ABSTRACT
Part II of this essay describes the author's participation in the laboratory course instituted by Eugene Landis at Harvard in 1943, a course that drew heavily on Thomas Lewis's example. He describes in detail his own methods of laboratory teaching at Utah and Michigan when, as department chair, he had the responsibility for organizing courses in physiology for medical students. In conclusion, the author laments the curtailment and eventual abolition of laboratory teaching in the 1970s that resulted from curriculum reform, student revolt, and faculty indifference.
Subject(s)
Laboratories/history , Physiology/education , Teaching/history , Animals , Boston , History, 20th Century , Humans , Michigan , Physiology/history , Teaching/methods , UtahABSTRACT
Part I of this essay sketches the history of laboratory teaching of medical physiology in England from the perspective of the author as a student at Oxford from 1935 to 1938. The systematic laboratory teaching that began in the 1870s at University College London under William Sharpey was carried to Oxford, as well as to other English and Scottish universities, by Sharpey's junior colleagues. C. S. Sherrington added mammalian experiments, and C. G. Douglas and J. G. Priestley added experiments on human subjects. The author describes his experience as a student in the Oxford courses and tells how he learned physiology by teaching it from 1941 to 1943 in the laboratory course established at the University of Pennsylvania by Oxford-trained physiologist Cuthbert Bazett.
Subject(s)
Education, Medical, Graduate/history , Laboratories , Physiology/education , England , History, 20th CenturySubject(s)
Epinephrine/physiology , Adrenal Glands/physiology , Animals , Blood Pressure/drug effects , Chemistry , Europe , History, 19th Century , History, 20th Century , Humans , Rabbits , Sheep , United StatesABSTRACT
An isolated segment of the greater curvature of a dog's stomach was perfused at constant flow through a single cannulated artery with donor blood containing 131I-albumin, 125I-fibrinogen, and papaverine. Perfusion pressure was 30-50 mmHg, and venous pressure was set at 15 mmHg. Venous blood was collected in 1-min samples for 60 min. Filtration of fluid and loss of labeled proteins were calculated as the difference between measured arterial inflow and venous outflow. Permeability-surface area products (PS) were calculated for the proteins, and reflection coefficients (sigma) were calculated from solute flux and filtration. Intraarterial infusion of histamine (1.6-1.9 microgram . ml-1) increased filtration and PS and decreased sigma for albumin but not fibrinogen. When protein-losing was established by topical irrigation with 10 mM dithiothreitol in neutral solution, filtration and PS increased, and sigma for albumin but not fibrinogen decreased. Irrigation of the mucosa with 10 mM salicylic acid in 100 mN HCl caused bleeding that was quantitated by addition of 51Cr-erythrocytes to perfusing blood. Filtration and PS increased, and sigma for albumin but not fibrinogen decreased. Hematocrit of blood lost remained low during extensive mucosal damage. Effects of histamine infusion were attenuated or abolished by cimetidine (4 mg . kg-1 loading, 1.4 mg . kg-1 . h-1 continuous infusion) or by pyrilamine maleate (5 mg . kg-1 bolus injection at beginning of irrigation, repeated at 40-50 min). Pyrilamine attenuated or abolished effects of topical dithiothreitol or salicylic acid. We conclude that during protein loss caused by dithiothreitol or salicylic acid, histamine released within the mucosa causes increased vascular permeability for plasma proteins.
