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Biomedical subjects

J R Wilson

Publications and source records attributed to J R Wilson.

At least 73 records · Page 4Linked to original sources
PubMed1996

Hemodynamic exercise testing. A valuable tool in the selection of cardiac transplantation candidates.

BACKGROUND: Peak exercise oxygen consumption (Vo2), a noninvasive index of peak exercise cardiac output (CO), is widely used to select candidates for heart transplantation. However, peak exercise Vo2 can be influenced by noncardiac factors such as deconditioning, motivation, or body composition and may yield misleading prognostic information. Direct measurement of the CO response to exercise may avoid this problem and more accurately predict prognosis. METHODS AND RESULTS: Hemodynamic and ventilatory responses to maximal treadmill exercise were measured in 185 ambulatory patients with chronic heart failure who had been referred for cardiac transplantation (mean left ventricular ejection fraction, 22 +/- 7%; mean peak Vo2, 12.9 +/- 3.0 mL. min-1.kg-1). CO response to exercise was normal in 83 patients and reduced in 102. By univariate analysis, patients with normal CO responses had a better 1-year survival rate (95%) than did those with reduced CO responses (72%) (P < .0001). Survival in patients with peak Vo2 of > 14 mL.min-1.kg-1 (88%) was not different from that of patients with peak Vo2 of < or = 14 mL.min-1.kg-1 (79%) (P = NS). However, survival was worse in patients with peak Vo2 of < or = 10 mL.min-1.kg-1 (52%) versus those with peak Vo2 of > 10 mL.min-1.kg-1 (89%) (P < .0001). By Cox regression analysis, exercise CO response was the strongest independent predictor of survival (risk ratio, 4.3), with peak Vo2 dichotomized at 10 mL. min-1.kg-1 (risk ratio, 3.3) as the only other independent predictor. Patients with reduced CO responses and peak Vo2 of < or = 10 mL.min-1.kg-1 had an extremely poor 1-year survival rate (38%). CONCLUSIONS: Both CO response to exercise and peak exercise Vo2 provide valuable independent prognostic information in ambulatory patients with heart failure. These variables should be used in combination to select potential heart transplantation candidates.

Analysis of Variance↗
PubMed1996

Circulatory status and response to cardiac rehabilitation in patients with heart failure.

BACKGROUND: We recently reported that some patients with heart failure and exercise intolerance exhibit severe hemodynamic dysfunction during exercise, whereas others have normal cardiac output responses to exercise. We postulated that patients with preserved cardiac output responses to exercise are limited by deconditioning and would respond to exercise training, whereas patients with reduced cardiac output responses are limited by skeletal muscle underperfusion and would not improve with exercise training. The present study was undertaken to test this hypothesis. METHODS AND RESULTS: Thirty-two patients with heart failure were studied. Hemodynamic response to maximal treadmill exercise was measured; then patients were enrolled in a standard 3-month cardiac rehabilitation program. Peak exercise VO2, lactate threshold, and quality-of-life questionnaires were assessed at 1, 2, and 3 months. Twenty-one patients had normal cardiac output responses to exercise. All 21 patients participated in the rehabilitation program without difficulty, and 9 (43%) responded to rehabilitation, defined as a > 10% increase in both peak exercise VO2 and the anaerobic threshold. Of the 11 patients with reduced cardiac output responses to exercise, 3 discontinued rehabilitation because of severe exhaustion, and only 1 qualified as a responder (9%; P < .04 versus preserved cardiac output). CONCLUSIONS: Patients with heart failure and normal cardiac output responses to exercise frequently improve with exercise training. Patients with severe hemodynamic dysfunction during exercise usually do not improve with training, which suggests that they are limited primarily by circulatory factors.

Blood Circulation↗
PubMed1996

Histamine-immunoreactive neurons and their innervation of visual regions in the cortex, tectum, and thalamus in the primate Macaca mulatta.

