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Biomedical subjects

R S Wright

Publications and source records attributed to R S Wright.

At least 37 records · Page 2Linked to original sources
PubMed1999

Evaluation of pollution prevention options to reduce styrene emissions from fiber-reinforced plastic open molding processes.

Pollution prevention (P2) options to reduce styrene emissions, such as new materials and application equipment, are commercially available to the operators of open molding processes. However, information is lacking on the emissions reduction that these options can achieve. To meet this need, the U.S. Environmental Protection Agency's (EPA) Air Pollution Prevention and Control Division, working in collaboration with Research Triangle Institute, measured styrene emissions for several of these P2 options. In addition, the emission factors calculated from these test results were compared with the existing EPA emission factors for gel coat sprayup and resin applications. Results show that styrene emissions can be reduced by up to 52% by using controlled spraying (i.e., reducing overspray), low-styrene and styrene-suppressed materials, and nonatomizing application equipment. Also, calculated emission factors were 1.6-2.5 times greater than the mid-range EPA emission factors for the corresponding gel coat and resin application. These results indicate that facilities using existing EPA emission factors to estimate emissions in open molding processes are likely to underestimate actual emissions. Facilities should investigate the applicability and feasibility of these P2 options to reduce their styrene emissions.

Air Pollutants, Occupational↗
PubMed1999

Hypersensitivity pneumonitis from Pezizia domiciliana. A case of El Niño lung.

A previously healthy woman developed severe dyspnea and was found to have restrictive lung disease and evidence of alveolitis. Open lung biopsy revealed extrinsic allergic alveolitis (hypersensitivity pneumonitis). The etiology was not initially apparent, but a home inspection showed an unusual mushroom growing in the patient's basement. Air sampling and serum precipitins against the fungal antigens confirmed that Pezizia domiciliana was the cause of the patient's hypersensitivity pneumonitis. This is the first described case of hypersensitivity pneumonitis cause by P. domiciliana. We speculate that unprecedented rainfall and flooding of the patient's basement as a result of El Niño rains produced ideal factors for the growth of this fungus.

Alveolitis, Extrinsic Allergic↗
PubMed1999

Polymyalgia, hypersensitivity pneumonitis and other reactions in patients receiving HMG-CoA reductase inhibitors: a report of ten cases.

Ten patients who take hydroxy-methylglutaryl coenzyme A reductase inhibitors, or statin medications, and experience adverse reactions are described. All patients experienced various manifestations of hypersensitivity while receiving the drugs. One patient is described with hypersensitivity pneumonitis, which was graphically demonstrated by both high resolution computerized axial tomography and open lung biopsy.

Aged↗
PubMed1997

Persistent cauda equina syndrome following bilateral aortoiliac dissection as a complication of cardiac angiography.

Cardiac angiography is accepted as an invasive yet safe procedure with well-characterized complications. We present a complication heretofore not described to our knowledge, in which a patient experienced the cauda equina syndrome following bilateral aortoiliac dissection during cardiac angiography. Similarities are noted between this complication and those documented in abdominal aortic aneurysm repair surgery.

Aged↗
PubMed1996

C-type natriuretic peptide-mediated coronary vasodilation: role of the coronary nitric oxide and particulate guanylate cyclase systems.

OBJECTIVES: We tested the hypothesis that C-type natriuretic peptide (CNP) mediates coronary vasodilation through activation of cyclic guanosine monophosphate (cGMP) by way of particulate guanylate cyclase. BACKGROUND: CNP has known peripheral vasodilator properties, and preliminary data have suggested that it can function as a coronary vasodilator. METHODS: The actions of CNP were studied in instrumented dogs and in organ chamber rings in the presence and absence of a known antagonist to particulate guanylate cyclase, HS-142-1. Additionally, the actions of HS-142-1 were tested on acetylcholine-mediated coronary vasodilation, and immunohistochemical staining was utilized to localize the presence of CNP in the coronary endothelium. RESULTS: CNP relaxed isolated coronary arteries with (mean +/- SEM 45.9 +/- 7%*) and without (72.0 +/- 7%*) an endothelium (*p < 0.05 for CNP effect alone, p < 0.05 for endothelium vs. no endothelium with CNP). Intracoronary infusions increased coronary blood flow (baseline, 64.6 +/- 5.1 ml/min; CNP-5, 79.9 +/- 6.1*; CNP-20, 103.3 +/- 13.6* [*p < 0.05 vs. baseline value]) and reduced coronary vascular resistance (baseline, 1.6 +/- 0.3 mm Hg/ml per min; CNP-5, 1.4 +/- 0.3*; CNP-20, 1.2 +/- 0.3*). Intracoronary injections increased coronary blood flow (delta baseline coronary flow, 30 +/- 9* ml/min [*p < 0.05]). HS-142-1 significantly attenuated these increases (delta coronary flow, 30 +/- 9* ml/min [CNP] to 14 +/- 6 [CNP + HS-142-1] [p < 0.05 CNP vs. CNP + HS-142-1]) and the relaxation of organ chamber rings (56 +/- 7% [CNP] to 18 +/- 6% [HS-142-1 + CNP]). Finally, CNP was localized to the coronary endothelium and smooth muscle by immunohistochemical staining. CONCLUSIONS: CNP functions as a coronary vasodilator through activation of cGMP by way of particulate guanylate cyclase. CNP-mediated coronary vasodilation is attenuated by intracoronary HS-142-1. Intracoronary HS-142-1 does not affect acetylcholine-mediated coronary vasodilation. These observations support a role for exogenous CNP as a potent coronary vasodilator.

