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Biomedical subjects

K R Cooper

Publications and source records attributed to K R Cooper.

At least 37 records · Page 2Linked to original sources
PubMed1989

Benefit of nasal CPAP in obstructive sleep apnea is due to positive pharyngeal pressure.

The purpose of this study was to determine if the mechanism of nasal continuous positive airway pressure's (CPAP's) effectiveness is to act as a pneumatic splint or to increase functional residual capacity (FRC) and consequently, upper airway caliber. Four subjects with obstructive sleep apnea underwent 3 nights of polysomnography: night 1, control; night 2, nasal CPAP; night 3, external subatmospheric pressure (ESAP). ESAP, a negative pressure body suit, increases FRC. We measured the changes in FRC with nasal CPAP and ESAP using the weighted spirometer technique. The dose used for the ESAP night was the dose that produced the same FRC as the subject's prescribed nasal CPAP dose. The mean number of arousals and the respiratory events index were higher on ESAP and control nights. Less severe oxygen desaturation occurred during non-rapid-eye-movement sleep on the nasal CPAP and ESAP nights. These preliminary results show that increasing FRC alone does not account for the effectiveness of nasal CPAP, and splinting of the collapsible upper airway is necessary.

Airway Obstruction↗
PubMed1988

Profound pulmonary shunting without edema following stereotaxic biopsy of hypothalamic germinoma. Case report.

Hypoxemia is a nearly constant accompaniment of head injury. Diverse theories have been proposed to explain this relationship. The authors report the case of a patient who suffered an episode of severe, transient, arterial oxygen desaturation during "controlled" brain trauma: an otherwise uneventful stereotaxic biopsy of a small germinoma of the hypothalamus. Evidence is provided that pure ventilation-perfusion mismatching, without pulmonary edema, underlay the hypoxemia. The hypothalamus is intimately involved in matching pulmonary ventilation to perfusion; the hypoxemia of various brain injuries may be mediated by perturbation of this structure.

Adolescent↗
PubMed1987

Behavioral and histological effects of acrylamide in rainbow trout.

A histological and behavioral study was used to assess whether acrylamide produced neurotoxic effects in rainbow trout. Swimming performance of trout exposed to 0, 12.5, or 25 mg/liter acrylamide for 15 days was unaffected. Swimming performance of animals exposed to 50 mg/liter acrylamide for a similar time period was compromised by morbidity and mortality of the animals in this treatment group. The absence of dose-related histological lesions in central neurons, peripheral neurons or muscle suggested that the observed deficit in swimming performance was due to a generalized toxic response. Acrylamide treatment produced dose-related lesions in the gill and liver of rainbow trout.

Acrylamide↗
PubMed1987

Monochloroacetic acid toxicity in the mouse associated with blood-brain barrier damage.

Monochloroacetic acid (MCA) causes front paw rigidity in 10% of mice surviving a single oral toxic dose (320-380 mg/kg). Mice exhibiting front paw rigidity were killed at various times after MCA treatment and their brains were prepared for histological examination. As early as 48 hr post-treatment, RBCs were found outside capillaries in several brain regions, especially the cerebellum. At time points up to 8 weeks after MCA, extracapillary RBCs were seen to be undergoing lysis, and there was loss of cerebellar Purkinje cells. Three hours after oral administration of an LD80 of MCA (380 mg/kg), entry of iv-injected [14C]inulin or [3H]dopamine (1.0 microCi) into all brain regions was significantly increased compared to controls. Increased entry of [14C]inulin into the brains of mice occurred as early as 2 hr after MCA, coinciding with the onset of signs of toxicity, and remained elevated for up to 8 hr following treatment. Further studies revealed that only those mice which were moribund but not those which were unaffected by MCA (380 mg/kg) 4-6 hr after treatment had significantly increased brain levels of [14C]inulin or [3H]dopamine. However, mice which survived an LD80 of MCA and exhibited front paw rigidity 24 hr later also had brain radiotracer concentrations significantly greater than controls. Both the lethal effects of MCA and the physical deficits observed in survivors may be associated with impairment of blood-brain barrier function.

