Masahiro Miyazaki

Effects of mild (33°C) and moderate (29°C). hypothermia on cerebral blood flow and metabolism, lactate, and extracellular glutamate in experimental head injury

AbstractThe effects of mild (33±C) and moderate (29±C) hypothermia were investigated to determine which temperature was more effective against compression-induced cerebral ischemia. Eighteen cats were anesthetized. The animals were divided into three groups according to deep-brain temperature (control, 37±C; mild hypothermia,33±C; and moderate hypothermia,29±C). Intracranial pressure (ICP) and cerebral blood flow (CBF) were monitored, the latter by hydrogen clearance. Arteriovenous oxygen difference (AVD02) and cerebral venous oxygen saturation (SCV02) were measured in blood samples from the superior sagittal sinus. The cerebral metabolic rate of oxygen (CMR02) and the cerebral metabolic rate of lactate (CMR lactate) were calculated. Extracellular glutamate was measured by microdia lysis. ICP was increased by inflation of an epidural balloon until CBF became zero, and this ischemia was maintained for 5 mint after which the balloon was quickly deflated. All parameters were recorded over 6 h. Evans blue was...

Pathophysiology of Brain Swelling after Acute Experimental Brain Compression and Decompression

Global ischemia was created by controlled expansion of an epidural balloon for 25 minutes in Group A (six cats) and for 5 minutes in Group B (six cats). The alterations of intracranial pressure, arteriovenous oxygen content difference, cerebral metabolic rate of oxygen, cerebral blood flow, and electroencephalogram were observed until brain death or 24 hours survival with normal intracranial pressure. The animals were then killed for brain histological examination. In four other cats, a 2% solution of Evans blue dye (4 mg/kg) was injected intravenously--immediately after deflation--resulting in 25 minutes of global ischemia. Two other cats received 5 minutes of global ischemia. The cats were killed 1 hour later. Abrupt swelling occurred in Group A, and no swelling was found in Group B. A transient absolute hyperemia was found immediately after deflation in both groups. The cerebral blood flow and cerebral metabolic rate of oxygen decreased markedly with low arteriovenous oxygen content difference and flat electroencephalogram in Group A, compared with gradual recovery of cerebral blood flow and cerebral metabolic rate of oxygen with high arteriovenous oxygen content difference and reappearance of electroencephalogram activity in Group B. The extravasation of Evans blue was observed on the compressed cerebral hemisphere, thalamus, hypothalamus, and brain stem in swelling animals and only on the compressed hemisphere in nonswelling animals. Histologically, the damage and congestive dilation of capillary, degeneration, and necrosis of neuronal and glial cell were found prominently on the hypothalamus and brain stem in the swelling group.(ABSTRACT TRUNCATED AT 250 WORDS)

The Role of the Central Monoamine System and the Cholinoceptive Pontine Area on the Oscillation of ICP “Pressure Waves”

Oscillation of ventricular fluid pressure in the form of pressure waves, Lundberg “A” or “B” waves, has been recognized since 1960 (4).

Effects of Mild and Moderate Hypothermia on Cerebral Metabolism and Glutamate in an Experimental Head Injury

In this study we sought to determine the optimal brain temperature for treating compression-induced cerebral ischemia. Six cats each were treated with a deep-brain temperature of 37 degrees C (control), 33 degrees C (mild hypothermia), or 29 degrees C (moderate hypothermia). Intracranial pressure (ICP) and cerebral blood flow (CBF) were monitored, as were arteriovenous oxygen difference (AVDO2) and cerebral venous oxygen saturation (ScvO2). The cerebral metabolic rate of oxygen (CMRO2) was calculated. Extracellular glutamate concentration was measured by microdialysis. ICP was increased by inflation of an epidural balloon until CBF became zero. This ischemia was maintained for 5 min, after which the balloon was deflated. Mild hypothermia showed coupled CBF-metabolic suppression, but moderate hypothermia resulted in disproportionately increased AVDO2, decreased ScvO2, and low CBF/CMRO2 (relative ischemia). Reactive hyperemia after balloon deflation was decreased after both mild and moderate hypothermia, as was the tissue volume showing Evans blue dye extravasation. Extracellular glutamate increased in control animals, an effect most effectively suppressed in the mild hypothermia group. These data favor 33 degrees C as the optimal temperature for treating compression-related cerebral ischemia.

