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Biomedical subjects

J L Kinney

Publications and source records attributed to J L Kinney.

16 recordsLinked to original sources
PubMed1998

Nomograms to follow recovery rate in status asthmaticus in a veteran population.

Data from 12 Department of Veterans Affairs patients hospitalized for status asthmaticus were analyzed to determine the rate and degree of response to therapy. The time to achieve recovery was directly related to the level of baseline obstruction at the time of hospital admission. The recovery rate was constant and could be described by a single second-degree polynomial regression equation. Nomograms were constructed showing this rate of improvement of pulmonary function over time at four levels of baseline pulmonary obstruction.

Aminophylline↗
PubMed1985

Sleep apnea syndrome and essential hypertension.

More than half of patients with essential hypertension have sleep apnea. The incidence of unrecognized sleep apnea in patients with essential hypertension was assessed. Twenty-three patients taking antihypertensive medication were selected at random from a hypertension clinic. They were evaluated by questionnaire for symptoms of sleep apnea, and during 3 hours of sleep, measurements were made of respiratory patterns using an impedance pneumograph, arterial O2 saturation with an ear oximeter and air flow at the mouth or nose with a face mask pneumotacograph. Abnormal sleep apneas (average 20 seconds) lasting for an average of 19% sleep time were found in 11 patients (48%). Significant arterial O2 desaturation, defined as a decrease of at least 4% and to less than 90%, was observed in 7 of these 11 (30%), with an average saturation of 87% at the end of the apneic episodes. Thus, almost one-third of patients randomly selected had significant arterial O2 desaturation during sleep because of sleep apnea, and it is suggested that sleep apnea may play a part in the development of essential hypertension.

Adult↗
PubMed1984

The effect of high dose glucocorticoid therapy on immunoglobulin E in asthma.

Serum IgE levels were measured before and after high dose intravenous methylprednisolone therapy in 14 patients with severe asthma. Eight patients received methylprednisolone 125 mg every 6 hours, four received methylprednisolone 60 mg every 6 hours, and two patients received hydrocortisone 100 mg every 6 hours. In patients receiving the higher dose, in extrinsic asthma, and in those not recently receiving corticosteroids, total serum IgE levels tended to decrease within a short interval after corticosteroid therapy.

Adult↗
PubMed1984

Antimalarial psychosis revisited.

Drug-induced psychosis resulted from the administration of quinacrine hydrochloride at a dosage of 100 mg twice daily for the treatment of discoid lupus. After two weeks of drug treatment, the patient exhibited symptoms similar to those seen in the manic phase of bipolar affective disorder. Although the incidence of antimalarial psychosis is unclear and perhaps small, we recommend close observation of patients for behavioral changes suggesting the development of antimalarial psychosis. Astute observation, leading to the early detection of behavioral changes, may help avert the development of a costly and disabling complication of drug therapy.

Female↗
PubMed1983

Delayed cutaneous hypersensitivity in normals: choice of antigens and comparison to in vitro assays of cell-mediated immunity.

In 81 normal subjects, ages 19 to 100 yr (mean 52), we studied the prevalence of positive 48 hr skin reactions to six antigens: fluid tetanus toxoid, Candida albicans, SK/SD, Trichophyton, PPD, and coccidioidin. Of these, C. albicans was most frequently reactive (92%); SK/SD (51%) and tetanus (49%) were less so. Each of the remaining three antigens was reactive in less than 42% of the subjects. The minimum number of antigens required to detect delayed hypersensitivity in 100% of subjects was two: C. albicans and tetanus. We found no correlation between skin reactivity at 20 min, 6 hr, and 48 hr for most of the antigens studied, suggesting different mechanisms for reactions occurring at each time. In 60 of the subjects, lymphocyte stimulation index (LSI) with tetanus toxoid and monocyte chemotaxis (MC) assays were done. The natural log of the area of induration at 48 hr after tetanus skin testing (I48) increased as a function of LSI (p less than 0.005) and MC (p less than 0.025) by multiple regression analysis. Skin testing was less sensitive than LSI as a test for cell-mediated immunity in our population. However, because of availability and correlation with LSI, delayed cutaneous hypersensitivity should be tested initially. For this purpose, tetanus toxoid appears to be a useful antigen when used in combination with C. albicans.

