Ocular silicone oil in the lateral cerebral ventricle

2013 ◽  
Vol 20 (9) ◽  
pp. 1312-1313 ◽  
Author(s):  
Garth Campbell ◽  
Shannon Milbourne ◽  
Umber A. Salman ◽  
Majid A. Khan
Radiology ◽  
1983 ◽  
Vol 148 (2) ◽  
pp. 529-531 ◽  
Author(s):  
D H Chinn ◽  
P W Callen ◽  
R A Filly

1988 ◽  
Vol 255 (1) ◽  
pp. R73-R81 ◽  
Author(s):  
T. J. Malkinson ◽  
K. E. Cooper ◽  
W. L. Veale

Adult male Wistar rats were anesthetized with urethan (1.5 g/kg). They were unable to maintain body temperature (Tb) in a warm (32 degrees C) or cool (9 degrees C) environment or at a laboratory room temperature of 22 degrees C. Tb was allowed to fall to 35.8, 34.5, or 33.3 degrees C, and prostaglandin E1 (PGE1, 400 ng) was delivered into a lateral cerebral ventricle. An immediate feverlike rise in Tb resulted, accompanied by vigorous shivering. Animals were vasoconstricted throughout. When Tb was raised to and maintained at 38.3 or 39.5 degrees C, animals also responded with a fever; however, the magnitude of the fever diminished as the starting Tb increased. In a series of experiments in which Tb was maintained (36.8-37.4 degrees C) by means of a heating pad, PGE1 delivered into a lateral cerebral ventricle or into the anterior hypothalamus caused a dose-dependent change in Tb, which was similar in time of onset, magnitude, and duration to that observed in conscious animals. This fever was accompanied by shivering and increased O2 uptake, heart rate, arterial blood pressure, respiratory rate, and intracranial pressure during the rising phase of the fever, and vasodilation of the paws occurred during defeveresence. Animals were also able to develop a dose-dependent rise in Tb in response to purified human interleukin 1.


1973 ◽  
Vol 44 (4) ◽  
pp. 417-420 ◽  
Author(s):  
P. L. Gildenberg ◽  
C. M. Ferrario ◽  
J. W. McCubbin

1. Infusion of angiotensin into both vertebral arteries or into a lateral cerebral ventricle of dogs anaesthetized with morphine-chloralose elicited a centrally mediated rise in blood pressure. 2. Heat coagulation of the area postrema and immediately adjacent structures abolished the pressor response to infusion of angiotensin into the circulation of the vertebral arteries, but did not alter the pressor response when the peptide was delivered into a cerebral lateral ventricle; transection of the midbrain eliminated the latter response but not the former. 3. It is concluded that there are at least two areas in the dog's brain that respond to angiotensin by inducing a raised blood pressure.


1988 ◽  
Vol 66 (8) ◽  
pp. 1082-1086 ◽  
Author(s):  
D. L. Jones

Input to the nucleus medianus of the preoptic region has been suggested to be involved in both the drinking and pressor responses elicited by the central administration of angiotensin II. Evidence in support of this suggestion has been gained principally from electrical lesion experiments. This lesion procedure does not differentiate between the cells of the region and fibers coursing through the region. To test the hypothesis that cells in this region are involved in both the pressor and drinking responses elicited by central administration of angiotensin II, injections of kainic acid were made to induce lesions of the cells, while sparing fibers of passage. Drinking and blood pressure responses were determined pre- and post-lesion in the chronically instrumented awake rat. Injections of 50 ng angiotensin II in a 2-μL volume into a lateral cerebral ventricle of the conscious rat elicited pronounced drinking and pressor responses with a latency of 3–5 min. Lesions of the median preoptic region produced by injecting 1.0 μg of kainic acid in 0.25 μL for 15 s attenuated or blocked the drinking response and increased the latency to drink induced by central injections of angiotensin II. However, kainic acid lesions did not significantly alter the pressor responses produced by angiotensin II administration. These results suggest that cells in the median preoptic region are involved in the drinking response but do not participate in the pressor response elicited by angiotensin II administration into a lateral cerebral ventricle of the conscious rat.


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