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Biomedical subjects

J C Ware

Publications and source records attributed to J C Ware.

At least 19 recordsLinked to original sources
PubMed1998

Sleep apnea in obese miniature pigs.

We postulated that three extremely obese Yucatan miniature pigs would have more sleep apnea than three nonobese Yucatan miniature pigs. Pigs were studied with the use of electroencephalograms, inductance plethysmography, oximetry, expired nasal CO2, or thermistors. All of the obese pigs, but none of the nonobese pigs, had both sleep apnea (8.5, 10.3, and 97.0 in obese pigs vs. O apnea + hypopnea/h in all nonobese pigs; P < 0.05) and oxyhemoglobin desaturation episodes during sleep [9.4 +/- 3.0 vs. 0 + 0.53 (SD) mean desaturation episodes/h in obese pigs vs. nonobese pigs, respectively; P < 0.05]. Two of the extremely obese pigs had obstructive sleep apnea, whereas the third obese pig had central sleep apnea. We conclude that sleep apnea occurs in extremely obese Yucatan minipigs and suggest that this animal can be used as a model for sleep apnea in obesity.

Animals↗
PubMed1998

Nasal patency and the effectiveness of nasal continuous positive air pressure in obstructive sleep apnea.

Nasal airway obstruction may exacerbate sleep apnea and is difficult to quantify on clinical examination. In this study, we examined the relationship among nasal patency, the frequency of sleep apnea events, and effective nasal continuous positive air pressures. Acoustic rhinometry was used as an objective measurement of nasal cross-sectional areas in 76 patients without nasal symptoms who underwent study with diagnostic polysomnography because of obstructive sleep apnea. Patients with persistent obstructive sleep apnea were titrated to nasal continuous positive air pressure in a split night study. All subjects had a mean apnea/hypopnea index of 28, and those with obstructive sleep apnea had a mean apnea/hypopnea index of 43. Mean cross-sectional areas 1 to 4 cm into the nose were 1.7, 1.1, 2.1, and 2.8 cm2, respectively (F = 39, p < 0.001). However, there was no correlation between the apnea/hypopnea index and the cross-sectional area at the four distances (r = 0.03, 0.06, 0.02, and 0.02, respectively, p = not significant). Correlations between nasal continuous positive air pressures and cross-sectional areas did not reveal a significant relationship at any of the four sites (r = 0.09, 0.07, -0.03, 0.00, respectively). Findings in patients with apnea were also compared with those in patients without apnea and significant differences were not found (F = 0.019, p = not significant). Although it would seem intuitive that increased nasal obstruction is associated with the severity of obstructive sleep apnea and difficulty with the use of nasal continuous positive air pressure, this study shows that nasal patency, as measured by acoustic rhinometry, does not correlate with the severity of obstructive sleep apnea, as determined by the apnea/hypopnea index or the effective nasal continuous positive air pressure.

Adult↗
PubMed1997

Sleep-related erections: absence of change following presleep sexual arousal.

We examined the effects of a brief period of sexual arousal before sleep on sleep-related erections (SREs) to add to our knowledge concerning those factors that affect SREs. Twelve subjects watched a 5 minute sexually explicit video before sleep. On other evenings they watched a dysphoric arousal video or a lecture (neutral) video. Sleep and SREs were recorded throughout the following night. Although the brief sexual arousal video produced a full or near full erection in all subjects, no significant effect on subsequent SREs occurred. We conclude that the control of SREs in young healthy subjects is insulated against the effect of a brief period of sexual arousal before sleep.

Adult↗
PubMed1997

Minimal rebound insomnia after treatment with 10-mg zolpidem.

This study examined rebound insomnia after discontinuation of chronic use of zolpidem (10 mg), a short elimination half-life imidazopyridine. The zolpidem group was bracketed by a placebo group and a positive control group taking 0.5 mg of triazolam (twice the recommended dose), which is known to produce rebound insomnia. Ninety-nine patients with sleep complaints that were polysomnographically documented participated in the study. After randomization, patients completed a 2-night, single-blind, placebo baseline period, a 28-night double-blind treatment phase, and a 3-night, single-blind, placebo substitution period. Polysomnographic and subjective sleep variables indicated a lack of rebound insomnia for the zolpidem group. The positive triazolam control group had rebound insomnia only on the first discontinuation night. There was no significant correlation between rebound insomnia and the level of initial insomnia, the degree of response to treatment in week 4, or the amount of tolerance that developed during drug use. During the 4-week treatment period, efficacy diminished for both drugs. From these data, it cannot be determined whether the lack of rebound insomnia with zolpidem is a result of drug dose or some property of the drug such as receptor selectivity.