Effect of intrathecal magnesium sulfate solution injection via a microcatheter in the cisterna magna on cerebral vasospasm in the canine subarachnoid haemorrhage model

Abstract Objective. To evaluate intracisternal injection of magnesium sulfate (MgSO4) solution via a lumbar catheter for the treatment of cerebral vasospasm in the canine subarachnoid haemorrhage (SAH) model. Materials and methods. SAH was induced in 7 beagle dogs using the dual haemorrhage model. Vertebral angiography was repeated on Day 1 (before SAH), and on Day 7 (during cerebral vasospasm) before and 1.5 hours after injection of 0.5 mL/kg of 15 mmol/L MgSO4 in Ringer solution via the tip of a microcatheter placed in the cisterna magna from the lumbar spine. Results. After injection of MgSO4 solution, the cerebrospinal fluid magnesium ion concentration significantly increased to 3.89 ± 0.97 mEq/L (P < 0.01) from the baseline value (1.49 ± 0.07 mEq/L). The arterial diameters of the basilar artery (BA), vertebral artery (VA), and superior cerebral artery (SCA) on Day 1 were 1.26 ± 0.19 mm, 1.10 ± 0.13 mm, and 0.74 ± 0.21 mm, respectively. On Day 7 before injection, the arterial diameters of the BA, VA, and SCA significantly decreased to 0.75 ± 0.27 mm, 0.74 ± 0.25 mm, and 0.36 ± 0.21 mm, respectively (P < 0.01), due to vasospasm, and were significantly increased to 0.91 ± 0.27 mm (P < 0.01), 0.91 ± 0.31 mm (P < 0.05), and 0.54 ± 0.14 mm (P < 0.01), respectively, after intracisternal injection of MgSO4 solution. Conclusions. Intracisternal MgSO4 therapy using a microcatheter from the lumbar spine may be effective against vasospasm in the clinical setting of endovascular treatment of ruptured aneurysm.

Control of ICP and the Cerebrovascular Bed by the Cholinergic Basal Forebrain

The involvement of the cholinergic basal forebrain in the control of ICP and the cerebrovascular bed was investigated by simultaneous measurement of CBF, BP, ICP and ETCO2 in rats and cats. Single unit spikes were also continuously recorded during ICP changes in the dorsomedial hypothalamic nucleus (DMH) of cats. Glutamate or acetylcholine (Ach) microinjection into the magnocellular basal nucleus (nucleus basalis Meynert: NBM, substantia innominata: SI) of rats or the DMH of cats caused persistent increases in ICP associated with slightly decreased BP. Microinjection of Ach into the NBM or the DMH also induced consistent increases in CBF in the cerebral cortex. Spike activities in DMH neurons increased before and during spontaneous ICP elevation. The firing rate of the DMH neurons increased in phase with the plateau wave-like ICP variations elicited by microinjection of Ach into the cholinoceptive pontine area or the contralateral DMH. Glutamate- or Ach-induced increases in ICP resulted from an increased CBV in response to a reduced cerebral vasoconstrictor tone. Activity within the cholinergic basal forebrain, as well as the central noradrenergic system, contribute to ICP changes and may be the intrinsic neuronal origin of the plateau waves occurring in some pathological conditions.

Control of ICP by The Medullary Reticular Formation

Spontaneous episodic elevation of intracranial pressure (ICP), named “plateau wave” by Lundberg [4], often occurs in patients with increased ICP caused by brain tumor, hydrocephalus and other conditions. There are two possible causes for the development of plateau waves: persistent intracranial hypertension and cerebral vasomotor reaction [2]. Plateau waves are associated with increased cerebral blood volume (CBV) [9] due to dilatation of the cerebral blood vessels, and apparently result from intact autoregulation responding to changes in cerebral perfusion pressure (CPP) [7, 10]. Previously, we investigated the function of noradrenergic cell groups, especially the dorsal noradrenergic system (locus coeruleus complex, LC), and the cholinoceptive pontine area (CPA) [3] in the generation of plateau waves in ICP-VI [5] and VII [6]. This study investigated the function of the ventral noradrenergic system [1] (medullary reticular formation, MRF) in the control of ICP and neuronal organizations between the CPA and MRF.

