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CARDIOVASCULAR RECULATION FOLLOWING CHANCES IN CENTRAL NERVOUS PERFUSION PRESSURE IN THE UNANAESTHETISED RABBIT
Author(s) -
Uther JB,
Guyton AC
Publication year - 1973
Publication title -
australian journal of experimental biology and medical science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0004-945X
DOI - 10.1038/icb.1973.29
Subject(s) - baroreceptor , bradycardia , blood pressure , medicine , cerebral perfusion pressure , anesthesia , mean arterial pressure , perfusion , cardiology , heart rate
Summary The effects on arterial pressure and heart rate of central nervous system ischaemia clue to elevated intracranial pressure were studied in intact unanaesthetised and anaesthetised rabbits, in acute pontine and spinal preparations and in unanaesthetised rabbits after inactivation of the arterial baroreceptor system. In the intact unanaesthetised rabbit elevation of intracranial pressure to high levels produced elevation of arterial pressure and bradycardia. The response was unchanged in pontine animals, but in spinal animals the arterial pressure rise was reduced and the bradycardia abolished, indicating that the ponto‐medullary cardiovascular centres were the major source of the observed effects. Comparison of the responses of unanaesthetised and anaesthetised intact rabbits indicated that anaesthesia did not alter the arterial pressure response. Comparison of the responses with and without the arterial baroreceptors system indicated that the arterial baroreceptors opposed the normal arterial pressure rise and caused the normal bradycardia. The responses produced by cerebral ischaemia occurred only at low central nervous system perfusion pressures, indicating that cerebral ischaemia cannot be an important regulator of arterial pressure within its normal physiological range in the intact unanaesthetised state.