Mechanisms of hyperbaric oxygen-induced neuroprotection in a rat model of subarachnoid hemorrhage.

Acute cerebral ischemia occurs after subarachnoid hemorrhage (SAH) because of increased intracranial pressure (ICP) and decreased cerebral perfusion pressure (CPP). The effect of hyperbaric oxygen (HBO) on physiological and clinical outcomes after SAH, as well as the expressions of hypoxia-inducible factor-1alpha (HIF-1alpha) and its target genes, such as BNIP3 and VEGF was evaluated. Eighty-five male SD rats (300 to 350 g) were randomly assigned to sham, SAH, and SAH+HBO groups. Subarachnoid hemorrhage was induced by endovascular perforation. Cortical cerebral blood flow (CBF), ICP, brain water content, brain swelling, neurologic function, and mortality were assessed. HBO (100% O2, 2.8 ATA for 2 h) was initiated at 1 h after SAH. Rats were sacrificed at 24 h to harvest tissues for Western blot or for histology. Apoptotic morphology accompanied by strong immunostaining of HIF-1alpha, VEGF, and BNIP3 were observed in the hippocampus and the cortex after SAH. Increased expressions of HIF-1alpha, VEGF, and BNIP3 were quantified by Western blot. HBO reduced the expressions of HIF-1alpha, VEGF, and BNIP3, diminished neuronal damage and improved CBF and neurologic function. HBO reduced early brain injury after SAH, probably by inhibition of HIF-1alpha and its target genes, which led to the decrease of apoptosis and preservation of the blood-brain barrier function.     

Impaired cerebral circulation and the effect of glycerol infusion in the acute stage of hypertensive intracerebral hematoma

The purpose of the present study was to clarify the mechanism of reduction in cerebral blood flow (CBF) in the acute stage of hypertensive intracerebral hematoma and the effect of glycerol infusion on the reduced CBF. We examined 55 cases. Thirty-eight cases showed putaminal hematoma and 17 presented thalamic hematoma. The range of consciousness was from alert to stupor. CBF was measured by single photon emission CT with Xe-133 inhalation within five days after the onset of the hemorrhage. A CBF map was obtained at a slice 5 cm above the OM-line and mean CBF of the affected and non-affected hemispheres was calculated. In 20 of 55 cases, 500 ml of glycerol was intravenously infused for 60 minutes and thereafter CBF was measured again. Epidural pressure was also recorded at the affected frontal area during glycerol infusion in three of the 20 cases. CBF reduced more profoundly in the area around the hematoma on the CBF map. Mean CBF of the affected hemisphere was negatively correlated with the volume of hematoma by a quadratic regression. After glycerol infusion, 13 of 20 cases showed a significant increase in mean CBF of the affected hemisphere, while the other seven cases showed no increase. Mean CBF increased with a higher percentage in cases with ventricular hemorrhage than without ventricular hemorrhage. In three cases where epidural pressure was measured during glycerol infusion, mean CBF increased and epidural pressure decreased. The increase in mean CBF was proportional to a rise in perfusion pressure calculated as pressure difference between mean systemic arterial pressure and mean epidural pressure, indicating impaired autoregulation in these cases.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of hyperoxemia on cerebral blood flow in subarachnoid hemorrhage patients

The effects of oxygen inhalation at atmospheric pressure (1 ATA.O2) on CBF were studied in subarachnoid hemorrhage (SAH) patients due to ruptured intracranial aneurysms to prove the usefulness of the "O2 response" test for the evaluation of the cerebral vascular response. "O2 response" means the CBF (or ICP) decrease during hyperoxemia. CBF was measured by 10 m Ci 133Xe intravenous injection method using rCBF analyzer BI-1400 (Valmet). Two-compartmental analysis was used for the calculation of initial slope index (ISI). Studied cases were 53 postoperative SAH patients and 100 times examinations were done under the condition of Rest-1 ATA.O2. The incidence of global disturbance of the O2 response was 33% from day 0 to 3, 31% during day 4 to 7, 30% during day 8 to 14, and 23% at day 15 to 30. But, after day 31, there was no case which revealed an impaired O2 response. It was not possible to detect focal or hemispheric abnormalities of the O2 response because of the limitation of noninvasive two-dimensional CBF measurement method employed. The causes of O2 response abnormality, within a month after the onset, were increased ICP, hydrocephalus and diffuse brain damage. Multiple regression analysis proved that elevated PaO2 is the major factor in reducing CBF. CBF and ICP correlation study showed that the higher the Rest ICP, the fewer the CBF decreases during pure O2 inhalation. This may indicate that the increase in ICP in the acute stage changes the O2 response according to the level of increased ICP.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of glycerol on local cerebral blood flow in patients with chronic ischemic cerebrovascular lesions]