Temporal Profile of the Effects of Intracisternal Injection of Magnesium Sulfate Solution on Vasodilation of Spastic Cerebral Arteries in the Canine SAH Model

PURPOSEnthe temporal profiles of the effects of intracisternal injection of magnesium sulfate (MgSO(4)) on vasodilation and cerebrospinal fluid (CSF) magnesium ion (Mg(2+)) concentration were investigated in the canine subarachnoid hemorrhage (SAH) model.nnnMETHODncerebral vasospasm was induced using the two-hemorrhage model in seven female beagles. On day 7, 0.5 ml/kg of 15 mmol/l MgSO(4) in Ringer solution was injected into the cerebellomedullary cistern. Angiography was performed on day 1 (before SAH), and before and 1, 3, and 6 h after the intracisternal injection on day 7. CSF Mg(2+) was measured at the same time.nnnRESULTSnthe diameters of the basilar artery (BA), vertebral artery (VA), and superior cerebellar artery (SCA) before the intracisternal injection on day 7 were 0.59 ± 0.15, 0.41 ± 0.17, and 0.35 ± 0.17 mm, respectively, and were significantly decreased (p < 0.01) compared with the baseline diameters on day 1. The BA diameters at 1 h (0.74 ± 0.16 mm) and 3 h (0.73 ± 0.13 mm), the VA diameter at 1 h (0.64 ± 0.14 mm), and the SCA diameter at 3 h (0.54 ± 0.08 mm) after the injection were significantly increased (p < 0.05). The CSF Mg(2+) concentration was significantly increased (p < 0.01) at 1 h (3.59 ± 0.76 mEq/l) and 3 h (2.00 ± 0.31 mEq/l) after the injection compared with the baseline value (1.35 ± 0.23 mEq/l).nnnCONCLUSIONSnthe reversible effect of intracisternal MgSO(4) solution injection on the spastic artery depends on maintenance of the optimal CSF Mg(2+) concentration.

The Roles of the Mutual Interaction Between the Locus Coeruleus Complex and the Chorioceptive Pontine Area in the Plateau Wave

Plateau waves are often observed in patients with intracranial hypertension from varying etiologies. Typical plateau waves are characterized by spontaneous and acute, rapid elevations in intracranial pressure (ICP).

Appropriate Cerebral Perfusion Pressure During Rewarming after Therapeutic Hypothermia

This study evaluated the cerebral ischemic parameters during the rewarming period after therapeutic hypothermia to determine the critical cerebral perfusion pressure (CPP) threshold to avoid ischemic deterioration. Cat experimental head injury was induced by inflation of an epidural rubber balloon to maintain intracranial pressure at 30 mmHg under hypothermia. During the rewarming period, CPP was maintained at > or = 120 mmHg, 90 mmHg, and 60 mmHg by controlling the blood pressure. CBF, CMRO2, AVDO2, and cerebral venous oxygen saturation (ScvO2) were measured. Brain extracellular glutamate concentrations were also measured by a dialysis electrode. Histological preparations of all brains were examined under an electron microscope. The cerebral metabolic parameters in animals with CPP of more than 90 mmHg returned to the base values after rewarming. However, ScvO2 was significantly lower (27 +/- 6%) and AVDO2 was significantly higher (9.4 +/- 1.8 ml/100 g/min) after rewarming in the animals with CPP = 60 mmHg, which indicated misery perfusion. Animals with CPP = 60 mmHg also showed increased extracellular glutamate concentration and histological ischemic damage (mitochondrial swelling). CPP of 60 mmHg during the rewarming period is associated with irreversible ischemia, which indicates continuation of cerebral vasoconstriction. Therefore, a CPP of greater than 90 mmHg is required to avoid cerebral ischemia.