Acetates↗
PubMed1987

Effect of sleep loss on beta-endorphin activity, epinephrine levels, and ventilatory responsiveness.

Sleep loss impairs ventilatory responsiveness to hypercapnia and hypoxia, and also interferes with performance on spirometry. To test the hypothesis that the decline in hypercapnic drive due to sleep loss is mediated by endorphin production, we measured loaded and unloaded CO2 response after injection of placebo and naloxone in 11 normal subjects who were alternately rested and sleep-deprived. Blood for beta-endorphin and epinephrine assay was drawn before testing each day. Unloaded CO2 response was lower after sleep loss than after sleep restoration; naloxone had no effect on this difference. Likewise, there was no difference between CO2 response after naloxone administration and CO2 response in control subjects. beta-Endorphin activity did not rise after sleep loss. Loaded CO2 response was reduced compared to unloaded response and was not affected by sleep loss or by naloxone. The serum epinephrine level rose significantly with sleep loss. We conclude that naloxone is not a respiratory stimulant in normal people, and that it does not reverse the fall in CO2 response that follows sleep loss.

Adolescent↗
PubMed1987

The effect of sleep loss on breathing in chronic obstructive pulmonary disease.

We have previously shown that one night of sleep deprivation results in significant deterioration of spirometric performance and ventilatory responsiveness to inhaled carbon dioxide in normal people. Since even a small decrease in pulmonary function may be clinically important in patients with chronic limitation of airflow, we undertook the present study to assess the effects of sleep loss on breathing in patients with chronic obstructive pulmonary disease (COPD). Criteria for inclusion in this study were a ratio of the forced expiratory volume in one second over the forced vital capacity (FEV1/FVC) of less than 60 percent, no hospital admission for pulmonary disease within two weeks of testing, stable (less than 30 percent variation) in tests of pulmonary function on two occasions within three months of testing, and no history of asthma. We studied 15 men (mean age, 57 +/- 3 years) on two consecutive mornings. Patients were studied with and without sleep deprivation in a randomized fashion. Patients were hospitalized for the study so that sleep deprivation, medications, smoking, and diet could be monitored and enforced. We found small but statistically significant falls in FEV1 (1.06 +/- 0.11 to 1.00 +/- 0.09 L; p less than 0.05) and in FVC (2.56 +/- 0.20 to 2.43 +/- 0.17 L; p less than 0.05) following sleep deprivation. Changes of similar magnitude which were not statistically significant occurred in maximal voluntary ventilation (MVV) and response to carbon dioxide. The arterial oxygen (PaO2) and carbon dioxide (PaCO2) tensions were not affected. Maximal expiratory pressure at the mouth increased slightly, but there was a fall in maximal inspiratory pressure (MIP) at the mouth. We conclude that sleep loss is associated with small but significant falls in FEV1 and FVC, as well as changes of similar magnitude in MVV, minute ventilation, and MIP in patients with severe COPD. Although the sleep loss which frequently accompanies exacerbations of COPD may be a slight additional stress of pulmonary reserve, a single night's loss of sleep in the patient with stable chronic airflow obstruction does not have major clinical consequences.

Aged↗
PubMed1986

Learning effect of repeated hypercapneic ventilatory response testing.

To determine whether hypercapneic ventilatory response (HCVR) is affected by repeated testing, the HCVR of 22 healthy subjects was determined daily for 4 consecutive days. The slope (S) of the HCVR increased to a maximum on Day 3, which was 14% greater than S on Day 1 (p less than 0.05). The increase in airway occlusion pressure during progressive hypercapnea (delta P0.1/delta PCO2) showed no significant change, indicating that although S and delta P0.1/delta PCO2 are both good measurements of ventilatory response, they are not totally interchangeable in normal subjects. A subgroup of 12 subjects (termed "increasers") was responsible for the overall increase in S. For this subgroup, S was significantly smaller on Day 1 than on each subsequent day. Increasers also had a significantly greater value of S on each day of the study than subjects who did not increase ("decreasers"). On Day 1, increasers' S was 3.77 +/- 1.31 L min-1 mm Hg-1, while decreasers' S was 2.46 +/- 1.00 (p less than 0.001). Some normal subjects demonstrate a learning effect during repeated daily testing of HCVR by the rebreathing technique, and those subjects whose S increases are those with large initial values of S.

