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Biomedical subjects

G K Adams

Publications and source records attributed to G K Adams.

44 records · Page 3Linked to original sources

Recovery of central respiratory function following anticholinesterase intoxication.

Spontaneous recovery of central respiratory function was studied in anesthetized guinea pigs intoxicated with pinacolyl methylphosphonofluoridate (Soman) or isopropyl methylphosphonofluoridate (Sarin). I.v adiministration of either agent produced an immediate disruption phrenic nerve activiity and resulting ventilatory failure. Animals were maintained on artifical respiration until spontaneous functional recovery was complete, as evidenced by the re-establishment of synchronized burst activity on the phrenic nerve and return of tracheal airflow. This usually occurred within 1 h. Animals were sacrificed at predetermined intervals after intoxication, and the brainstem homogenates were analyzed for AChE activity. Results showed no significant return of AChE activity after 1 h, although functional recovery of respiration was complete within this time. Additional doses of the agents were administered at various times after recovery from the respiratory blockade. Following spontaneous restoration of ventilatory function, subsequent injections of the organophosphorus compounds failed to reinstate central respiratory paralysis, although they further depressed brainstem AChE levels. These data suggest that spontaneous recovery of central respiratory function after intoxication with Soman or Sarin may not be related to the return of AChE activity.

Acetylcholinesterase↗

Collection of normal canine tracheobronchial secretions.

A technique is described for the collection of tracheobronchial secretions from the upper trachea of anesthetized dogs. The method is simple, relatively quantitative, and provides secretory material in quantity suitable for biochemical or rheological studies. In 42 experiments comprising 184 individual samples we have found the collection rate of tracheobronchial secretions to be 1.0 +/- 0.1 mg/min per kg (mean +/- SEM).

Animals↗

Experimental study of a potential anti-asthmatic agent: SCH 15280.

A forced oscillations technique for measuring total respiratory system resistance was used to quantitate the bronchomotor activity of Sch 15280: (5[4-(N-methyl)-piperidylidine]5H-[1]-benzopyrano[2,3,b]-pyridine maleate) and to compare its potency to that of standard bronchodilator agents. By the intravenous route, Sch 15280 was 48 times more potent than aminophylline and 1/78 as potent as atropine in inhibiting methacholine-induced bronchoconstriction in rabbits. In cats Sch 15280 was 1/12 as potent as ephedrine in inhibiting histamine-induced bronchoconstriction and had a greater protective activity against histamine-induced bronchoconstriction and had a longer duration of action than 0.5% solution of isoproterenol. Statistical tests of parallelism revealed a significant difference between the log dose-response curves of Sch 15280 and ephedrine but not between those of Sch 15280, atropine and aminophylline. The results suggest that Sch 15280 can act via, a nonadrenergic mechanism to block both histaminergically and cholinergically mediated responses in the tracheobronchial tree. This pharmacologie profile may have important therapeutic application in the type I immediate hypersensitivity reactions of man.

Adrenergic beta-Antagonists↗

Induced rhinovirus infection under controlled exposure to sulfur dioxide.

The interaction between short-term sulfur dioxide (SO2) exposure and experimentally induced rhinovirus infection was studied in thirty-two volunteers divided into two groups balanced with respect to age, antibody levels, and nasal mucus flow rates. One group was exposed to SO2 exposure at the threshold limit value (TLV) of 5 ppm during 4 hours; the other group served as controls exposed to pollution-free air under the same conditions. The SO2 exposure caused a 50% decrease in nasal mucus flow rate in the anterior parts of the nose, but there was no difference in the number of colds which developed in the two groups. The group exposed to SO2 had fewer symptoms and a possibly shorter incubation period (P = .06), and virus shedding was at a lower level but more persistent than in the control group. No differences were found in antibody response. The rhinovirus infection in the control group caused a gradual decrease in nasal mucus flow rate starting 2 days after the virus instillation, and after 5 days the rate was less than half its initial value. For future experiments on the interaction between airborne pollutants and rhinovirus infections, a virus challenge by aerosol inhalation is recommended. Our study supports an earlier observation that growth of influenza virus in the nasal cavity of mice was inhibited by exposure to SO2 concentrations of 6 or 20 ppm.

Adolescent↗