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Biomedical subjects

J R Wilson

Publications and source records attributed to J R Wilson.

At least 199 records · Page 11Linked to original sources
PubMed1984

Sequential changes in regional coronary flow during pacing-induced angina pectoris: coronary flow limitation precedes angina.

To investigate the sequence of changes in regional myocardial perfusion which precedes stress-induced angina, we measured great cardiac vein flow (GCVF), draining the anterior left ventricle, during incremental atrial pacing in 10 patients with normal anterior perfusion (group I) and in 11 patients with greater than or equal to 50% diameter stenosis of the left main or proximal left anterior descending coronary artery (group II). Pacing produced angina in 11 of 11 and regional lactate production in 9 of 11 group II patients. Both groups had comparable resting GCVF (group I = 62 +/- 7 ml/min vs group II = 76 +/- 9 ml/min; p = NS) and both exhibited progressive increases in GCVF with pacing. However, the entire flow-demand relationship was displaced downward in group II, as evidenced by a reduction in the percent increase in GCVF both following the first 20-beat pacing increment (group I = 46 +/- 6% vs group II = 16 +/- 4%; p less than 0.001) and at angina (group I = 113 +/- 16% vs group II = 44 +/- 9%; p less than 0.001). The first 20-beat pacing increment increased the heart rate to only 77 +/- 2 bpm in group II whereas angina and ECG changes did not occur until a pacing rate of 117 +/- 6 bpm. These data indicate that regional flow abnormalities precede the onset of pacing-induced angina in patients with coronary disease (CAD) and that these flow abnormalities frequently are detectable at heart rates substantially below the anginal threshold.

Adult↗
PubMed1984

Standards for product safety design: a framework for their production.

Accident reduction can be achieved through improved standards of product design and associated safety performance standards. Although many problems exist in terms of data production, reporting, collection and dissemination, it is suggested that a useful design data bank could be contructed and applied. The discussion of data requirements, classification and application is oriented particularly towards the problem of child safety.

Journal Article↗
PubMed1984

Effect of hydralazine on nutritive flow to working canine gracilis skeletal muscle.

The direct smooth muscle vasodilator hydralazine has been used to treat exertional fatigue in patients with chronic heart failure. However, prior studies suggest that arteriolar vasodilators such as hydralazine may actually impair nutritive flow to working skeletal muscle by interfering with the distribution of blood flow within muscle. To investigate this possibility, tension development and metabolism were measured in nine vascularly isolated gracilis muscle preparations perfused at 90 mm Hg and stimulated to contract progressively at rates of 1, 3 and 6/s with each stage lasting 3 minutes. Studies were then repeated after 30 minutes of intraarterial hydralazine (0.02 to 0.12 mg/min). At rest, hydralazine decreased mean vascular resistance (+/- SEM) from 15.1 +/- 1.4 to 8.6 +/- 0.9 X 10(2) units (p less than 0.001) and increased blood flow from 6.4 +/- 0.7 to 11.4 +/- 1.2 ml/min (p less than 0.001), but did not change oxygen consumption (VO2) control, 18 +/- 1 versus hydralazine, 17 +/- 2 microliter/min). Hydralazine also decreased vascular resistance and increased flow at a contraction rate of 1/s, but not at 3 and 6/s. Hydralazine had no effect on maximal VO2 (control, 254 +/- 18 versus hydralazine, 236 +/- 19 microliter/min), maximal developed tension (control, 353 +/- 90 versus hydralazine, 334 +/- 74 kg X min) or the response in venous lactate (control, 20.6 +/- 2.3 versus hydralazine, 18.1 +/- 2.0 mg/dl). Hydralazine also did not change muscle metabolism and function at contraction rates of 1 and 3/s. These data suggest that hydralazine does not adversely affect nutritive flow to working skeletal muscle.

Animals↗
PubMed1984

Exercise intolerance in patients with chronic heart failure: role of impaired nutritive flow to skeletal muscle.