The histaminergic system is involved in the control of arousal in the brain and may impact significantly on visual processing. However, little is known about the histaminergic innervation of visual areas, or the histamine system in the primate brain, in general. We examined in Macaca mulatta the location of histamine-immunoreactive neurons and the innervation of important cortical and subcortical visual areas by histamine-immunoreactive axons. Brain sections were treated with an antibody to histamine and processed with standard immunohistological procedures. Histamine-immunoreactive neurons (20-45 microns in diameter) were localized bilaterally in the hypothalamus, particularly in ventral, lateral, posterior, and perimammillary hypothalamic areas. These hypothalamic cells appear to provide the sole neural source of histamine in the macaque brain. A plexus of varicose histamine-immunoreactive axons was present throughout the superior colliculus, the dorsal and ventral lateral geniculate nuclei of the thalamus, the reticular nucleus of the thalamus, the lateral posterior/pulvinar complex, and the visual cortex, including areas 17, 18, and the nearby extrastriate cortex. The axons nearly homogeneously innervated every region and layer in these structures, except for an increase in density in layer 1 of the visual cortex and in the superficial-most layers of the superior colliculus. Histaminergic axons broadly innervated every visual region examined. In comparison with the other aminergic and the cholinergic projection systems, which show considerable projection specificity, the histaminergic projection exhibited great homogeneity. The breadth of the distribution of histaminergic axons ensures that virtually all levels of visual processing in the primate can be influenced, either directly or indirectly, by the neuromodulatory effects of histamine.

Animals↗
PubMed1996

Evaluation of skeletal muscle fatigue in patients with heart failure.

Exertional fatigue is a major limiting symptom in patients with heart failure. Nevertheless, the mechanism responsible for this fatigue remains unclear. Reduced skeletal muscle blood flow, altered muscle oxidative enzymes, decreased muscle mass and altered muscle contractility have all been implicated but the precise contribution of these factors remains to be determined. Clinically, the severity of muscle fatigue is usually determined from the patient history. This approach is unreliable since symptoms reported during normal daily activities correlate poorly with objective measures of exercise performance. The degree of perceived fatigue noted during formal exercise testing also correlates poorly with objective measures of muscle behavior, such as blood lactate levels. Cardiopulmonary exercise testing can be used to identify the onset of lactate release, or the anaerobic threshold, and therefore provides more objective information about muscle behavior. However, an increase in blood lactate does not necessarily indicate muscle fatigue. Surface recordings of muscle electromyograms during exercise permits detection of increasing EMG signal, an indicator of fatigue. This technique is potentially valuable but is technically challenging. Finally, muscle fatigue can be assessed by monitoring developed tension during repetitive contractions of the quadriceps muscle. This index of muscle fatigability correlates relatively closely with maximal exercise performance and provides the best index of fatigue currently available. However, further studies are needed to document the clinical utility of this methodology.

Cardiac Output, Low↗
PubMed1996

Expression of the type 2 metallothionein-like gene MT2 from Arabidopsis thaliana in Zn(2+)-metallothionein-deficient Synechococcus PCC 7942: putative role for MT2 in Zn2+ metabolism.

Zn2+ proteins pervade metabolism and are essential for gene expression. However, no proteins have been ascribed the central roles of Zn2+ donation to, or removal from, metalloproteins, or Zn2+ storage in vegetative plant tissue. In animals, such functions have been proposed for metallothioneins. Plants contain multiple metallothionein-like genes but their predicted products, which differ significantly from animal metallothioneins, remain to be isolated from vegetative tissue and their roles are uncertain. The type 2 metallothionein-like gene from Arabidopsis, MT2, was expressed under the control of Zn2+-responsive elements derived from the cyanobacterial metallothionein divergon, smt. Zn2+-dependent expression of MT2 transcripts in Synechococcus PCC 7942 was confirmed by northern analysis. The Arabidopsis MT2 gene partly complemented Zn2+ hypersensitivity in mutants of Synechococcus PCC 7942 which are functionally deficient in an endogenous Zn2+-metallothionein gene, smtA. MT2 was also expressed as a recombinant fusion protein in Escherichia coli, purified and shown to bind Zn2+ in vitro. The mean pH of half displacement of Zn2+ from MT2 was estimated to be 5.05. This suggests that MT2 has a greater affinity for Zn2+ than phytochelatins. The results presented here reveal that MT2 is capable of binding Zn2+ in vitro, conferring tolerance to elevated [Zn2+] in vivo within cyanobacteria and is likely to compete with other polypeptides for cellular Zn2+ in planta.

Amino Acid Sequence↗
PubMed1996

GABA immunopositive axons in the optic nerve and optic tract of macaque monkeys.