The effect of glycerol on local cerebral blood flow was examined in patients with chronic ischemic cerebrovascular diseases (CVD). Twelve patients with minor completed stroke (10 cases) or transient ischemic attacks (2 cases) were subjected to the study (8 males, 4 females, the age ranging 27 to 70 with average of 56 +/- 15 years). Cerebral blood flow (CBF) was measured with stable xenon computerized tomography (Xe-CT). Each patient had 3 sequential Xe-CTs; resting, with intravenous administration of 200 ml of glycerol (group A) or lactated Ringer's solution (group B), and with intravenous administration of 1 g of acetazolamide. The resting CBF, CBF with glycerol, and CBF with acetazolamide were 30.4 +/- 1.6 ml/100 g/min (ml), 35.1 +/- 2.6 ml, 44.2 +/- 2.2 ml in group A, and 29.9 +/- 2.0 ml, 28.5 +/- 1.9 ml, 45.0 +/- 3.2 ml in group B, respectively. Glycerol increased CBF significantly in patients with chronic CVD, and seemed to be effective in ameliorating chronic low perfusion state in these patients.     

The effect of stable xenon on ICP

Recent studies have suggested that under certain conditions, inhalation of stable xenon can cause an increase in CBF or intracranial pressure (ICP). We reviewed the ICP changes that occurred during 48 stable xenon/CT CBF studies in 23 comatose head-injured patients to determine if the concentration (32%) and duration of inhalation (4.5 min) of stable xenon we used caused an increase in ICP. In the group as a whole, there was no significant difference between the mean ICP at the start of xenon inhalation and the mean ICP immediately after completion of the studies. An increase in ICP also was not found in subgroups with low, normal, or high global CBF, or groups with or without intracranial hypertension. Changes in ICP that occurred during individual studies usually were related to corresponding changes in the arterial pCO2 (p less than 0.0001, Pearson's correlation test). Our data suggest that 32% stable xenon administered for 4.5 min does not cause a significant increase in ICP during xenon/CT CBF studies.     

重型脑创伤患者脑细胞间液甘油浓度研究

目的研究重型脑创伤后影响脑细胞间液甘油(Gly)浓度变化的因素。方法连续监测53例重型颅脑创伤患者近损伤区脑细胞间液Gly浓度和局部脑血流(CBF),同时监测颅内压(ICP)及脑灌注压(CPP)。选择每小时CPP和CBF的最小值及ICP的最大值与该小时的Gly浓度匹配。根据局部CBF、ICP、CPP及预后将所有Gly样品分组。结果(1)Gly、CCP及CBF与预后的关系:与中残或重残组比较,植物生存或死亡组患者Gly显著增高而CCP及CBF显著降低(P<0.05);与恢复良好组比较,中残或重残组Gly显著增高而CCP及CBF显著降低(P<0.05)。(2)ICP,CCP,CBF对Gly的影响:ICP>15mmHg组、CCP<70mmHg组及CBF<50AU分别比ICP<15mmHg组、CCP>70mmHg及CBF50￣150AU组Gly浓度显著增高(P<0.01)。(3)病理类型和Gly浓度的关系:弥漫性轴索损伤Gly浓度最高,比硬膜外血肿及硬膜下血肿显著增高(P<0.05),但与脑挫裂伤患者无显著差异。结论Gly浓度可以反映原发和继发性脑损伤的严重程度,是细胞膜降解和脑缺血的可靠指标。     

The effect of hyperoxemia on cerebral blood flow in normal humans

The aim of this study was to evaluate the effect of various degrees of hyperoxemia on cerebral blood flow (CBF), including the hyperbaric oxygenation (HBO) environment. Study subjects were 28 healthy volunteers (17 males and 9 females) from 26 to 60 (average: 42 +/- 11) years old. CBF measurements were done by 19 mCi 133Xe intravenous injection method using rCBF analyzer BI-1400 (Valmet). Two-compartmental analysis was used for the calculation of Fast, Slow Flow and initial slope index (ISI). The three CBF study series included: Rest (before HBO 1 ATA.air)-1 ATA.O2-2 ATA.O2 series in 8 cases; Rest-1 ATA.O2 50% N2 50%-1.5 ATA.O2 series in 10 cases; and Rest-2.5 ATA.O2-after HBO (1 ATA.air) series in 8 cases. CBF measurements commenced 5 to 10 minutes after fixing a mask for oxygen inhalation. Arterial blood gas analyses using IL-813 (IL) and blood pressure measurements were done immediately after CBF measurements. CBF changes evaluated by ISI, estimating resting flow as 100% (PaO2: 93 +/- 8 mmHg), were 91% at 1 ATA.O2 50% (PaO2: 201 +/- 50 mmHg), 79% at 1 ATA.O2 (PaO2: 432 +/- 44 mmHg), 77% at 1.5 ATA.O2 (PaO2: 693 +/-79 mmHg) and 71% at 2 ATA.O2 (PaO2: 838 +/- 95 mmHg). CBF gradually decreased to the level shown for 2 ATA.O2, but CBF showed a tendency to increase somewhat at 2.5 ATA.O2 (81%, PaO2: 1103 +/- 111 mmHg). CBF decreases were statistically significant at 1 ATA.O2, 1.5 ATA.O2, 2 ATA.O2 and also 2.5 ATA.O2 compared with Rest (P less than 0.05). Arterial blood gas analyses clearly showed the stepwise increase in PaO2 to the level of 2.5 ATA.O2 (P less than 0.01). Changes in PaCO2 and blood pressure were slight and not significant statistically in each series. Since the data showed no significant change in the PaCO2 level in each series, it was concluded that the CBF decrease was due to vasoconstriction caused by the elevated PaO2. The mechanism of cerebral vasoconstriction caused by hyperoxemia is not yet clearly understood, but the direct vasoconstrictive effect of oxygen, neurogenic control and the metabolic effect of an elevated cerebral tissue oxygen level may contribute to the CBF decrease. CBF decrease during elevated PaO2 may be a protective physiological response to maintain normal brain metabolism and function against the excessive oxygen supply. Disturbance of this regulatory mechanism may result in oxygen poisoning of the central nervous system.(ABSTRACT TRUNCATED AT 400 WORDS)     