Adult↗
PubMed1996

Narcolepsy.

Narcolepsy is a commonly under diagnosed or misdiagnosed problem that results in severe daytime sleepiness. There is a strong genetic component with some immune system involvement. It may occur in combination with other sleep disorders such as sleep apnea complicating its treatment. An objective diagnosis requires a polysomnogram and Multiple Sleep Latency Test. Management depends on the careful use of stimulant medication to control the sleepiness and other medications to control the auxiiliary symptom of cataplexy.

Amphetamines↗
PubMed1994

The acute effects of nefazodone, trazodone and buspirone on sleep and sleep-related penile tumescence in normal subjects.

This study examined the effects of nefazodone, trazodone and buspirone on sleep and sleep-related penile tumescence. Trazodone is a sedating antidepressant without anticholinergic properties. Nefazodone is a new antidepressant that is a structural analogue of trazodone but is less sedating. Buspirone is a nonsedating, nonbenzodiazepine anxiolytic with antidepressant properties. Nefazodone was compared to trazodone and buspirone in a double-blind, placebo-controlled crossover study in 12 normal healthy males. Nefazodone increased rapid eye movement (REM) sleep, whereas trazodone and buspirone suppressed REM sleep. The drugs only minimally affected other sleep stages. Trazodone increased total tumescence time by delaying the onset of detumescence; nefazodone increased total tumescence time only insofar as it increased REM sleep; buspirone did not change total tumescence time when compared to placebo. The results support a growing body of data indicating that not all antidepressants suppress REM sleep. The results also are consistent with the interpretation of an earlier study showing that trazodone prolongs penile tumescence during sleep as a result of its alpha-adrenergic blocking properties that suppress detumescence. Nefazodone, with less alpha-adrenergic blocking activity, did not abnormally penile tumescence beyond REM sleep.

Adult↗
PubMed1992

Characteristics of penile erections during sleep recorded from normal subjects.

The results of penile tumescence recordings from first- and second-night polysomnograms from 146 normal subjects are presented for four age groups. The data are in close agreement with basic tumescence parameters that have been presented earlier. In addition, results from first and second nights are compared, and data are presented from base and coronal sulcus (tip) recordings locations. The results indicate that tumescence parameters that are most correlated with rapid-eye-movement sleep are those most likely to significantly differ from the first to the second night. Base and tip recordings closely paralleled each other. Additionally, tumescence periods were also divided into three phases that are likely to correspond to different physiological states. These three phases, Tup, Tmax, and Tdown, vary in their sensitivity to night and age effects. It is hypothesized that changes in different tumescence phases may reflect different pathophysiologies.

Adult↗
PubMed1991

Pathophysiology of prolonged penile erection associated with trazodone use.

Treatment with the antidepressant trazodone has been associated with the occurrence of prolonged penile erection and priapism. To evaluate the effect of trazodone on erection we monitored the periodic physiological sleep-related erections in 6 healthy volunteers in a double-blind crossover study comparing the effect of trazodone, trimipramine (a tricyclic antidepressant) and placebo. In addition, to determine the effects of trazodone on the neurovascular control of penile smooth muscle we performed in vitro studies on corpus cavernosum tissue obtained from patients undergoing penile prosthesis implantation. Trazodone significantly increased the total interval of nocturnal erectile activity, while trimipramine had no effect. During the high dose treatment (nights 4 and 5) the average duration of erectile activity per night with placebo was 158 +/- 41 minutes (mean +/- standard deviation) for night 4 and 177 +/- 21 minutes for night 5. During trazodone treatment the erectile activity per night was significantly prolonged to 285 +/- 115 minutes during night 4 and 232 +/- 86 during night 5 (p less than 0.01). Analysis of the erectile activity in relation to the rapid eye movement sleep period during which erectile activity usually occurs revealed that the detumescence phase of erection, under sympathetic control, was significantly prolonged an average of 2.4 times by trazodone compared to placebo (p less than 0.05). In vitro, trazodone at concentrations comparable to those reached in plasma significantly impaired corporeal smooth muscle contractions elicited by electrical stimulation of adrenergic nerves and antagonized contractions induced by exogenous norepinephrine. We conclude that trazodone can enhance penile erection in man and propose a mechanism related to the alpha-adrenoceptor blocking properties of trazodone by interference with the sympathetic control of penile detumescence.