Using an antibody to gamma-aminobutyric acid (GABA), we examined the optic nerves and optic tracts from macaque monkeys at the light and electron microscopic levels to determine if there is a possible inhibitory projection from the retina to the brain. All of the monkeys (n = 5) had GABA immunopositive axons that were evenly distributed in their optic nerves. These immunopositive axons were slightly larger than the axons around them and comprised an average of 2.6% of the axons in the nerves. Thus, their estimated total was about 44,000 axons per nerve. In the optic tracts, the GABA immunopositive axons were not distributed evenly, but were concentrated mostly in the ventromedial part, indicating that this retinal pathway probably goes to a midbrain destination such as the superior colliculus. The present findings provide further evidence that there is a GABAergic retinal projection to the brain in primates with currently unknown physiological influences.

Animals↗
PubMed1996

Effects of cold acclimation and central opioid processes on thermoregulation in rats.

Two experiments, using centrally administered [D-Ala2-MePhe4-Gly(ol)5]enkephalin (DAMGO), a selective mu-opioid agonist, assessed the thermoregulatory consequences of cold acclimation. Experiment 1 assessed whether cold acclimation influenced DAMGO hyperthermia at room temperature. Sialo-adenectomized rats were implanted with ICV cannulae and IP Mini-Mitters. After 3 weeks of exposure to 5 degrees C (cold acclimation) or 22 degrees C (non-cold acclimation) rats were pretreated with IP naltrexone HCl (2 mg/kg b.wt.) or vehicle (0.15 M saline) and later administered a 5-microliters ICV injection of 0.15 M saline, 0.1, or 1.0 microgram DAMGO. Cold acclimation exerted little effect on core temperature but potentiated DAMGO hyperthermia in a dose-dependent, naltrexone-reversible, activity-independent manner. Experiment 2 assessed the effect these same manipulations exerted on operant escape from a convective source of mild heat (37 degrees C). Duration of heat escape increased with cold acclimation in a naltrexone-resistant manner, yet was not influenced by DAMGO in either non-cold-acclimated or cold-acclimated rats. These findings suggest that two central adaptations occur with cold acclimation: A non-mu-opioid process that increases heat sensitivity and a mu-opioid process that potentiates hyperthermia but fails to alter heat escape due to mu-opioid-mediated analgesia.

Acclimatization↗
PubMed1996

Blood conservation in neonatal and pediatric populations.

Blood conservation in infants and children has benefits even beyond those seen with the adult populations. For instance, acquired blood borne diseases such as cytomegalovirus not only cause illness but also can have deleterious effects on the growth and development of infants and children. Decreasing blood transfusions is especially important in preventing sensitization over a lifetime, which may require further transfusion and even organ transplantation. A less striking benefit, but one equally as significant, is decreasing the occurrence of graft-versus-host disease when blood conservation negates the need for multiple transfusions. The limitation of alternative transfusion practices in children and infants increases the benefits of blood conservation. Autologous blood donation may be an alternative to allogeneic transfusion in older children, but is not possible with neonates who may be born anemic and who experience a normal physiologic anemia during the first 2 months of life. Critical care nurses are instrumental in helping blood conservation by understanding blood salvaging techniques, including correct collection techniques, noninvasive monitoring, evaluation of diagnostic sample needs, and administration of erythrocyte-stimulating factors.

Adult↗
PubMed1995

Synaptic inputs to single neurons in the lateral geniculate nuclei of normal and monocularly deprived squirrel monkeys.

Neurons in the dorsal lateral geniculate nucleus (dLGN) of normal and monocularly lid-sutured squirrel monkeys were recorded electrophysiologically, and some were injected intracellularly with horseradish peroxidase (HRP) to examine and compare their synaptic inputs. Limited tests of the receptive field properties did not show any differences between the normal, nondeprived, or deprived neurons. Sixteen injected neurons were examined at the light microscopic level with most of these located in the P-laminae (n = 14). Ten of these were either from normal monkeys (n = 9) or received input from the nondeprived eye of a monocularly deprived monkey (n = 1). The remaining six neurons received input from the deprived eye. The dendritic trees of deprived neurons did not differ from those of normal or nondeprived neurons. Three normal and five deprived neurons from the P-laminae were examined at the electron microscopic level. Afferent distributions were not significantly different between normal and deprived neurons. Retinal, cortical, and gamma aminobutyric (GABA)ergic afferents accounted for nearly all inputs (avg., 42%, 23%, and 32%, respectively) and selectively contacted proximal, distal, or all parts of the dendrites. Overall, synaptic densities (synapses per length of dendrite) were high proximally and decreased with distance from the soma. However, the synaptic densities onto deprived neurons were higher at all distances compared to those onto normal neurons. Furthermore, HRP-filled deprived neurons received an average of 25 synapses onto their somata compared with only an average of 7 somal synapses on the HRP-filled normal neurons. Most of the increase in the number of synapses onto the deprived neurons was from GABAergic type profiles. This abnormality of the deprived neurons of the dLGN could be the underlying cause of their lesser responses compared with normal or nondeprived dLGN neurons. It could also be the initial stage that causes blindness in monocularly lid-sutured primates.

