temporal response in left ventricular filling (Qlvf) to a change in Qrvo. To quantify series interaction we used a three-element, two-parameter model of the pulmonary circulation. The parameters represented the pulmonary arterial and venous resistance and pulmonary vascular compliance. Using beat-to-beat values of mean pressure and flow measured at the input and output of the pulmonary circulation during the transient response to caval or pulmonary artery occlusion, we estimated the parameters for this model in eight open-chest dogs under control conditions, after autonomic blockade, and after fully opening the pericardium. From 110 separate data episodes, the average values of the pulmonary arterial and venous resistance and pulmonary vascular compliance were 0.14 +/- 0.08 mm Hg.sec/ml and 4.81 +/- 3.17 ml/mm Hg (+/- SD). These estimates were insensitive to the simultaneous effects of autonomic reflexes and direct ventricular interaction, so they uniquely measure the bulk transport properties of the pulmonary circulation. The time constant, which measures the response of Qlvf to a change in Qrvo, averaged 0.26 +/- 0.15 second, which implies that effects of series interaction on Qlvf are manifest within one beat. The model was also able to predict the dynamic response of Qlvf to changes in Qrvo and thus can be used to measure and predict the effects of series interaction in the intact cardiopulmonary system.

Animals↗
PubMed1989

Beat-to-beat regulation of left ventricular function in the intact cardiovascular system.

A variety of regulatory mechanisms have evolved to control the heart's pump function because the cardiovascular system must continually adapt to the changing demands that body functions place on it. This regulation takes place through many physiological systems; however, fine adjustments in cardiac pumping probably require adaptations more quickly than external control mechanisms (such as the autonomic nervous system) can compensate. Thus cardiac pumping is also regulated by mechanisms intrinsic to the heart. To better understand these intrinsic control mechanisms, we studied the beat-to-beat response of left ventricular function to continually varying changes in loading conditions produced by transiently occluding the pulmonary artery, venae cavae, and aorta. We used multiple linear regression to identify and quantify the important beat-to-beat determinants of left ventricular systolic function, quantified as stroke work. We could not adequately explain or predict beat-to-beat changes in stroke work with traditional determinants of ventricular function, preload, afterload, and heart rate, because a large systematic error remains after taking these traditional determinants of function into account. To eliminate this systematic error, we had to include some function of previous beat stroke volume and end-systolic size and pressure. This additional information significantly improved both our ability to model the observed transient changes in left ventricular stroke work and to predict additional observations that were not used to develop our model. We conclude that previous beat contraction history is an important determinant of left ventricular function and implies an important regulatory mechanism whereby the left ventricle can fine tune its function from beat to beat in response to continually changing loading conditions.

Animals↗
PubMed1989

Left ventricular volume measurement by conductance catheter in intact dogs. Parallel conductance volume depends on left ventricular size.

The conductance catheter is a promising new instrument for continuously measuring left ventricular (LV) volume. Absolute LV volume (V[t]) is related to uncorrected conductance volume, B(t), according to the equation: V(t) = (1/alpha)(B(t) - alpha Vc). The alpha Vc factor represents parallel-conductance volume due to conducting material outside the LV blood pool, and may be estimated by transiently changing blood conductivity using a bolus injection of hypertonic saline. alpha is the slope in the relation between B(t) and true LV volume. We tested the assumption that alpha Vc and alpha are constant over a range of hemodynamic conditions. We performed multiple hypertonic saline alpha Vc determinations in seven intact dogs during control conditions and subsequent temporary balloon occlusions of inferior vena cava (IVCO), aorta (AO), and pulmonary artery (PAO). We also compared B(t) with simultaneous biplane angiographic LV volume during similar control and intervention conditions. The saline-derived alpha Vc was 76 +/- 2 ml during control and fell significantly by -7 +/- 2 ml during IVCO (p less than 0.001) but not during AO or PAO. According to multiple linear regression analyses, the strongest predictor of saline-derived alpha Vc was uncorrected end-systolic Bes, with a sensitivity coefficient of 0.60 +/- 0.06 ml/ml (p less than 0.001). Angiographically derived alpha Vc showed a similar dependence on Bes, with a coefficient of 0.77 +/- 0.14 ml/ml (p less than 0.001). Angiographically determined alpha also showed significant variation with hemodynamic interventions, largely reflecting an underlying dependence on alpha Vc. The variation in alpha Vc and alpha with LV size may stem from nonlinearity in the B(t)-V(t) relation. Although the conductance catheter provides a useful measure of relative LV volume, measurement of absolute LV volume over a wide hemodynamic range using constant alpha Vc and alpha factors is unrealistic. This result calls into question the current use of this technique for the measurement of the absolute end-systolic--pressure-volume relation.