Animals↗
PubMed1994

Interrelationships between pulmonary and extrapulmonary involvement in systemic sclerosis. A longitudinal analysis.

PURPOSE: (1) To evaluate the relationship between the degree of pulmonary involvement by systemic sclerosis (SSc) and the degree of involvement of other organ systems by SSc at baseline. (2) To assess the degree of impairment in lung function at presentation and the annual rate of change in lung function to predict the rate of progression of involvement of extrapulmonary organ systems by SSc over time. (3) To determine whether survival in patients with SSc can be predicted from the degree of lung function impairment at baseline or from the annual rate of change in lung function. METHODS: Semiquantitative indices of pulmonary and extrapulmonary involvement and pulmonary function tests (PFTs) were analyzed and compared in 62 nonsmoking scleroderma patients enrolled in a 3-year prospective drug trial, vs 47 in a "study group" who underwent serial evaluation. The other 16 "early withdrawals" withdrew prior to the second evaluation. The indices of organ system involvement were based on clinical, physiologic, and biochemical findings as previously published. The PFTs included total lung capacity (TLC), forced vital capacity (FVC), FEV1, and single-breath diffusing capacity for carbon monoxide (Dsb). Annualized rates of change in PFTs and indices of extrapulmonary involvement were calculated for each subject from data collected on at least 2 separate occasions at least 6 months apart. Spearman rank correlations were performed between individual baseline PFTs (expressed as percent predicted) and (a) indices of extrapulmonary involvement at baseline, (b) annualized rates of change in PFTs, and (c) annualized rates of change in indices of extrapulmonary involvement. Correlations also were performed between the rate of change in each lung function measure and rates of change in indices of extrapulmonary involvement. The ability of PFTs at baseline and their rates of change to predict cumulative survival was assessed by Cox stepwise regression. RESULTS: The degree of impairment in baseline PFTs was related to involvement of the right side of the heart but not to other extrapulmonary system involvement. Baseline PFTs were not related to the rate of subsequent decline of lung function or worsening of extrapulmonary organ system involvement. Subsequent annual rates of decline in lung function were related to worsening skin and upper gastrointestinal involvement. Cumulative survival may be related to the rate of decline in DCO, TLC, and FVC, but was not predicted by impairment in any measure of lung function. CONCLUSION: With the exception of involvement of the right side of the heart consistent with cor pulmonale, the degree of pulmonary involvement by SSc was not correlated with the extent of extrapulmonary involvement. The degree of pulmonary involvement by SSc did not predict subsequent worsening of either pulmonary or extrapulmonary involvement. Worsening pulmonary involvement by SSc, in general, does not correlate with worsening involvement of extrapulmonary organ systems, except for the skin and upper gastrointestinal tract. A rapid decline in DCO or lung volumes may predict poor survival.

Bone Diseases↗
PubMed1994

Pleural effusion associated with ipsilateral breast and arm edema as a complication of subclavian vein catheterization and arteriovenous fistula formation for hemodialysis.

A 38-year-old woman with end-stage kidney disease presented with a pleural effusion and profound edema of the ipsilateral arm and breast. A patent hemodialysis arteriovenous fistula access was present in the involved extremity. Brachiocephalic vein stenosis, as a result of previous dialysis catheter placement in the subclavian vein, was demonstrated by ultrasound imaging and Doppler analysis. Takedown of the arteriovenous fistula in the edematous arm along with living-related kidney transplantation caused immediate resolution of the breast and arm edema and rapid clearing of the effusion. An anatomic explantation for the findings is offered.