High ICP as trigger of proinflammatory IL-6 cytokine activation in aneurysmal subarachnoid hemorrhage

Abstract

Objective: There is a rising debate about the role of inflammation in the pathogenesis of complications after aneurysmal subarachnoid hemorrhage (SAH) such as intracranial hypertension (intracranial pressure, ICP >20 mmHg). This study aimed to analyse the origin of interleukin-6 (IL-6) in respect to ICP and cerebral metabolism in SAH patients.

Methods: Prospectively, IL-6 was measured in three compartments, the extracellular fluid (ECF) monitored by cerebral microdialysis (MD), cerebrospinal fluid (CSF) and plasma for 10 days after SAH (days 0–4, three times daily; days 5–10, two times daily). Patients were classified having intracranial hypertension (n=7) or normal ICP (n=17) during 10 days after bleeding. Glasgow outcome scale (GOS) was assessed after 3 and 6 months.

Results: Patient groups were comparable for age, WFNS and Fisher grade. Intracranial hypertension was associated with an inflammatory response, indicating activation of the inflammatory cascade in the brain (ECF) and systemic circulation with high IL-6 and C-reactive protein (CRP) plasma levels after SAH, the latter associated with unfavourable outcome. The data suggest the ECF but not the CSF as main origin of IL-6 in the systemic circulation in the presence of intracranial hypertension in SAH.

Discussion: Intracranial hypertension is associated with a strong activation of the inflammatory cascade in the brain and systemic circulation, and might be underestimated as proinflammmatory trigger in the pathogenesis of complications after SAH. Future therapies targeting anti-inflammatory response in plasma may help to reduce the inflammatory cascade responsible for development of intracranial hypertension.     

Effect of nimodipine on cerebral blood flow and cerebrovascular reactivity after subarachnoid haemorrhage

The aim of the present study was to investigate the effect of nimodipine on autoregulation of cerebral blood flow (CBF), CO2 reactivity and cerebral oxygen metabolism (CMRO2) in patients with subarachnoid haemorrhage (SAH). Eight patients with severe SAH were studied with repeated CBF and CMRO2 measurements on the first day of the bleeding and after at least 12 h of treatment of nimodipine. An initial resting study, an autoregulation study and a hyperventilation study was performed. CBF was measured using the 133-Xenon intravenous method. CMRO2 was calculated as AVDO2 x CBF. Nimodipine did not significantly change CBF and CMRO2 in the initial resting study. After induced arterial hypotension intact autoregulation was found before as well as after treatment with nimodipine. Beneficial effects of nimodipine were found on CO2 reactivity and CMRO2 during hypotension that may be explained as a positive effect on cerebral ischaemia.     

Hypertonic fluid resuscitation from subarachnoid hemorrhage in rats: a comparison between small volume resuscitation and mannitol