Afferent Pathways↗
PubMed1995

Dissociation between exertional symptoms and circulatory function in patients with heart failure.

BACKGROUND: Patients with heart failure frequently report exertional dyspnea and fatigue. These symptoms are usually attributed to circulatory dysfunction and therefore are typically treated with cardiovascular medications. Serial assessment of exertional symptoms has also become the principal method used to assess drug efficacy in heart failure. Nevertheless, the relation between exertional symptoms in heart failure and circulatory dysfunction remains uncertain. METHODS AND RESULTS: This study was undertaken to investigate the relation between exertional symptoms, ventilatory and skeletal muscle dysfunction, and circulatory function in patients with heart failure. To this end, 52 ambulatory patients with heart failure underwent hemodynamic monitoring during maximal treadmill exercise testing. During exercise, the severity of dyspnea and fatigue was evaluated on a scale of 6 to 20 (Borg scale). The level of perceived exercise intolerance during daily activities was evaluated with the Minnesota Living With Heart Failure Questionnaire and the Yale Dyspnea-Fatigue Index. Maximal treadmill exercise increased the VO2 to 13.4 +/- 2.8 mL.min-1.kg-1, the dyspnea score to 15.7 +/- 2.3, the fatigue score to 14.8 +/- 3.4, the pulmonary wedge pressure to 28 +/- 11 mm Hg, and the pulmonary artery lactate concentration to 34.5 +/- 16.3 mg/dL and decreased the pulmonary artery hemoglobin oxygen saturation to 30 +/- 9%. The level of perceived dyspnea had no relation to the pulmonary wedge pressure and correlated only minimally with the level of excessive ventilation (r = 39). The level of perceived fatigue correlated only weakly with blood lactate concentration (r = .55). Eleven patients (21%) exhibited a normal cardiac output and wedge pressure < 20 mm Hg during exercise, 22 (42%) exhibited a normal cardiac output but wedge pressure > 20 mm Hg during exercise, and 19 (37%) exhibited reduced cardiac output and wedge pressure > 20 mm Hg during exercise. Despite these markedly different hemodynamic responses, all three groups exhibited similar levels of fatigue and dyspnea at comparable workloads and had comparable total scores for the Minnesota Living With Heart Failure Questionnaire and the Yale Dyspnea-Fatigue Index. There was no relation between the Living With Heart Failure Questionnaire and peak exercise VO2 and only a weak correlation between the Dyspnea-Fatigue Index and peak VO2 (r = .48). CONCLUSIONS: The level of exercise intolerance perceived by patients with heart failure has little or no relation to objective measures of circulatory, ventilatory, or metabolic dysfunction during exercise. In patients who report severe exertional symptoms, it may be desirable to directly measure hemodynamic response to exercise to ensure that these symptoms are due to circulatory dysfunction.

Adult↗
PubMed1995

Sources of subcortical afferents to the macaque's dorsal lateral geniculate nucleus.

BACKGROUND: The dorsal lateral geniculate nucleus (dLGN) is the thalamic region responsible for transmitting retina signals to cortex. Brainstem pathways to this nucleus have been described in several species and are believed to control the retinocortical pathway depending on the state of the animal (awake, asleep, drowsy, etc.). The purpose of this study was to determine all of the subcortical sources of afferents to the dLGN in a higher primate, the macaque monkey, whose visual system is similar to that of humans. METHODS: Injections of horseradish peroxidase (HRP), with or without conjugation to wheat germ agglutinin, were made into the dLGNs of seven macaque monkeys, followed by perfusion, brain sectioning, and analyses of neurons in the brainstem, thalamus, and hypothalamus that contained the retrogradely transported marker. RESULTS: The reticular nucleus of the thalamus, pedunculopontine nucleus, parabigeminal nucleus, pretectal nucleus of the optic tract, superior colliculus, dorsal raphe nucleus, and tuberomammillary region of the hypothalamus contained many retrogradely labeled neurons ipsilateral to the injections. In the contralateral brainstem, HRP-labeled cells were found only in the pedunculopontine nucleus, nucleus of the optic tract, and dorsal raphe nucleus. The number of labeled neurons on the contralateral side was about one-half of that in corresponding ipsilateral nuclei. The locus coeruleus contained no labeled neurons in four of the macaques that had injections limited to the dLGN. CONCLUSION: There are seven subcortical regions that send afferents to the dLGNs of macaque monkeys. Except for the locus coeruleus, these are the same as observed for other species, such as the cat and rat, and indicate the possible sources of subcortical control over the dLGNs of humans.