The maximal exercise capacity of patients with chronic heart failure is frequently reduced. To investigate whether this exercise intolerance is caused by inadequate nutritive flow to skeletal muscle, we compared cardiac outputs, leg blood flow, and leg metabolism during maximal bicycle exercise in seven patients with normal maximal oxygen uptake (VO2) (greater than 20 ml/min/kg; group A), eight patients with heart failure and moderately reduced maximal VO2 (15 to 18 ml/min/kg; group B), and eight patients with heart failure and markedly reduced maximal VO2 (less than 14 ml/min/kg; group C). As the severity of exercise intolerance increased from group A to group C there was a progressive decline in cardiac output and leg blood flow at any given workload accompanied by a progressive decline in maximal cardiac output (liters/min) (A, 12.4 +/- 1.0; B, 8.7 +/- 0.9; C, 5.5 +/- 0.7), maximal leg flow (liters/min) (A, 4.0 +/- 0.3; B, 2.6 +/- 0.4; C, 1.4 +/- 0.2), and maximal leg VO2 (ml/min) (A, 564 +/- 49; B, 403 +/- 41; C, 213 +/- 35 ml/min). All patients terminated exercise because of severe leg fatigue. At termination of exercise, all three groups exhibited similar marked levels of leg O2 extraction (%) (A, 80 +/- 2; B, 83 +/- 3; C, 89 +/- 1) and high femoral-arterial lactate gradients (mg/dl) (A, 15.4 +/- 2.6; B, 18.3 +/- 3.5; C, 19.2 +/- 3.6), suggesting that exercise was limited when a critical level of muscle underperfusion was reached. These data suggest that the reduced maximal exercise capacity of patients with chronic heart failure is primarily due to impaired nutritive flow to skeletal muscle and resultant muscular fatigue.

Adult↗
PubMed1984

Exercise testing in the evaluation of the patient with chronic cardiac failure.

A single progressive upright treadmill or upright bicycle exercise test may be used to safely evaluate the functional aerobic capacity of patients with chronic cardiac failure of varying severity and origin. The non-invasive monitoring or respiratory gas exchange and the determination of VO2 max and the anaerobic threshold may be used to objectively grade the severity of chronic cardiac failure and the heart's pumping reserve. The serial monitoring of these indices of exercise performance should prove useful in following the natural history of cardiac disease and in assessing the response to various therapeutic interventions.

Cardiac Output↗
PubMed1983

Exercise intolerance in patients with chronic left heart failure: relation to oxygen transport and ventilatory abnormalities.

Circulatory, metabolic, and ventilatory responses to maximal and submaximal symptom-limited exercise were studied in 13 patients with chronic stable heart failure. Maximal exercise was sustained 6.5 +/- 0.6 minutes (mean +/- standard error of the mean) and increased minute oxygen consumption (VO2) to 940 +/- 65 ml/min, whereas submaximal exercise was sustained for 15.4 +/- 2.3 minutes and increased VO2 to 825 +/- 49 ml/min (both p less than 0.01 compared with maximal exercise). Both exercise protocols were terminated because of fatigue and both were associated with reduced cardiac output relative to VO2, marked systemic oxygen extraction (80 +/- 2% maximal versus 78 +/- 2% submaximal) and similarly elevated blood lactate concentrations (37 +/- 4 mg/dl maximal versus 36 +/- 4 mg/dl submaximal), suggesting inadequate oxygen delivery to working muscle. Minute ventilation during both types of exercise was also more than twice normal relative to carbon dioxide production. However, during submaximal exercise, dyspnea was noted in only 3 patients despite these ventilatory abnormalities. During maximal exercise, dyspnea was noted in 11 patients but did not force termination of exercise or preclude achievement of marked systemic oxygen extraction and lactate production. These data suggest that patients with chronic stable cardiac failure are limited during both maximal and submaximal exercise primarily by inadequate oxygen transport to working muscle.

Cardiac Output↗
PubMed1983

Determinants of circulatory response to intravenous hydralazine in congestive heart failure.

To determine whether the circulatory response to hydralazine in heart failure is influenced by initial hemodynamic status or left ventricular (LV) chamber size, 28 patients with chronic LV dysfunction were studied. Hemodynamic measurements and echocardiographic LV end-diastolic dimension were correlated with the response to 20 mg of intravenous hydralazine and to a dose titrated in each patient to reduce systemic resistance by greater than or equal to 20%. Hydralazine, 20 mg, decreased systemic resistance from 23 +/- 8 to 18 +/- 8 U (p less than 0.01) and increased the cardiac index from 2.0 +/- 0.5 to 2.5 +/- 0.6 liters/min/m2 (p less than 0.01) and the stroke work index from 21 +/- 11 to 24 +/- 9 g . m/m2 (p less than 0.05). Titrating the dose to decrease systemic resistance by greater than or equal to 20% increased the cardiac index further to 2.7 +/- 0.6 liters/min/m2 and the stroke work index to 32 +/- 9 g . m/m2. The change in systemic resistance produced by 20 mg of hydralazine correlated only with initial systemic resistance (r = 0.53), suggesting that vascular response to hydralazine is a direct function of initial vascular resistance. The percentage change in stroke work index produced by 20 mg of hydralazine correlated directly with indexes of LV preload-end-diastolic wall stress (r = 0.69) and pulmonary wedge pressure (r = 0.43) and inversely with stroke work index (r = -0.49), an index of ventricular work. Similar but less close correlations were observed when the dose of hydralazine was titrated. The hemodynamic response to hydralazine did not correlate with LV end-diastolic dimension or right atrial pressure. Thus, vascular response to moderate doses of hydralazine is related to initial systemic vascular resistance. LV pump response is related to the level of initial LV pump dysfunction but not to LV chamber size or right atrial pressure.