Adult↗
PubMed1986

Respiratory failure after percutaneous cordotomy.

A 33-year-old woman who had Ondine's curse after high cervical cordotomy for relief of chronic pain maintained adequate ventilation while awake but became apneic as she progressed from light sleep toward stages of deep sleep. After 14 months of successful nocturnal ventilatory support, she died suddenly. Central sleep apnea is common after cervical cordotomy and will usually resolve after several weeks, but can be permanent. Diaphragmatic pacing and mechanical ventilation can be offered for long-term ventilatory support.

Adult↗
PubMed1985

Treatment of theophylline toxicity with oral activated charcoal.

We treated 14 patients who had an initial serum theophylline concentration greater than 30 micrograms/ml (48.3 +/- 19.4 micrograms/ml) and symptoms of theophylline toxicity with oral activated charcoal (OAC). Thirty-gram doses of OAC were administered approximately every two hours for two to four doses. Ten patients tolerated OAC and demonstrated a reduction in theophylline half-life to 5.6 +/- 2.5 hours with resolution of symptoms. Three of these ten patients were treated in the emergency department and discharged, making hospitalization unnecessary. The four patients with the highest initial theophylline concentrations (76.6 +/- 17.7 micrograms/ml) vomited all doses of OAC. Three of these four patients were treated with charcoal hemoperfusion with a reduction in the half-life to 5.2 +/- 1.0 hours. These data support the use of OAC as the primary therapeutic modality in the management of patients with theophylline toxicity. Patients with very high theophylline concentrations (greater than 50 micrograms/ml), however, usually vomit the OAC and may require charcoal hemoperfusion.

Administration, Oral↗
PubMed1985

Safe use of PEEP in patients with severe head injury.

Thirty-three patients with severe head trauma were studied to determine whether the use of positive end-expiratory pressure (PEEP) would cause an increase in intracranial pressure (ICP). Changes in ICP induced by PEEP were then correlated with a panel of physiological variables to try to explain these changes. Mean ICP increased from 13.2 +/- 7.7 mm Hg (+/- standard deviation) to 14.5 +/- 7.5 mm Hg (p less than 0.005) due to 10 cm H2O PEEP, but the eight patients with elevated baseline ICP experienced no significant increase. Cardiac output and venous admixture (Qs/Qt) declined significantly, while central venous pressure, peak inspiratory pressure, functional residual capacity, and arterial pCO2 increased significantly due to PEEP. Blood pressure and cerebral perfusion pressure were unchanged. The change in ICP due to PEEP correlated significantly with a combination of cardiac output, peak inspiratory pressure, Qs/Qt, and changes in blood pressure and arterial pCO2 due to PEEP, indicating that the effect of PEEP on ICP could be largely explained by its effect on hemodynamic and respiratory variables. No patient deteriorated clinically due to PEEP. It is concluded that 10 cm H2O PEEP increases ICP slightly via its effect on other physiological variables, but that this small increase in ICP is clinically inconsequential.

Brain Injuries↗
PubMed1985

Sleep apnea in active acromegaly.

Previous case reports have shown an association between acromegaly and the sleep apnea syndrome (SAS). Some of the patients described had central SAS, raising the possibility that an elevation of the growth hormone (GH) level may cause a defect in respiratory drive. We determined the prevalence of SAS in 21 patients with a history of acromegaly. We separated them into two groups based on serum GH concentrations. Ten patients had active acromegaly (mean GH concentration, 62.2 ng/mL; range, 12.6 to 148 ng/mL), while 11 patients had inactive acromegaly (mean GH, 3.2 ng/mL; range, 0.7 to 6.4 ng/mL). Four of the ten patients with active acromegaly had SAS; none of the 11 patients with inactive acromegaly had SAS. Three patients with SAS had the purely obstructive type, and one had the mixed central and obstructive type. The hypercapnic ventilatory response was normal in all patients tested and was not influenced by the GH level. We conclude that SAS is associated with active acromegaly and that the GH level does not affect the hypercapnic ventilatory response. The absence of SAS in successfully treated patients suggests that it may resolve after a normal GH level is restored.