Adult↗
PubMed1993

Atrial natriuretic peptide in heart failure.

Atrial natriuretic peptide hormone of cardiac origin, which is released in response to atrial distension and serves to maintain sodium homeostasis and inhibit activation of the renin-angiotensin-aldosterone system. Congestive heart failure is a clinical syndrome characterized by increased cardiac volume and pressure overload with an inability to excrete a sodium load, which is associated with increased activity of systemic neurohumoral and local autocrine and paracrine mechanisms. Circulating atrial natriuretic peptide is greatly increased in congestive heart failure as a result of increased synthesis and release of this hormone. Atrial natriuretic peptide has emerged as an important diagnostic and prognostic serum marker in congestive heart failure. In early heart failure, it may play a key role in preserving the compensated state of asymptomatic left ventricular dysfunction. Despite increased circulating atrial natriuretic peptide in heart failure, the kidney retains sodium and is hyporesponsive to exogenous and endogenous atrial natriuretic peptide. The mechanism for the attenuated renal response is multifactorial and includes renal hypoperfusion, activation of the renin-angiotensin-aldosterone and sympathetic nervous systems. Therapeutic strategies to potentiate the biologic actions of atrial natriuretic peptide may prolong the asymptomatic phase and delay progression to overt congestive heart failure.

Animals↗
PubMed1993

Cardiorenal and neurohumoral function in a canine model of early left ventricular dysfunction.

BACKGROUND: Recent studies have reported that asymptomatic left ventricular dysfunction (ALVD) in humans is characterized by early neurohumoral activation. Specifically, atrial natriuretic factor (ANF) and norepinephrine are activated without activation of the renin-angiotensin-aldosterone system (RAAS). The current study describes hemodynamic and renal function associated with this neurohumoral profile in a canine model of early and presumably "asymptomatic" ventricular dysfunction. We hypothesized that the neurohumoral profile observed in ALVD is associated with preservation of renal function despite significant hemodynamic compromise. METHODS AND RESULTS: ALVD was produced by ventricular pacing at 180 beats per minute for 10 days. Intravascular volume expansion was performed before and after producing ALVD in eight conscious dogs. The model of ALVD was characterized by decreases in ejection fraction (48 +/- 2 to 29 +/- 4%), cardiac output (4.64 +/- 0.29 to 2.89 +/- 0.17 L/min), and mean arterial pressure (119 +/- 4 to 108 +/- 4 mm Hg). Atrial pressures and systemic vascular resistance were increased. ANF (60 +/- 19 to 165 +/- 27 pg/mL) and norepinephrine (382 +/- 127 to 690 +/- 211 pg/mL) were activated, whereas the RAAS was not. Creatinine clearance and sodium excretion (UNa V) were unchanged after producing ALVD. The natriuretic response to volume expansion in ALVD was completely intact, with increases in UNa V similar to that observed with volume expansion in ALVD was completely intact, with increases in UNa V similar to that observed with volume expansion before producing ALVD. CONCLUSIONS: The current study demonstrates that significant ventricular dysfunction with peripheral vasoconstriction can be associated with normal renal function and thus suggests an important functional role for the neurohumoral profile of ALVD in preserving sodium balance.

Animals↗
PubMed1992

Effects of smoked marijuana of varying potency on ventilatory drive and metabolic rate.

Ventilatory responses to hypercapnia in experienced marijuana smokers have previously been shown to decrease, increase, or not change acutely after marijuana. In one study, minute ventilation (VE) and O2 consumption (VO2) increased but hypoxic ventilatory response did not change after smoking marijuana. We further investigated the effects of marijuana of increasing potency (0, 13, and 20 mg THC) on ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia in 11 young, healthy men who smoked marijuana regularly but refrained from any smoked substance, alcohol, caffeine, or other drugs for greater than or equal to 12 h before study. Ventilatory and P0.1 responses to hypoxia and hypercapnia were measured on 3 separate days before and 5 and 35 min (hypoxia) and 15 and 45 min (hypercapnia) after smoking. In a companion 3-day study, 12 young male habitual marijuana smokers underwent measurements of VE, VO2, and CO2 production (VCO2) before and 5 to 135 min after smoking marijuana containing 0, 15, or 27 mg THC. None of the active marijuana preparations caused significant changes in ventilatory or P0.1 responses to either hypercapnia or hypoxia or in resting VE, VO2 or VCO2. We conclude that smoking marijuana (13 to 27 mg THC) has no acute effect on central or peripheral ventilatory drive or metabolic rate in habitual marijuana smokers. These conclusions cannot be applied to infrequent users of marijuana without further study.

