Cardiovascular Effects of Acutely Raised Intracranial Pressure

1956 ◽  
Vol 185 (3) ◽  
pp. 510-514 ◽  
Author(s):  
Faith K. Brown

Cardiovascular effects of acute elevations of intracranial pressure were studied, with special reference to three questions: a) whether vasoconstriction or cardiac stimulation is primarily responsible for the pressor response to this stimulus; b) whether the ultimate nature of the stimulus is neurogenic or humoral; and c) whether or not changes in venous tone occur in response to ICP elevation. It is concluded from the experimental findings that vasoconstriction was the dominant factor in the response, that the reflex is primarily neurogenic, and that the venomotor system shows an active constriction which accompanies the arterial pressure rise.

Author(s):  
Lamkordor Tyngkan ◽  
Nazia Mahfouz ◽  
Sobia Bilal ◽  
Bazla Fatima ◽  
Nayil Malik

AbstractTraumatic brainstem injury can be classified as primary or secondary. Secondary brainstem hemorrhage that evolves from raised intracranial pressure (ICP) and transtentorial herniation is referred to as Duret hemorrhage. We report a 25-year-old male who underwent emergency craniotomy, with evacuation of acute epidural hematoma, and postoperatively developed fatal Duret hemorrhage. Duret hemorrhage after acute epidural hematoma (EDH) evacuation is a very rare complication and the outcome is grave in most of the cases.


1991 ◽  
Vol 74 (4) ◽  
pp. 799-799
Author(s):  
Frederick E. Sieber

2002 ◽  
Vol 249 (9) ◽  
pp. 1292-1297 ◽  
Author(s):  
Frank Winkler ◽  
Stefan Kastenbauer ◽  
Tarek A. Yousry ◽  
Ulrich Maerz ◽  
Hans-W. Pfister

1980 ◽  
Vol 59 (s6) ◽  
pp. 235s-237s ◽  
Author(s):  
R. W. Rockhold ◽  
J. T. Crofton ◽  
L. Share

1. The cardiovascular effects of an enkephalin analogue were examined in spontaneously hypertensive and normotensive Wistar-Kyoto rats. (D-Ala2)-methionine enkephalin caused a biphasic increase in blood pressure and an increase in heart rate after intracerebroventricular injection. 2. The initial pressor response to (D-Ala2)-methionine enkephalin was greater in hypertensive than in normotensive rats. No difference was noted between groups during the secondary pressor response. Heart rate increases paralleled the secondary increase in blood pressure. 3. Naloxone pretreatment abolished the secondary increase in blood pressure and the tachycardia, but did not blunt the initial pressor response in female Wistar-Kyoto rats. 4. Plasma levels of arginine vasopressin were depressed during the plateau phase of the pressor response in hypertensive rats given intracerebroventricular (d-Ala2)-methionine enkephalin. 5. The results suggest that the cardiovascular effects of central enkephalin are not due to vasopressin, but may involve activation of the sympathetic nervous system.


Sign in / Sign up

Export Citation Format

Share Document