Female↗
PubMed1983

Respiratory gas analysis during exercise as a noninvasive measure of lactate concentration in chronic congestive heart failure.

Measurement of blood lactate during exercise in patients with chronic congestive heart failure provides a useful index of oxygen (O2) availability in working muscle. Bicarbonate buffering of lactate produces carbon dioxide (CO2) in excess of that resulting from oxidative metabolism. Therefore, calculation of excess CO2 production from measured CO2 production and O2 uptake may offer a noninvasive quantitative index of changes in blood lactate during exercise in these patients. To investigate this possibility, 22 patients with congestive heart failure and depressed left ventricular function were studied during progressive maximal upright bicycle exercise. Oxygen uptake, expired carbon dioxide, arterial lactate, O2 extraction, and cardiac output were measured at each 20 W incremental work load and peak exercise. Exercise increased VO2 from 3.5 +/- 0.9 ml/min/kg at rest to 13.1 +/- 2.9 ml/min/kg, O2 extraction from 49 +/- 9% at rest to 78 +/- 6%, lactate from 12 +/- 5 mg/dl at rest to 41 +/- 15 mg/dl, and cardiac index from 1.7 +/- 0.4 at rest to 3.8 +/- 1.2 liters/min/m2. The increase in lactate at each work load was linearly related to excess CO2 production (r = 0.92, p less than 0.01). Exercise was repeated the following day in 10 patients; measurements of excess CO2 production was highly reproducible (r = 0.98, p less than 0.01). Excess CO2 production also correlated with the decrease in bicarbonate produced by exercise (r = 0.81), supporting the hypothesis that excess CO2 is produced by bicarbonate buffering of lactate. Thus, calculation of excess carbon dioxide production from noninvasive measurement of respiratory gas exchange provides a reliable and reproducible method of continuously assessing alterations in lactate throughout bicycle exercise in patients with chronic congestive heart failure.

Bicarbonates↗
PubMed1983

Pressures and procedures for the design of safe consumer products.

An assessment is provided of the current position regarding changes in UK or EEC civil law under which injured parties can obtain redress in respect of injuries caused by defective products. One effect of proposed systems of strict liability in tort will be to shift some of the burden of proof from the injured party on to the producer of the product claimed to have caused injury. It is argued that this is a just and logical change, given the unfairness and anomalies in present systems and the relative abilities of consumers and producers to avoid such incidents and to bear or to offset the cost of the consequences. Cases of apparent misuse of a product by a consumer may frequently be induced by the design of that product and could thus be prevented by more thoughtful design. In order that producers can ensure their own viability and satisfy the consumer market, their products must be safe, efficient, comfortable and satisfying to use, as well as durable, serviceable and realistically priced. One requirement for achieving this has been said to be the input of accident and ergonomics data early in the product development process; the present paper examines this proposition. Evidence is provided by research into the design and manufacture of consumer products for the UK market, carried out at Birmingham University. Examined in particular are the extent to which formal development processes and design safety review procedures are used, and the degree of utilisation of accident, ergonomics, user testing and market feedback data, identifying barriers to the widespread use of these. Safe and ergonomic design of products must aim to be seen as a positive business activity, rather than as a cost-centre. The benefits to a company of a comprehensive design safety programme will more than outweigh the costs given the pressures identified earlier.

Journal Article↗
PubMed1983

Effect of atrial pacing on intracoronary thromboxane production in coronary artery disease.

