Biomedical subjects

R W Robinson

Publications and source records attributed to R W Robinson.

At least 19 recordsLinked to original sources

PubMed1996

Safety assessment of a nematode-resistant tomato by a simple, short-term rat feeding study.

A simple, 11-week, weanling rat feeding period was used to determine general safety of a nematode-resistant tomato cultivar. Comparison of growth, mean blood hemoglobin, hematocrit, red blood cell count, and total white blood cell count of Fisher rats fed a complete diet containing 40% "VFN 8" tomato (nematode-resistant) cultivar to two other groups of rats, fed either a "New Yorker" tomato (nematode-susceptible) or a control diet, showed normal and similar results. Although the expressed product of the Mi gene necessary for nematode resistance is unknown, this short, comparative study of a whole plant food shows no unexpected toxicants influencing animal growth and hematology. However, human exposure of this resistant tomato would be needed to definitely determine consumer safety regarding allergenicity and hypersensitivity.

Animal Feed↗

PubMed1987

Relationship of respiratory drives to dyspnea and exercise performance in chronic obstructive pulmonary disease.

Frequently, patients with COPD with similar spirometric impairment have marked differences in dyspnea and exercise limitation. As the classic "blue bloater" with attenuated respiratory drive is described as being less dyspneic than his "pink puffer" counterpart, we wondered whether the variability in dyspnea and exercise tolerance in a group of patients with COPD with relatively similar degrees of air-flow obstruction might be partly explained by the variability in resting respiratory drives (unstimulated P0.1 and hypoxic and hypercapnic P0.1 responses). Therefore, we measured unstimulated mouth occlusion pressure (P0.1), hypoxic response (-delta P0.1/delta SaO2), hypercapnic response (delta P0.1/delta PCO2), 6-min walk distance, VO2max, steady-state exercise VE/VO2, exercise SaO2, and dyspnea using an oxygen cost diagram in 15 subjects with severe COPD (mean FEV1% 35.2 +/- 1.9 SEM). No correlations between spirometric impairment and either dyspnea or exercise performance were seen. Unstimulated P0.1 correlated inversely with spirometric impairment but did not correlate with dyspnea, VO2max or 6-min walk distance. Both hypoxic and hypercapnic responses were significantly correlated with greater exercise ventilation (VE/VO2), less exercise O2 desaturation, and a greater VO2max, but not with dyspnea or 6-min walk distance. The results of this study do not support the concept that depressed respiratory drives are associated with less dyspnea or greater exercise capability in COPD.

Adult↗

PubMed1987

Effects of oral narcotics on sleep-disordered breathing in healthy adults.

Alcohol and benzodiazepines may increase sleep-disordered breathing by decreasing activity of pharyngeal dilating muscles, favoring the development of obstructive apneas and hypopneas. Narcotics cause greater depression of wakeful respiration than the previously mentioned drugs; however, the influence of narcotics on the upper airway and breathing during sleep has not been studied. We, therefore, examined, in 12 healthy adults, the effects of oral hydromorphone hydrochloride (2 and 4 mg) on breathing during sleep and on a variety of awake respiratory variables (minute ventilation, gas exchange, and chemoresponsiveness). In addition, awake pharyngeal inspiratory airflow resistance was determined before and after narcotic administration to assess the drug's influence on patency of the upper airway. Following both doses, minute ventilation decreased, and carbon dioxide pressure increased. The 4-mg dose of hydromorphone hydrochloride also produced a significant decrement in the hypoxic ventilatory response, whereas hypercapnic responsiveness and pharyngeal resistance did not change following either dose of the drug. Despite the respiratory depression during wakefulness described previously, no significant change was observed in any measure of sleep-disordered breathing after either dose of narcotic. We conclude that in healthy individuals without suspected sleep apnea, oral hydromorphone in standard dosages does not significantly increase sleep-disordered breathing. This result may be due to a lack of selective depression of upper-airway muscular function by the doses of narcotic used.

Adult↗

PubMed1985

Moderate alcohol ingestion increases upper airway resistance in normal subjects.

Apnea during sleep has been associated with both increased pharyngeal resistance and nasal obstruction. Alcohol can worsen obstructive sleep apnea, but its influence on pharyngeal resistance and nasal patency has not been evaluated. Accordingly, we determined the effects of alcohol on pharyngeal and nasal resistances in 11 normal awake subjects on 2 separate days. Baseline pharyngeal resistance prior to placebo and alcohol was not significantly different. After placebo, pharyngeal resistance did not change significantly. However, after alcohol, pharyngeal resistance increased from 1.9 +/- 0.5 (SEM) to 3.3 +/- 0.8 cm H2O/L/s at 45 min (p less than 0.05) and returned to near baseline level by 90 min. Baseline nasal resistance varied considerably within subjects on the 2 days, but the mean values for baseline nasal resistance on alcohol and placebo days were not significantly different. Nasal resistance did not change after placebo, but after alcohol, nasal resistance increased from 2.4 +/- 0.9 at baseline to 3.7 +/- 0.8 at 45 min (NS) and to 4.3 +/- 1.2 cm H2O/L/s at 90 min (p less than 0.05). We conclude that a decrease in pharyngeal airway size and an increase in nasal resistance may account for alcohol's ability to worsen obstructive sleep apnea.

Adult↗

PubMed1985

The effect of drugs on breathing during sleep.

We hope that the reader is impressed with the relatively limited amount of information available about the effects of drugs on breathing during sleep in both normal subjects and patients with sleep-disordered breathing. Although more reports are appearing, well-controlled evaluations remain limited in number. We believe that this information gap will quickly close because it is now increasingly appreciated that either spontaneous or drug-induced breathing abnormalities measured during wakefulness may be strikingly magnified during sleep. Therefore, this area of investigation is exciting. Finally, we hope the reader shares our view that, to date, drug therapy for sleep apnea has limited efficacy.

Almitrine↗

PubMed1985

Sleep and respiration: a postscript.

The recent advances in our understanding of breathing in sleep include an evolution in the selection and surgical therapy of patients with the sleep apnea syndrome. Recent work suggests that shorter polysomnographic studies may be adequate for diagnostic purposes in many sleep apnea patients. It is now clear that central apnea may occur, paradoxically, in patients with either very blunted chemical drives to breathe or increased drives to breathe.

Acetazolamide↗

PubMed1985