Adolescent↗
PubMed1991

Diagnosis and treatment of insomnia and depression.

Disturbed sleep is a common problem particularly among depressed patients. Diagnostic and treatment considerations are reviewed for two of the more common insomnia problems, psychophysiological insomnia and insomnia associated with depression. Studies of the actual sleep patterns of patients with these disorders reveal reliable differences that are important to understand for optimized treatment outcome. As the differentiation of sleep disorders becomes more precise and the pharmacologic armamentarium becomes greater, emphasis needs to be placed on both understanding the etiology of the sleep complaint and selecting a drug that is best matched to correct the underlying problem.

Antidepressive Agents↗
PubMed1990

Estazolam and flurazepam: a multicenter, placebo-controlled comparative study in outpatients with insomnia.

A multicenter, double-blind placebo-controlled clinical trial was designed to compare the safety and efficacy of estazolam compared with flurazepam as hypnotics. Outpatients complaining of insomnia were randomized to receive either estazolam 2 mg, flurazepam 30 mg or placebo for 7 consecutive nights. The analysis of efficacy was based on the patients' daily assessments of sleep and the investigators' global evaluations. Adverse events which were considered by the investigator to be attributable to, or of unknown relationship to the test medication were analyzed. The patient subjective questionnaire indicated that estazolam and flurazepam significantly improved all parameters (P less than .05) as compared to placebo. A marked or moderate improvement in sleep was reported by 81% (58/72), 78% (63/81) and 36% (27/76) of estazolam, flurazepam, and placebo recipients, respectively. There were no significant differences in hypnotic effect between estazolam and flurazepam. All efficacy parameters of the investigators' global evaluation improved significantly more (P less than .05) for patients receiving estazolam or flurazepam (except quality of sleep) than for those receiving placebo. The percentage of patients reporting any adverse experience was greatest for flurazepam (72%), followed by estazolam (59%), and placebo (43%). Somnolence and hypokinesia were the most commonly reported adverse events. An analysis of the global evaluation of side effects showed that flurazepam had a significantly worse side effect profile than estazolam (P less than .05) or placebo (P = .001). Estazolam and flurazepam effectively, and comparably, relieved insomnia when administered for 7 nights in adult patients complaining of insomnia. Estazolam demonstrated a more favorable side effect profile than flurazepam.

Ambulatory Care↗
PubMed1990

Increased deep sleep after trazodone use: a double-blind placebo-controlled study in healthy young adults.

The effects of trazodone on sleep were compared with those of placebo and the sedating tricyclic antidepressant trimipramine in a double-blind crossover study in six healthy young men. Only trazodone significantly increased deep sleep without otherwise altering the normal architecture of sleep. The alpha-adrenergic receptor-blocking property of trazodone and a relative lack of noradrenergic reuptake blocking and the lack of anticholinergic effects are hypothesized to be responsible for the effects on sleep.

Adolescent↗
PubMed1989

Effects of clomiphene citrate on episodic luteinizing hormone secretion throughout the menstrual cycle.

Pituitary luteinizing hormone secretory dynamics (pulse frequency and amplitude) were evaluated in eight normal women administered clomiphene citrate or placebo. After 5 days of treatment clomiphene citrate was found to increase mean luteinizing hormone secretion by increasing the amount of pituitary luteinizing hormone released per pulse. No change in pituitary luteinizing hormone interpulse interval was found in the follicular phase of the cycle, although a faster pulse frequency in the luteal phase was found after clomiphene citrate when compared with placebo. No differences were found in the luteal phase (pulse frequency, amplitude, and mean luteinizing hormone level) after clomiphene citrate versus placebo in the volunteers. These data suggest that the principal mechanism of action of clomiphene citrate is an increase in the concentration of hypothalamic gonadotropin releasing hormone into the hypothalamic-pituitary portal circulation, with a resultant increase in pituitary luteinizing hormone secretion.

