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Biomedical subjects

D A Leon

Publications and source records attributed to D A Leon.

60 records · Page 4Linked to original sources

Bereavement and cancer: some data on deaths of spouses from the longitudinal study of Office of Population Censuses and Surveys.

Registration of cancer and mortality after the death of a spouse were assessed using data from the longitudinal study of the Office of Population Censuses and Surveys (OPCS). The study population comprised 1% of the people counted in England and Wales in the 1971 census, for whom data on subsequent vital events were linked with their census records. There was little evidence of an increase in registrations of cancer after the death of a spouse and only a slight suggestion of increased mortality from cancer. For other causes of death there was some evidence of increases in mortality during widow(er)hood. In so far as the death of a spouse is often a very stressful event, these data may be interpreted as providing little support for the hypothesis that stress is implicated in the aetiology of cancer.

Death↗

Comparison of local anesthetics as bronchodilator aerosols.

Lidocaine aerosols have been ineffective at preventing airway constriction provoked by non-reflex stimuli. To determine if there were any advantages to using more potent amide-type local anesthetics or local anesthetics from other chemical classes, the authors compared the protection afforded by pretreatment with aerosols of lidocaine, bupivacaine, hexylcaine, and procaine against a subsequent prolonged challenge (5 min) with 10% citric acid aerosols in barbiturate-anesthetized Basenji-Greyhound dogs. The local anesthetics were administered as aerosols (4% solutions) for 10 min immediately preceding the citric acid challenge. In control experiments, that employed pretreatment with aerosols of isotonic saline rather than local anesthetics, the citric acid challenge aerosol increased pulmonary resistance by an average of 3.3 +/- 0.8 (+/- SE) cmH2O X 1(-1) X s during the first 15-min postchallenge, and reduced dynamic compliance by one-third during this time. None of the local anesthetics prevented citric-acid-induced changes in pulmonary mechanics. The average increases in pulmonary resistance (0-15 min postchallenge) elicited by citric acid aerosols in dogs pretreated with lidocaine, hexylcaine, bupivacaine, and procaine were 2.1 +/- 0.6, 2.1 +/- 0.6, 3.2 +/- 1.3, and 3.3 +/- 1.0 cmH2O X 1(-1) X s, respectively. The authors concluded that local anesthetic aerosols have little or no effect against other than reflex bronchoconstriction, and none of those tested were more effective than lidocaine.

Anesthetics, Local↗

The Basenji-Greyhound dog: antigen-induced changes in lung volumes.

Subdivisions of lung volume, closing volume (CV), pulmonary resistance (RL) and dynamic pulmonary compliance (Cdyn) were measured before and after bronchial challenge with Ascaris suum in seven ascaris-sensitive Basenji-Greyhound (BG) crossbreed dogs. RL increased from a control value of 1.41 +/- 0.43 (mean +/- SE) cm H2O/L/sec to 21.4 +/- 5.15 (P Less Than 0.01) and Cdyn decreased from 163 +/- 32 ml/cm H2O to 43 +/- 11 (P Less Than 0.01) in the first 15 min following ascaris-antigen aerosol (AAA) challenge. Vital capacity (VC) decreased from 1581 +/- 147 ml to 944 +/- 86 (P Less Than 0.005) ml and residual volume (RV) increased from 381 +/- 63 to 577 +/- 68 ml (P Less Than 0.005) following AAA challenge. We conclude that the pulmonary mechanical changes in the BG dog following antigen challenge more closely resemble the changes observed in acute human asthma than do changes occurring in the mongrel dog.

Aerosols↗

Mechanism of tracheal constriction by succinylcholine.

The purpose of this study was to identify the mechanism by which succinylcholine produced large increases in endotracheal tube cuff pressure in barbiturate-anesthetized dogs (n = 7). Cuff pressure was measured in vivo by a transducer connected to a fluidfilled, high-volume, low-pressure cuff. Intravenous succinylcholine, 0.5 and 1 mg/kg, produced mean increases in cuff pressure of 12 +/- 2 (+/-SE) and 27 +/- 5 cm H2O, respectively, which reached peak effect in 1 to 3 min and declined slowly over the next 10 min. Bilateral vagotomy, intravenous administration of atropine (0.2 mg/kg) and hexamethonium (5 mg/kg) prevented or terminated succinylcholine-induced increases in cuff pressure. Isolated preparations from an additional three dogs were employed to study the direct actions of succinylcholine on trachealis muscle in vitro. In organ baths, succinylcholine (10(-6) to 10(-3) M) did not contract canine trachealis muscle, and concentrations of 10(-5) M and above significantly relaxed carbamylcholine-induced contractions. The authors conclude that succinylcholine elicits contraction of trachealis muscle by a stimulant action on parasympathetic pathways rather than by a direct action on airway smooth muscle. Since vagotomy prevented the succinylcholine response, the site of stimulant action is not at autonomic ganglia.

Animals↗

Basenji-greyhound dog model of asthma: pulmonary responses after beta-adrenergic blockade.

To understand the mechanism underlying bronchial hyperreactivity in the Basenji-Greyhound (BG) dog, the effects of propranolol (2 mg/kg) and hexamethonium (5 mg/kg) on base-line pulmonary mechanics and on the bronchial response to aerosol challenges of citric acid and methacholine were studied in five BG dogs. Both propranolol and hexamethonium increased base-line pulmonary resistance (RL) from 0.69 +/- 0.05 (means +/- SE) cmH2O.l-1.s to 1.67 +/- 0.10 (P less than 0.05) and 2.22 +/- 0.45 cmH2O.1-1.s (P less than 0.05) and decreased dynamic compliance (Cdyn) from 190 +/- 10 ml/cmH2O to 154 +/- 9 (P less than 0.05) and 140 +/- 9 (P less than 0.05) ml/cmH2O, respectively. Both propranolol and hexamethonium potentiated the pulmonary response to 10% citric acid given for 5 min (P less than 0.05). RL postchallenge was 4.4 +/- 0.23, 8.1 +/- 0.81, and 7.8 +/- 0.31 cmH2O.l-1.s, and Cdyn was 78 +/- 5, 58 +/- 6, and 51 +/- 3 ml/cmH2O in untreated, propranolol-pretreated, and hexamethonium-pretreated animals. In untreated BG dogs, methacholine (0.075 mg/ml) increased RL from 0.94 +/- 0.25 to 2.2 +/- 0.21 cmH2O.l-1.s (234%) and decreased Cdyn from 223 +/- 39 to 141 +/- 14 ml/cmH2O (63%). In the same animals pretreated with propranolol, methacholine (0.075 mg/ml) increased RL from 1.9 +/- 0.66 to 4.8 +/- 1.37 cmH2O.l-1.s (253%) and decreased Cdyn from 144 +/- 35 to 81 +/- 15 ml/cmH2O (56%). We conclude that propranolol produces airway constriction in BG dogs, as in asthmatic humans and that the effects of propranolol on airways in BG dogs are not due to parasympathetic or alpha-adrenergic predominance.

Adrenergic beta-Antagonists↗