Adult↗
PubMed1982

A comparison of skin and bronchial reactivity in asthmatic patients using single, group related and unrelated antigen mixtures.

To test the hypothesis that mixtures of antigens may provide an efficient technique for bronchial challenge, the authors measured the airway response to challenge with individual antigens and groups of related and unrelated antigens. The data suggest that the hypothesis is correct for grass antigens. Grass antigens were associated with all positive challenges observed in the group challenges. Positive bronchial challenges were not found in the mixtures that did not contain grass antigen.

Adult↗
PubMed1980

A comparison of diluent and methacholine challenge with spirometry and the body plethysmograph.

Bronchial reactivity to inhaled diluent and methacholine was determined for asthmatics using automated spirometry. These data were compared with challenge data from a matched group of asthmatics previously studied plethysmographically. High correlations were obtained between all indices both groups, suggesting that spirometry is adequate for the clinical characterization of the methacholine response.

Adult↗
PubMed1980

The asthmatic airway response to inhaled antigen.

The airway response to inhaled antigen was measured in asthmatic patients at 5, 10 ad 20 minutes following bronchial challenges. The over-all frequency of positive responses in the 26 individual challenges was 27%. There were no significant differences between the 5-, 10- or 20-minute responses. Patients with positive responses to bronchial challenge manifested high grade skin reactivity by intradermal tests. Positive responses to bronchial challenge occurred only at 1 X 10(-3) weight/volume (w/v) concentration of inhaled antigen. Although the degree of methacholine reactivity was related to positive antigen challenge, two subjects with a positive challenge had minimal methacholine reactivity.

Adult↗
PubMed1977

Cardiorespiratory effects of temperature in the turtle, Pseudemys floridana.

Weight specific VO2 of resting Pseudemys floridana at body temperatures (BT) between 12 to 38 C was studied in relationship to VE, VT, f, pulmonary and systemic blood flow, and blood PO2, PCO2, pH and O2 content. The slope of the curve for VO2 against body mass was similar to that for mammals and differed from that of lizards. VE increased with BT while VE/VO2 fell, resulting in an elevation of arterial PCO2 and a decline in arterial pH of 0.013 unit/degrees C [HCO-3] and total CO2 remained constant. Increments in VE were achieved by decreasing apneic time and increasing VT up to VT of 18 ml.kg-1 when further rise in VE was exclusively on account of breathing frequency. Mean pulmonary and arterial blood flows were incremented in direct proportion to VO2, and no net intracardiac shunts was demonstrable. Ventilation-perfusion ratio fell with BT while EO2 increased. Arterial hemoglobin saturation varied inversely with BT while the arteriovenous O2 difference remained constant. EO2 was found to be highly dependent on the constant blood convection requirement as VE/VO2 fell. At similar BT, VE/VO2 was similar to that for man while Qpul/VO2 was in inverse proportion to maximum O2 capacity of the blood for the two species.

Acid-Base Equilibrium↗
PubMed1977

Oxidative cost to ventilation in a turtle, Pseudemys floridana.

Estimates of oxidative cost of ventilation for Pseudemys floridana were obtained by comparison of mean resting VO2 with that obtained while artificially ventilating the lungs with a constant air flow in excess of the normal VE, a circumstance during which the animals remained apneic due to reduction in alveolar PCO2. At a body temperature of 22 degrees C, the oxidative cost attributable to ventilation was 0.0047 ml O2/ml gas ventilated, a value about 10 times that of man. This cost of ventilation is then related to values of VO2 and VE at various body temperatures. The oxidative cost of ventilation, expressed as a percentage of resting VO2, is given by the equation: cost = 0.47 VE/VO2. Relative cost declines with body temperature since VE/VO2 (resting) declines according to the equation: VE(BTPS)/VO2 = -0.017 BT -0.025 log Wt + 2.01 where units are in ml, kg and min. At body temperatures of 10 and 37 C relative costs were 30 and 10% VO2, respectively. While the inverse relation between VE/VO2 and body temperature has important implications for regulation of arterial pH through influencing arterial PCO2, it has the additional meaning of reducing the relative oxidative cost of ventilation as VO2 increases.