Adult↗
PubMed1989

Effects on sleep: a double-blind study comparing trimipramine to imipramine in depressed insomniac patients.

Trimipramine, a sedating tricyclic antidepressant, and imipramine were compared on polysomnographic parameters during a 4-week double-blind trial in depressed patients with insomnia and anxiety. Trimipramine eliminated objective evidence of sleep disturbance. This was not the case with imipramine, although depression improved similarly in both groups. Subjects' sleep appeared unchanged or more disturbed at the end of the treatment with imipramine. For trimipramine, the major changes in sleep parameters occurred during the first week of drug administration and did not parallel the gradual changes seen in the measures of depression. Additionally, trimipramine did not suppress REM sleep even in a subgroup of six trimipramine patients who had short rapid-eye-movement (REM) sleep latencies during the placebo baseline period, even though their depression was alleviated. The data demonstrate that (a) antidepressants may vary in their effects on sleep, even though they have similar effects on depression; (b) REM sleep suppression does not necessarily accompany improvement in depression; and (c) reports of improved sleep by patients undergoing antidepressant therapy may not reflect improvement on objective measures of sleep. The different sleep effects suggest the possibility of different antidepressant pathways.

Adolescent↗
PubMed1989

Impotence and aging.

Taking into account the normal changes that occur with aging and the large number of pathologies, pharmacologic agents, and social situations that the elderly are subject to, it is perhaps more surprising that 25 per cent of those over 80 years of age do report normal sexual functioning. Loss of erectile capability appears to be multifactorial in many patients, although the exact degree is uncertain due to unsystematic assessment in the majority of current studies. Unfortunately, impotence is often ignored by the patients' physicians. Physicians do not routinely ask about erectile functioning in their patients, perhaps because they do not know how to systematically evaluate and treat the complaint. Any follow through that might result from a complaint is often chaotic. And, rarely are treatment possibilities systematically and clearly presented to the patient. This is particularly true for the elderly patients whose physicians may be surprised that an elderly patient would still be interested in sexual behavior. No matter how subtle, this "dirty old man" response by the physician does not foster a good therapeutic environment. Inappropriate and unsystematic evaluations of impotent patients leads to a literature replete with contradictory statements. Because of the prevalence of impotence in the elderly, as a group they are hurt the most by unsystematic evaluation techniques and therefore have the most to gain from the application of systematic evaluation and treatment procedures.

Adult↗
PubMed1988

Destructive bruxism: sleep stage relationship.

Despite apparent similar amounts of bruxism, two groups that had been evaluated polysomnographically differed dramatically in symptomatology. Patients with severe symptoms were referred to as the destructive bruxism group and were compared with (a) a group with sleep disturbance complaints who had bruxism and (b) a group of insomniac depressed patients chosen without regard to bruxism. It was hypothesized that not only the presence of bruxism during sleep but its pattern and sleep stage relationship were factors affecting clinical symptoms. The results indicated that the sleep stage relationship was an important factor. Patients with severe symptoms attributed to nocturnal bruxism were likely to have more bruxism in REM sleep than the other groups. These results if replicated prospectively would help explain some of the discrepancies in the literature concerning sleep stage relationship of bruxism, as well as help explain differences in symptomatology of bruxism patients.

Adult↗
PubMed1988

Peripheral vasoconstriction in patients with sleep related periodic leg movements.

Two patients complaining of insomnia had sleep-related periodic leg movements (nocturnal myoclonus) on polysomnographic evaluation. Both also complained of cold feet and had abnormal peripheral pulse examinations. Treatment with phenoxybenzamine, alpha-adrenergic blocker, normalized the peripheral pulse responses, reduced the complaint of insomnia, and reduced the sleep related leg movements but resulted in only mild sleep improvements. Peripheral pulse examinations of ten other patients with sleep-related periodic leg movements revealed abnormal responses in four. From these and other results, it is hypothesized that the sympathetic nervous system may mediate the periodicity of sleep related periodic leg movements.

Adrenergic alpha-Antagonists↗