Acute intracranial hypertension and brain-stem blood flow

Nagao, Seigo; Sunami, Norio; Tsutsui, Takako; Honma, Yutaka; Momma, Fumiyuki; Nishiura, Tsukasa; Nishimoto, Akira

doi:10.3171/jns.1984.60.3.0566

Cited by 43 publications

(10 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These findings indicate that the increase in MABP (the Cushing response) is ac tivated at ICP levels between 30 and 50 mm Hg, which corresponds to previous findings in experi mental intracranial hypertension (Johnston et al , 1972;Nagao et al, 1984;Schrader et al, 1985a,b;Zierski, 1987;Hartmann et al, 1989;Barz6 et al , 1991).…”

Section: Discussion Baseline Valuessupporting

confidence: 89%

Cerebral Blood Flow Autoregulation in Acute Intracranial Hypertension

Hauerberg

Juhler

1994

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Summary: The present series of experiments was carried out to investigate CBP autoregulation during fixed levels of acute increased intracranial pressure (ICP). Three groups of six rats each, one with normal ICP (8 mm Hg), one with moderately increased ICP (30 mm Hg), and one with severely increased ICP (50 mm Hg), were investi gated. ICP was maintained by continuous infusion of lac tated Ringer solution into the cisterna magna. Cerebral perfusion pressure (CPP), calculated as mean arterial blood pressure -ICP, was increased by intravenously infused norepinephrine and decreased by controlled bleeding. In all groups the corresponding autoregulation curve included a plateau where CBP was independent of Abbreviations used: CPP, cerebral perfusion pressure; CVR, cerebrovascular resistance; ICP, intracranial pressure; JVP, jug ular venous pressure; LL, lower limit of autoregulation; MABP, mean arterial blood pressure. 519changes in CPP, demonstrating intact autoregulation. However, a significant shift of the lower limit of autoreg ulation (LL) toward lower CPP levels during severe in tracranial hypertension was observed (p < 0.006). In the controls the LL was found at CPP = 73 ± 6 mm Hg, in moderately increased ICP the LL was 59 ± 4 mm Hg, and in severely increased ICP the LL was 51 ± 4 mm Hg. These results indicate that an acute elevation of ICP ac tivates a reserve capacity of cerebral resistance vessels that dilate further below the normal physiological LL to maintain CBP at low levels of CPP.

show abstract

Section: Discussion Baseline Valuessupporting

confidence: 89%

Cerebral Blood Flow Autoregulation in Acute Intracranial Hypertension

Hauerberg

Juhler

1994

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…Finally, a high local perfusion pressure was maintained until just before final collapse. This finding is consistent with the previously reported, relative maintenance of medullary blood flow, following a lethal supratentorial expanding lesion (15,25) even in the presence of an isoelectric EEG (29). These findings suggest that medullary compression, secondary to foramen magnum herniation, is not a prerequisite for a lethal outcome following a supratentorial epidural haemorrhage.…”

Section: Anatomical Shifts and Compressions And Physiological Variablessupporting

confidence: 92%

Changes in Intracranial Morphology, Regional Cerebral Water Content and Vital Physiological Variables during Epidural Bleeding

Ganz¹,

Thuomas²,

Vlajkovic³

et al. 1993

Acta Radiol

View full text Add to dashboard Cite

Epidural bleeding was produced in 8 anaesthetised and heparinised dogs by an artificial system. Changes in vital physiological variables were related to intracranial shifts and tissue water content assessed with MR imaging. Six animals survived while 2 succumbed. In the surviving animals intracranial shifts and compressions remained unchanged from an early stage. The cerebral perfusion pressure was reduced from between 80 and 110 mm Hg to between 40 and 60 mm Hg. Some increase in supratentorial white matter tissue water was observed. In the lethal experiments cerebral perfusion pressure fell to less than 40 mm Hg. Moreover, secondary delayed anatomical changes were seen including hydrocephalus. Increase in cerebral tissue water was more intense and widespread than in the survivors. These findings indicate that the outcome of epidural bleeding is related to cerebral perfusion pressure with secondary deterioration resulting from additional volume loading from increased tissue water and hydrocephalus.

show abstract

“…These consistently and more frequently observed responses in many cats may be preferentially assumed to have a primary functional meaning on the regulation or modification of ICP as well as BP. The mutual relationship and interference among ICP, BP, and activities of the pressor and depressor sites are explained by the series of events supposed to occur following activation of the pressor or depressor sites, since changes in cardiovascular activity and CBF were observed by an increase in ICP (LITTLE and OBERG, 1981;SADOSHIMA et al, 1981;MATSUURA et al, 1984;NAGAO et al, 1984) and an alteration in BP (KONTOS et al, 1978;KUMADA et al, 1979). A schematic diagram in Fig.…”

Section: Resultsmentioning

confidence: 99%

Changes in intracranial pressure and arterial blood pressure following electric stimulation to restricted regions in the cat brainstem.

et al. 1986

View full text Add to dashboard Cite

The brainstem of anesthetized cats was electrically stimulated to examine the changes in the Intracranial pressure (ICP). There were pressor and depressor sites, which preferentially produced an immediate increase and decrease in ICP in association with the arterial pressor and depressor responses, respectively. A preferential increase in ICP was also observed by stimulation of some depressor sites. The stimulus-induced ICP responses were usually different from the secondary ICP changes due to nonneurogenic alteration of arterial blood pressure (BP) as evoked by arterial bleeding and infusion of saline solution; the stimulus-induced increase in ICP was greatly enhanced when the stimulation to the pressor sites was applied at lowered BP levels and at moderately elevated ICP levels. In addition, when a gradual elevation in ICP was spontaneously observed with the lowering of the BP level, the pressor site-induced increase in ICP exceeded 70-100 mmHg at the peak plateau-like waves, regardless of the magnitude of accompanying arterial pressor response. We propose that the stimulus-induced ICP responses cannot be explained merely by the metabolic changes, the decreased intracranial compliance, and the secondary transmural action on the intracranial space of the arterial pressor and depressor responses. A neurogenic mechanism that directly affects Intracranial blood diameter may be involved in the ICP responses, especially those observed ,at a lower BP level, in addition to extracranic action of sympathetic and parasympathetic nerve activities.

show abstract

Acute intracranial hypertension and brain-stem blood flow

Cited by 43 publications

References 14 publications

Cerebral Blood Flow Autoregulation in Acute Intracranial Hypertension

Cerebral Blood Flow Autoregulation in Acute Intracranial Hypertension

Changes in Intracranial Morphology, Regional Cerebral Water Content and Vital Physiological Variables during Epidural Bleeding

Changes in intracranial pressure and arterial blood pressure following electric stimulation to restricted regions in the cat brainstem.

Contact Info

Product

Resources

About