Animals↗
PubMed1995

Dissociation between peak exercise oxygen consumption and hemodynamic dysfunction in potential heart transplant candidates.

OBJECTIVES: The purpose of this study was to determine how often peak exercise oxygen consumption (VO2) misclassifies the severity of cardiac dysfunction in potential heart transplant candidates. BACKGROUND: Cardiopulmonary exercise testing is being used to help select heart transplant candidates on the basis of the assumption that a low peak exercise VO2 indicates severe hemodynamic dysfunction and a poor prognosis. However, noncardiac factors, such as muscle deconditioning, can also influence exercise capacity. Therefore, peak exercise VO2 may overestimate the severity of cardiac dysfunction in some patients. METHODS: Hemodynamic and respiratory responses to maximal treadmill exercise were measured in 64 sequential patients undergoing evaluation for heart transplantation, all of whom had an ejection fraction < 35% and reduced peak exercise VO2 levels (mean [+/- SD] 13.3 +/- 2.7 ml/min per kg). RESULTS: Twenty-eight (44%) of 64 patients exhibited a reduced cardiac output response to exercise and pulmonary wedge pressure > 20 mm Hg at peak exercise, consistent with severe hemodynamic dysfunction. Twenty-three patients (36%) exhibited a normal cardiac output response to exercise but a wedge pressure > 20 mm Hg at peak exercise, suggesting moderate hemodynamic dysfunction. Thirteen patients (20%) exhibited a normal cardiac output and wedge pressure < 20 mm Hg at peak exercise, suggesting mild hemodynamic dysfunction. Despite these markedly different hemodynamic responses, all three groups exhibited similar peak exercise VO2 levels (mild dysfunction 14.2 +/- 3.5 ml/min per kg, moderate dysfunction 13.9 +/- 2.7 ml/min per kg, severe dysfunction 12.4 +/- 2.1 ml/min per kg). A peak exercise VO2 level < 14 ml/min per kg, considered to reflect severe hemodynamic dysfunction, was observed in 18 of the patients with a normal cardiac output response to exercise, whereas 7 patients with severe hemodynamic dysfunction had a peak VO2 level > 14 ml/min per kg. CONCLUSIONS: More than 50% of potential heart transplant candidates with a reduced peak exercise VO2 level exhibit only mild or moderate hemodynamic dysfunction during exercise. Hemodynamic responses to exercise should be directly measured in potential transplant candidates to confirm severe circulatory dysfunction.

Adult↗
PubMed1995

Self-esteem, compliance, and cervical screening.

A computerized version of the semantic differential was administered to 57 respondents and 43 nonrespondents to invitations for a cervical smear test. 26 concepts pertaining to emotional, social, parental, and health-related domains were tested. The semantic differential was followed by a personal questionnaire. Analysis indicated that fear, worry, and embarrassment were negatively correlated with the decision to have a cervical smear test. Respondents seemed to have higher self-esteem and better relationships with their husbands than nonrespondents.

Adult↗
PubMed1995

Clenbuterol: a substitute for anabolic steroids?

Clenbuterol is a recently popular drug used by athletes in many sports for its purported anabolic effects and reduction of subcutaneous fat. It is a beta-2 (beta 2) agonist prescribed overseas as a bronchodilator, but not approved for use in this country. It is on the banned substance list of the United States Olympic Committee. To avoid any erosion of confidence, physicians caring for athletes need accurate information regarding clenbuterol. Such information is unavailable within the routine medical environs. A review of the literature of animal husbandry reveals that this drug, when administered in doses far greater than those required for bronchodilation, does indeed increase the deposition rate of lean mass and retard adipose gain. There are no human studies available. Animal studies were conducted on laboratory and slaughter stock. No investigation into long-term cardiovascular side effects has been undertaken. The rate of extrapolation from animal studies to unsupervised human usage is alarming. If this category of drugs does preserve lean mass in humans, there are legitimate medical applications. Trials of efficacy and safety are needed.

Adipose Tissue↗