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Biomedical subjects

A C Pugliese

Publications and source records attributed to A C Pugliese.

7 recordsLinked to original sources
PubMed1980

Respiratory consequences of methadone: the response to added resistance to breathing.

Respiratory responses to hypercapnia and added airway resistance were studied before and after methadone intake in 7 normal subjects (Group I) and 7 subjects receiving chronic methadone maintenance therapy (Group II). Before taking the drug, both groups exhibited similar ventilatory responses to CO2 without the resistance and equivalent augmentation of the airway occlusion pressure or "respiratory drive" responses to CO2 with the resistance. In Group I subjects, analgesic dosages of methadone depressed ventilation and ventilatory responsiveness to hypercapnia, and abolished the increase in respiratory drive elicited by the resistance. In contrast, patients receiving methadone maintance therapy exhibited no changes in either ventilatory responses or respiratory drive after intake of their daily doses of the drug. The data show that narcotic drugs may abolish the respiratory compensation, i.e., the enhanced ventilatory drive that accompanies increased airway resistance, although tolerance develops with chronic use. Because this compensation has been reported to play an important role in the respiratory response to diffuse obstructive disease, the findings suggested a mechanism for the frequent inordinate respiratory depressant effects of narcotic drugs in such diseases.

Adult↗
PubMed1977

Control of breathing during methadone addiction.

Chemical control of breathing was studied before and after the administration of the daily dose of methadone in 14 former heroin addicts who were enrolled in a methadone maintenance program and taking 60 to 100 mg/day. Two major groups were identified: group 1 in which subjects (n=6) had taken the drug for less than two months, and group 2 in which the subjects (n=6) had taken the drug from eight to 43 months. Prior to the daily dose of methadone, the levels of arterial carbon dioxide tension were significantly higher and ventilatory response to hypoxia significantly lower in group 1 than in group 2. Ventilatory responses to carbon dioxide (CO2) were also lower in group 1, but the difference was not statistically significant. Following the daily dose of methadone, the subjects in group 1 manifested significant reductions of ventilation and arterial oxygen tension, significant increases in arterial carbon dioxide tension and significant depressions of ventilatory responses to both CO2 and hypoxia in comparison to values before the administration of methadone. In contrast, subjects in group 2 manifested only a significant decrease in ventilatory responsiveness to hypoxia with no change in ventilation, arterial blood gas tensions or ventilatory responsiveness to CO2 following the daily dose. Two intermediate subjects (five and seven months) behaved as long-term subjects with regard to arterial carbon dioxide tension and CO2 responses but as short-term subjects with regard to responsiveness to hypoxia. Thus, during the first two months of methadone maintence, there is continual alveolar hypoventilation due to depression o both central (CO2) and peripheral (hypoxia) chemoreception. After five months, alveolar hypoventilation is abolished as the CO2-sensitive chemoreflex acquires full tolerance to methadone at the maintenance dose level. In contrast, tolerance of the hypoxia-sensitive chemoreflex is developed more slowly and is never complete.

Adult↗