Acromegaly↗
PubMed1984

Bioconcentration and metabolism of picric acid (2,4,6-trinitrophenol) and picramic acid (2-amino-4,6-dinitrophenol) in rainbow trout Salmo gairdneri.

The bioconcentration and metabolism of picric acid and picramic acid were determined for rainbow trout. The bioconcentration factor (BCF) in the epaxial muscle at 42 d for both of these compounds was less than 1; the skin had a BCF value of 1 and 9, respectively. The half-life (t1/2) elimination for the high and low dose of picric acid was 12.0 and 12.5 d, respectively; and for picramic acid was 9.0 and 9.5 d, respectively. In separate experiments, approximately 34% of the injected [14C]picric acid was metabolized to picramic acid, glucuronide conjugates, and an unidentified group of compounds, and 42% of the [14C]picric acid was metabolized to picric acid, glucuronide conjugates, and an unidentified group of compounds. The low bioconcentration in the trout muscle may be due to the trout's ability to excrete the parent compound and metabolites. The higher radioactivity observed on the skin may be due to the water route of exposure and the binding of the parent compounds to protein.

2,4-Dinitrophenol↗
PubMed1984

Different humidification systems for high-frequency jet ventilation.

This study examined the effect of several different high-frequency jet ventilation (HFJV) humidification techniques on tracheobronchial mucosa. Six groups (2 in each group) of mongrel dogs, chronically instrumented, were cared for in an intensive care-like setting for data acquisition. Four groups received HFJV with different humidification systems during 72 h of continuous ventilation. Two groups served as controls (conventional ventilation with and without humidity). Although there was significant damage to tracheal mucosa during ventilation without humidification, there were no significant pathologic differences in bronchial mucosa between humidified and nonhumidified groups. Several techniques of HFJV humidification produced no pathologic evidence of mucosal damage and could be clinically useful.

Animals↗
PubMed1984

Spinal cord compression due to an aspergilloma.

Aspergilloma is a common complication of cystic lung disease; it is widely considered to be a saprophytic colonization and local or disseminated invasion is unusual. We describe a patient with stage IV sarcoidosis and bilateral aspergillomas in whom locally invasive disease led to spinal cord compression.

Adolescent↗
PubMed1984

Correlation of benzene metabolism and histological lesions in rainbow trout (Salmo gairdneri).

Rainbow trout metabolized benzene to phenol and catechol, and excreted them primarily as glucuronide conjugates. Treatment with benzene or toluene resulted in spleenomegaly that may be a more generalized solvent effect on the circulating RBCs. Anemia was observed only in the benzene-treated animals. This may be a result of decreased erythropoiesis in the head kidney or a direct effect of the principal metabolite (phenol) or its reactive intermediate. Both the spleen and liver metabolized benzene in vitro, while no metabolism was observed in the head kidney or trunk kidney. This fact, along with the observed "covalently" bound material in the liver, spleen, and kidney in vivo, can be interpreted as indicating that a reactive metabolite is formed outside the head kidney and is transported to the head kidney where it results in the observed hematopoietic damage. A similar hypothesis has been suggested for the observed protection by partial hepatectomy against bone marrow effects in mammalian species. The effects observed in trout are similar to those reported for higher mammalian species, but the metabolic profile is simpler, and studies in these animals may shed light on the mechanism of benzene toxicity. The techniques developed for monitoring benzene toxicity in trout can also be used for examining other environmental pollutants that may affect the hematopoietic system of fish.

Animals↗