Animals↗
PubMedDate not supplied

Variability of pulmonary function tests in stable corticosteroid dependent asthma patients.

We studied 24 corticosteroid dependent asthmatic patients over a period of 10 months to establish a baseline for future therapeutic trials with corticosteroid sparing agents. Clinical symptoms, steroid dose, peak expiratory flow rate (PF), forced expiratory volume in 1 second (FEV1), and forced vital capacity (FVC) were recorded at clinic visits. Correlation was sought between PF and FEV1, steroid dose versus PF and symptom severity, and PF versus time and symptoms. There was considerable weekly variability of PF and FEV1. However, when viewed over almost a year, 54% had no significant change in PF. 29% actually worsened and 17% improved. The data suggest that to assess the effect of a steroid-sparing agent accurately, one must first establish a reliable baseline over several months to eliminate weekly variability. The current trend of obtaining a baseline over a 1 to 2 month interval is inadequate in this study population. We also found that neither patient assessment of severity of symptoms nor corticosteroid dosage correlate with objective spirometric measurements.

Adult↗
PubMedDate not supplied

Nomifensine maleate: a new second-generation antidepressant.

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, drug interactions, dosage, and formulary recommendations for nomifensine maleate are reviewed. Nomifensine is a potent inhibitor of norepinephrine but has little effect on serotonin. It is unique in that it is a potent reuptake inhibitor of dopamine. Nomifensine is rapidly and completely absorbed and is widely distributed throughout the body. The major route of elimination is through the kidneys. Because of its short half-life and resultant lack of accumulation, nomifensine is usually given in divided doses. Nomifensine is approved for the treatment of depression. In clinical trials with imipramine, amitriptyline, nortriptyline, maprotiline, and various investigational antidepressant drugs, it has been found to be as effective as the standard antidepressant agents. In general, nomifensine has been well tolerated by patients and has caused few side effects. It also has not been associated with serious toxic effects in overdose situations. The usual effective dose of nomifensine maleate is 100-200 mg daily given in divided doses. It appears to be a good choice for patients with profoundly retarded depression and for those who cannot tolerate the side effects of traditional antidepressant drugs. Nomifensine should not be used alone in patients with schizoaffective disorders or in patients with agitated depression. Nomifensine is a safe and effective antidepressant with a fairly unique pharmacological profile. Because the drug is relatively safe and causes little sedation, it may offer substantial advantages over the more traditional antidepressants and should be considered for formulary addition.

Chemical Phenomena↗
PubMedDate not supplied

Evaluation of amoxapine.

The pharmacology, pharmacokinetics, clinical trials, side effects, and dosage of amoxapine are reviewed. Amoxapine is a tricyclic dibenzoxazepine antidepressant that is chemically similar to the antipsychotic agent loxapine. In animal tests, amoxapine and its metabolites block reuptake of the neurotransmitter norepinephrine, with little effect on serotonin. It is rapidly and virtually completely absorbed when administered orally; peak serum concentrations occur one to two hours after ingestion. Amoxapine is widely distributed throughout body tissues and is 90% bound to serum proteins. Aromatic hydroxylation in the liver produces two major metabolites, which are excreted in the urine primarily but also in the feces. Amoxapine's elimination half-life is eight hours; one of the metabolites has a long half-life (30 hours). In clinical trials, amoxapine has been compared with amitriptyline and imipramine in several types of depressed patients. In some studies, amoxapine's therapeutic effects were measurable earlier (at one or two weeks after initiation of therapy) than those of the amitriptyline or imipramine, but generally only a portion of the depression-rating scales yielded statistically significant differences. Side effects noted during amoxapine therapy include hypotension (42%), drowsiness (14%), xerostomia (14%), constipation (12%), blurred vision (7%), fatigue (5%), and vertigo (5%). Amoxapine is approved by FDA for use in patients with neurotic or reactive depressive disorders, endogenous or psychotic depression, and depression accompanied by anxiety or agitation. The usual adult dosage is 200-300 mg daily, either in divided doses or a single bedtime dose. Amoxapine is a safe and effective antidepressant with no striking advantages over other available agents.

Amitriptyline↗