Animals↗
PubMed1988

Multiple linear regression is a useful alternative to traditional analyses of variance.

Physiologists often wish to compare the effects of several different treatments on a continuous variable of interest, which requires an analysis of variance. Analysis of variance, as presented in most statistics texts, generally requires that there be no missing data and often that each sample group be the same size. Unfortunately, this requirement is rarely satisfied, and investigators are confronted with the problem of how to analyze data that do not strictly fit the traditional analysis of variance paradigm. One can avoid these pitfalls by recasting the analysis of variance as a multiple linear regression problem. When there are no missing data, the results of a traditional analysis of variance and the corresponding multiple regression problem are identical; when the sample sizes are unequal or there are missing data, one can use a regression formulation to analyze data that cannot be easily handled in a traditional analysis of variance paradigm and thus overcome a practical computational limitation of traditional analysis of variance. In addition to overcoming practical limitations of traditional analysis of variance, the multiple linear regression approach is more efficient because in one run of a statistics routine, not only is the analysis of variance done but also one obtains estimates of the size of the treatment effects (as opposed to just an indication of whether such effects are present or not), and many of the pairwise multiple comparisons are done (they are equivalent to t tests for significance of the regression parameter estimates). Finally, interaction between the different treatment factors is easier to interpret than it is in traditional analysis of variance.

Analysis of Variance↗
PubMed1987

Left ventricular mechanical adaptation to chronic aortic regurgitation in intact dogs.

Increased end-diastolic wall stress has been hypothesized to stimulate left ventricular (LV) hypertrophy following volume overload. We instrumented intact-chest dogs with radiopaque markers in both ventricles and created volume overload by puncturing one aortic valve cusp. End-diastolic stress increased immediately, then fell over 3 mo as the heart hypertrophied. End-systolic stress did not change significantly. Chamber contractility, quantified as Emax, the end-systolic pressure-volume line slope, increased. Emax normalized by multiplying by LV mass increased following the lesion before but not after beta-blockade with propranolol and did not change significantly over time, suggesting that chamber contractility changed because of increased mass and sympathetic tone rather than changed intrinsic muscle function. LV mass did not initially correlate with lesion size, but steady-state mass did. Over the range of lesions we produced, increased end-diastolic wall stress appears to stimulate hypertrophy at a fixed rate, which stops when end-diastolic wall stress has been reduced to an acceptable level.

Adaptation, Physiological↗
PubMed1987

Chronic pressure overload hypertrophy decreases direct ventricular interaction.

We studied the relative roles of direct (via the interventricular septum) and series (via the pulmonary circulation) ventricular interaction in hearts with concentric left ventricular hypertrophy by using statistical models to analyze the transient responses in right and left ventricular pressures and dimensions to occlusions of the venae cava and pulmonary artery in five open-chest anesthetized dogs. The left ventricles of these dogs had moderate concentric hypertrophy (31% increase in mass) induced by 3 mo of renovascular hypertension [peak left ventricular pressure = 160 +/- 13 (SD) mmHg]. At end diastole we found that direct interaction was only about one-tenth as important as series interaction in determining left ventricular size with the pericardium around the heart. At end systole we found that direct interaction was about one-fifth as important as the end-systolic pressure-volume relationship in determining left ventricular size. Removing the pericardium decreased the importance of direct interaction. Direct interaction is less important in these hearts than in normal hearts, probably because the septum is thicker and, hence, less distensible. This change in the relative importance of direct ventricular interaction with hypertrophy complicates comparison of pressure-volume relationships between normal and hypertrophied hearts.

Animals↗
PubMed1979

Determination of frequency response from step response: application to fluid-filled catheters.

The performance of a fluid-filled catheter can be described by reporting its undamped natural frequency and damping ratio. These parameters can be measured by subjecting the catheter to sinusoidally varying pressures at a wide variety of frequencies to obtain the frequency response. They can also be computed from the response to a step change in pressure, which is often easier to produce. This paper derives the required equations and includes a graph which permits one to look up the undamped natural frequency after measuring the period and decay rate of the oscillation following a step change in pressure.

Cardiac Catheterization↗