Biomedical subjects
K E Cooper
Publications and source records attributed to K E Cooper.
Potentiation of fever, produced by intravenous leucocyte pyrogen, following the injection of paraffin oil in the cerebral ventricles of the unanesthetized rabbit.
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Studies of the mechanism of the Jarisch-Herxheimer reaction in louse-borne relapsing fever: evidence for the presence of circulating Borrelia endotoxin.
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The effect of injecting an inert oil into the cerebral ventricular system upon fever produced by intravenous leucocyte pyrogen.
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Some physiological and clinical aspects of pyrogens.
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Sudden failure of swimming in cold water.
To investigate the effect of cold water on swimming four men who declared themselves good swimmers were immersed fully clothed on separate days in water at 23.7 degrees and 4.7 degrees C. The time that they were able to swim in the cold water was much shorter than in the warm. The two shortest swims ended after 1.5 and 7.6 minutes, before rectal temperature fell, when the men suddenly floundered after developing respiratory distress with breathing rates of 56-60/min. The other cold swims, by the two fattest men, ended less abruptly with signs of general and peripheral hypothermia.It is concluded that swimming in cold water was stopped partly by respiratory reflexes in the thin men and hypothermia in the fat, and partly by the cold water's high viscosity. The longer swimming times of the fat men are attributed largely to their greater buoyancy enabling them to keep their heads above water during the early hyperventilation.The findings explain some reports of sudden death in cold water. It is clearly highly dangerous to attempt to swim short distances to shore without a life-jacket in water near 0 degrees C.
Observations on the site & mode of action of pyrogens in the rabbit brain.
1. Leucocyte pyrogen has been injected bilaterally into various parts of the rabbit brain. It caused fever when injected into the pre-optic area and the anterior hypothalamus, but not when injected into the posterior hypothalamus, the mid-brain, the pons, the cerebellum or the cerebral cortex.2. The mean time which elapsed between a leucocyte pyrogen injection into the anterior hypothalamus and the onset of fever was 7.8 min. For similar injections of bacterial pyrogen the time lag was 24.8 min. The mean time lag between bilateral injections of noradrenaline into the anterior hypothalamus and the onset of fever was 7.4 min.3. The amount of leucocyte pyrogen required to cause fever when injected into the anterior hypothalamus was less than 1/100 of that required to cause a similar fever on intravenous injection. The quantity of bacterial pyrogen injected into the hypothalamus was of the same order as that which would cause a similar fever on intravenous injection.4. Control injections of saline, plasma, cerebrospinal fluid, heated leucocyte pyrogen and red cells into the anterior hypothalamus did not cause fever.5. After attempts to deplete the hypothalamus of its monoamine stores by intraventricular injections of reserpine, the rabbit had fever as a result of an intravenous injection of bacterial pyrogen.6. We conclude that the anterior hypothalamus and the pre-optic area are sites at which leucocyte pyrogen acts to cause fever in the rabbit. The mechanism of this febrile response is not clear, but it appears that part, at least, of the response could be mediated by a mechanism other than release of noradrenaline or failure to release 5-HT.
Pyrogens and monoamine oxidase inhibitors.
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Temperature regulation and the hypothalamus.
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Gene effect in carriers of anhidrotic ectodermal dysplasia.
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Effects of intraventricular and intrahypothalamic injection of noradrenaline and 5-HT on body temperature in conscious rabbits.
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The role of the hypothalamus in the genesis of fever.
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Quantitative observations in disordered temperature regulation.
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Round table on antibiotic assay methods.
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The umbilical blood flow in the foetal sheep.
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A method for measuring the blood flow in the umbilical vessels.
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Measurement of intracranial pressure in the unanesthetized rabbit.
A method is described for the measurement of intracranial pressure in the unanesthetized, minimally restrained rabbit utilizing a modified subarachnoid screw system. The pressures are transmitted from within the cranium via a flexible saline filled catheter to a fixed external pressure transducer. An index of the relative vertical position of the animal's skull as compared to the fixed transducer is given by means of a second open-ended pressure measuring catheter, the open end of which is fixed to the subarachnoid screw assembly on the animal's skull. The system was found to be a reliable method of measurement of intracranial pressures in the minimally restrained rabbit, and could easily be adapted to other animal species. The method is currently being used to assess the effects of fever on intracranial pressures.
Antipyresis: its effect on mortality rate of bacterially infected rabbits.
The effect of an antipyretic drug administered directly into the preoptic-anterior hypothalamus was measured in order to investigate the role of fever on mortality of bacterially infected mammals. New Zealand white rabbits (Oryctolagus cuniculus) were injected intravenously with Pasteurella multocida and either sodium salicylate or a control solution was infused directly into the preoptic-anterior hypothalamus. Both groups developed fevers, but the fever of the rabbits infused with the antipyretic was reduced by 50% during the initial stage of infection. Hypothalamic sodium salicylate infusions produced a lower average fever than control infusions over an initial 5 hour period of infection, reducing average 5 hour fevers from 1.56 degrees C to 0.72 degrees C. All of the infected rabbits infused with sodium salicylate died whereas only 29% of the infected control rabbits died. Rabbits receiving sodium salicylate alone did not die. The increased mortality could possibly be the result of a fulminating infection caused by rapidly multiplying bacteria during the initial, attenuated phase of the febrile course in the salicylate-treated rabbits.