[Interaction between neurogenic and metabolic factors upon deterioration in cerebrovascular tonus--experimental study on the etiology of cerebral vasoparesis].
It is widely accepted that a tremendous increase in cerebral blood volume (CBV) due to progressive cerebral vasoparesis is an essential to the development of acute brain swelling. This study was designed to determine whether neurogenic and/or metabolic factors are predominant and how these interact with each other in producing cerebral vasoparesis. Fifty-one awake cats immobilized with pancuronium bromide were divided into 4 groups: group I, control; group II, normocapnic hypoxia (PaO2 = 50 mmHg); group III, normoxic hypercapnia (Pa-CO2 = 70 mmHg), and group IV, increased intracranial pressure (ICP = 40 mmHg) by brain compression. Systemic arterial pressure (BP), CBV (photoelectric method), and ICP (epidural pressure) were continuously recorded. The dorsomedial hypothalamic nucleus (DM) and the reticular formation of the midbrain (MB-RF) were bilaterally coagulated by a stereotaxic technique (3mA, 1 min). Therefore alterations in cerebrovascular tonus created by destruction of the cerebral vasomotor centers were examined in the animals with metabolically induced cerebral vasodilatation to various degree's. In group I, vasomotor center destruction resulted in an immediate and transient decrease in BP (DM; -14.1 +/- 6.7 mmHg, MB-RF; -10.2 +/- 4.8 mmHg) and simultaneous increase in CBV and ICP (DM; 7.6 +/- 7.0 mmHg, MB-RF; 6.0 +/- 5.6 mmHg) for 3 to 4 minutes. Increase in ICP by destruction of vasomotor centers reduced significantly in group II (DM; 2.3 +/- 2.6 mmHg, MB-RF; 1.6 +/- 1.2 mmHg) and reduced slightly in group IV (DM; 7.5 +/- 4.0 mmHg, MB-RF; 4.8 +/- 3.2 mmHg). In these 3 groups, autoregulation of cerebral blood flow and CO2 vasoreactivity were not changed by destruction of vasomotor centers.(ABSTRACT TRUNCATED AT 250 WORDS)
Honma
Y
Y
Department of Neurological Surgery, Okayama University Medical School, Japan.
Nagao
S
S
Tsutsui
T
T
Sunami
N
N
Momma
F
F
Kuyama
H
H
Nishimoto
A
A
D000818:Animals; D002415:Cats; D002560:Cerebrovascular Circulation; D004108:Dilatation, Pathologic; D006935:Hypercapnia / Q000150:complications; D000860:Hypoxia / Q000150:complications; D007427:Intracranial Pressure; D002546:Ischemic Attack, Transient / Q000209:etiology* / Q000503:physiopathology; D009422:Nervous System Diseases / Q000150:complications; D014664:Vasodilation; D014666:Vasomotor System / Q000503:physiopathology