Adult↗
PubMed1990

Ventilatory and diffusion abnormalities in potential heart transplant recipients.

Few data are available concerning pulmonary function in patients with severe chronic congestive heart failure. Of 315 patients evaluated for potential cardiac transplantation at UCLA, 132 underwent pulmonary function tests. The latter patients had severe heart failure with a mean left ventricular ejection fraction of 19 percent and mean cardiac index of 2.1 L/min/m2. Diffusion impairment either alone or combined with restrictive and/or obstructive ventilatory defects occurred in 67 percent of the patients evaluated. Diffusion impairment occurred as the sole abnormality in 31 percent of the patients and in combination with a restrictive ventilatory defect in 21 percent. A reduction in diffusing capacity has not been previously described as a frequent finding in patients with chronic congestive heart failure. In contrast to other studies involving patients with acute heart failure, obstructive ventilatory defects were uncommon. None of the lung function abnormalities was associated with smoking status, prior drug use, chest roentgenographic changes, hemodynamic findings, or clinical features, including duration of congestive heart failure. The mechanism for the diffusion impairment is unclear but could be due to chronic passive congestion with pulmonary fibrosis and/or recurrent pulmonary emboli. Recognition of diffusion impairment as a common finding in patients with severe chronic congestive heart failure who are candidates for heart transplantation is important for proper interpretation of possible post-transplant changes in diffusing capacity due to other causes.

Adult↗
PubMed1990

Propionate inhibits hepatocyte lipid synthesis.

Oat bran lowers serum cholesterol in animals and humans. Propionate, a short-chain fatty acid produced by colonic bacterial fermentation of soluble fiber, is a potential mediator of this action. We tested the effect of propionate on hepatocyte lipid synthesis in rats using [1-14C]acetate, 3H2O, and [2-14C]mevalonate as precursors. Propionate produced a statistically significant inhibition of cholesterol biosynthesis from [1-14C]acetate at a concentration of 1.0 mM and from 3H2O and [2-14C]mevalonate at concentrations of 2.5 mM. Propionate also produced a significant inhibition of fatty acid biosynthesis at concentrations of 2.5 mM using [1-14C]acetate as a precursor. The demonstration of propionate-mediated inhibition of cholesterol and fatty acid biosynthesis at these concentrations suggests that propionate may inhibit cholesterol and fatty acid biosynthesis in vivo and may mediate in part the hypolipidemic effects of soluble dietary fiber. Further studies are needed to clarify this action of propionate and to establish the exact mechanisms by which the inhibition occurs.

Animals↗
PubMed1989

Neurogenic pulmonary edema after trigeminal nerve blockade.

Acute neurogenic pulmonary edema developed immediately after injection of bupivacaine hydrochloride into the trigeminal cistern of a 32-year-old man with atypical facial pain and no prior history of cardiopulmonary problems. This complication of trigeminal nerve blockade has not been reported previously, to our knowledge. Associated neurologic deficits suggest a key role for the brain stem in the pathogenesis of this disorder.

Adult↗
PubMed1985

The course of steroid release by intact ovarian follicles of Atlantic salmon (Salmo salar) incubated in vitro with and without gonadotrophin.

Intact ovarian follicles were dissected from a single ovary and groups of follicles incubated in balanced saline at 6 degrees with and without a pacific salmon gonadotrophin (GTH) preparation. Aliquots of the incubation media were withdrawn at intervals, the steroids were extracted with solvent, and 17 alpha, 20 beta-dihydroxy-4-pregnen-3-one (17 alpha 20 beta P), 17 alpha-hydroxyprogesterone, progesterone, androstenedione, testosterone, and oestradiol were separated chromatographically and measured by radioimmunoassay. The main findings were (1) germinal vesicle breakdown commenced on Day 8 under the influence of GTH, (2) after an induction period of about 2 days there was a dramatic and continuing release of 17 alpha 20 beta P in the presence of GTH, (3) GTH promoted a moderate release of 17 alpha-hydroxyprogesterone, (4) GTH stimulated testosterone release up to Day 6 but thereafter levels fell, reflecting either absorption or catabolism of the released steroid, (5) GTH induced a precipitous release of androstenedione during the first few hours of incubation, and (6) progesterone and oestradiol release were little affected by GTH. Steroid concentrations were also measured in ova stripped from naturally ovulating wild fish and the relative amounts were shown to bear some similarity to those released into the incubation medium in the presence of GTH. The routes of biosynthesis and functions of these steroids are considered in light of the results.

17-alpha-Hydroxyprogesterone↗