The effect of atrial pacing on intracoronary thromboxane production was investigated in 35 patients with stable (n = 19) or unstable (n = 16) angina. Arterial and coronary sinus thromboxane B2, the stable metabolite of thromboxane A2, myocardial lactate extraction and thermodilution coronary sinus flow were measured before, during and immediately after atrial pacing until the onset of angina. Pacing did not significantly increase coronary sinus thromboxane B2 (rest, 233 +/- 107 pg/ml; pacing, 249 +/- 154 pg/ml; postpacing, 330 +/- 309 pg/ml) (mean +/- standard deviation) despite a moderate increase in arterial thromboxane B2 (rest, 270 +/- 170 pg/ml; pacing, 387 +/- 364 pg/ml; postpacing, 446 +/- 420 pg/ml) (all changes probability [p] less than 0.05). A positive transmyocardial thromboxane B2 gradient, suggesting intracoronary thromboxane A2 production, occurred in only five patients at rest (gradient = 60 +/- 35 pg/ml). During pacing, a transmyocardial thromboxane B2 gradient was not observed despite myocardial lactate production in 18 patients. A postpacing gradient was observed in eight patients (gradient = 284 +/- 349 pg/ml). These gradients were significantly more frequent in patients who produced lactate during pacing (7 of 18) than in patients without lactate production (1 of 17) (p less than 0.05). In patients with and without a postpacing gradient, coronary vascular resistance decreased with pacing and returned to rest levels immediately after pacing, suggesting that a postpacing thromboxane gradient does not significantly alter coronary tone. These data suggest that: 1) pacing-induced angina is usually not associated with substantial intracoronary thromboxane A2 production; 2) in a minority of patients who develop intracoronary thromboxane A2 production, the amount is small and does not produce significant coronary vasoconstriction.

Angina Pectoris↗
PubMed1983

Selective breeding for a multivariate index of ethanol dependence in mice: results from the first five generations.

Starting with a population of genetically heterogeneous mice (HS/lbg), selection for a multivariate index of the ethanol withdrawal syndrome has been initiated. The study uses within-litter selection to minimize inbreeding and includes replicate high, low, and control lines. After five generations, results indicate that selection is proceeding successfully. There is evidence of asymmetry in the selection, i.e., selection is proceeding more rapidly for signs of severe withdrawal than for mild withdrawal signs. The realized heritability after five generations of within-family selection is approximately 0.15. These selected lines should eventually prove useful in determining some of the underlying genetic, physiological, and biochemical mechanisms involved in ethanol dependence.

Alcohol Drinking↗
PubMed1983

Development of neuronal response properties in the cat dorsal lateral geniculate nucleus during monocular deprivation.

We measured response properties of X- and Y-cells from laminae A and A1 of the dorsal lateral geniculate nucleus of monocularly lid-sutured cats at 8, 12, 16, 24, and 52-60 wk of age. Visual stimuli consisted of small spots of light and vertically oriented sine-wave gratings counterphased at a rate of 2 cycles/s. In cats as young as 8 wk of age, nondeprived and deprived neurons could be clearly identified as X-cells or Y-cells with criteria previously established for adult animals. Nonlinear responses of Y-cells from 8- and 12-wk-old cats were often temporally labile; that is, the amplitude of the nonlinear response of nondeprived and deprived cells increased or decreased suddenly. A similar lability was not noted for the linear response component. This phenomenon rarely occurred in older cats. At 8 wk of age, Y-cell proportions (number of Y-cells/total number of cells) in nondeprived and deprived A-laminae were approximately equal. By 12 wk of age and thereafter, the proportion of Y-cells in deprived laminae was significantly lower than that in nondeprived laminae. At no age was there a systematic difference in response properties (spatial resolution, latency to optic chiasm stimulation, etc.) for Y-cells between deprived and nondeprived laminae. Spatial resolution, defined as the highest spatial frequency to which a cell would respond at a contrast of 0.6, was similar for nondeprived and deprived X-cells until 24 wk of age. In these and older cats, the mean spatial resolution of deprived X-cells was lower than that of nondeprived X-cells. This difference was noted first for lamina A1 at 24 wk of age and later for lamina A at 52-60 wk of age. The average latency of X-cells to optic chiasm stimulation was slightly greater in deprived laminae than in nondeprived laminae. No such difference was seen for Y-cells. Cells with poor and inconsistent responses were encountered infrequently but were observed far more often in deprived laminae than in nondeprived laminae. Lid suture appears to affect the development of geniculate X- and Y-cells in very different ways. Not only is the final pattern of abnormalities quite different between these cell groups, but the developmental dynamics of these abnormalities also differ.

Animals↗