OBJECTIVE: Death and severe morbidity after subarachnoid hemorrhage (SAH) are mainly caused by global cerebral ischemia through increased intracranial pressure (ICP) and decreased cerebral blood flow (CBF). We have recently demonstrated neuroprotective effects of small volume resuscitation (7.5% saline in combination with 6% dextran 70) in an animal model of SAH, leading to normalization of increased ICP, reduced morphological damage and improved neurological recovery. In the present study, we compared the concept of small volume resuscitation represented by two clinically licenced hypertonic-hyperoncotic saline solutions with the routinely used hyperosmotic agent-mannitol-and investigated their effects on ICP, CBF, neurological recovery and morphological damage after SAH in rats. METHODS: 60 dextran-resistant Wistar rats were subjected to SAH by an endovascular filament. ICP, MABP (mean arterial blood pressure) and bilateral local CBF were continuously recorded. All animals were randomly assigned to four groups: (I) NaCl 0.9% (4 ml/kg bw), (II) 7.5% NaCl+6% dextran 70 (4 ml/kg bw), (III) 7.2% NaCl+HES 200,000 (4 ml/kg bw) and (IV) 20% mannitol (9.33 ml/kg bw) given 30 min after SAH. Neurological deficits were assessed on days 1, 3 and 7 after SAH. The morphological damage was evaluated on day 7 after SAH. RESULTS: The induction of SAH resulted in an immediate ICP increase to 46.6+/-3.2 mm Hg (mean+/-S.E.M.) and 29.6+/-1.3 (mean+/-S.E.M.) mm Hg 90 min post-SAH. While a treatment with both hypertonic saline solutions (II, III) decreased ICP as well as the 20% mannitol solution, only the group treated with hypertonic saline and dextran 70 (II) showed an increase of ipsilateral CBF for 20 min after the infusion and significantly more surviving neurons in the motorcortex and caudoputamen. Mortality was reduced from 60% (I) and 73% (III and IV), respectively, to 40% in group II. CONCLUSION: Of all hypertonic solutions investigated, small volume resuscitation with NaCl 7.5% in combination with 6% dextran 70 evolved to be most effective in terms of reducing the initial harmful sequelae of SAH, leading to lowered ICP and less morphological damage after SAH in the rat.     

Independent compartment phenomena: characteristics of dynamics in cerebral tissue oxygen metabolism under increased intracranial pressure in immature brain: an experimental study

The aim of this study is to clarify the specific pathophysiology of increased intracranial pressure in an immature brain in relation to its unique cerebral blood flow dynamics and brain tissue oxygen metabolism. Thirteen puppies were used for an experimental model of brain herniation due to a massive intracerebral hematoma. Along with increasing size of the hematoma, the intracranial pressure (ICP), carotid blood flow (CBF) and cerebral tissue oxygen (CTPO2) were measured simultaneously and continuously. The tolerance capacity for an acutely expanding mass lesion, or intracranial compliance, was studied. The ratio of hematoma volume/body weight was obviously higher by more than 200% in a group of younger puppies with open cranial sutures. Dynamic changes of CTPO2 were noted to be independent in the cerebral subcortical region and the medulla oblongata, when Doppler detection of arterial pulsations showed no flow in the anterior circulation in association with increased intracranial pressure caused by a supratentorial expanding mass lesion. A case with open cranial sutures (1,500 g of body weight) clearly demonstrated this and survived over 24 hours. With acutely increasing ICP CTPO2 was elevated modestly in the cerebral subcortical region (p < 0.1) and prominently in the medulla oblongata (p < 0.005). In conclusion, the posterior fossa structure (brain stem and cerebellum) in the immature age group is protected from an acutely expanding mass lesion in the supratentorial compartment. The posterior fossa behaves as an independent compartment with more prominent CBF and CTPO2 reactivity in the dynamic changes. The author proposed to name these findings as "independent compartment phenomena".     

Cerebral effects of hyperbaric oxygen breathing: a CBF SPECT study on professional divers

We investigated the effects on cerebral blood flow (CBF) of pure oxygen breathing exposure during dives in a group of professional divers, in both the normobaric (NBO) and the hyperbaric oxygen (HBO) breathing conditions. Using single photon emission computerized tomography (SPECT) and Tc-99m hexamethylpropylenamine oxime (HM-PAO), we studied 10 young divers and six normal volunteers. Divers were studied by SPECT in the NBO and HBO conditions, in two different sessions. The HBO state was obtained in a hyperbaric chamber at 2.8 ATA for 15 min. By ANOVA, we did not observe any significant difference in CBF distribution between controls and divers in both NBO and HBO conditions. By individual analysis, divers showed a decreased CBF in a total of 33 regions of interest (ROIs) during NBO and 46 ROIs during HBO with respect to control values. In particular, two divers showed a remarkable increase in the number of hypoperfused ROIs during HBO (+7 and +5 ROIs, respectively). Pure oxygen breathing exposure in young divers is associated with a patchy distribution of brain areas of hypoperfusion. This phenomenon is more pronounced in the HBO state than in the NBO state. Further studies on CBF are needed to help identify divers potentially prone to harmful oxygen effects.     

The time course of intracranial pathophysiological changes following experimental subarachnoid haemorrhage in the rat

The rat subarachnoid haemorrhage (SAH) model was further studied to establish the precise time course of the globally reduced CBF that follows and to ascertain whether temporally related changes in cerebral perfusion pressure (CPP) and intracranial pressure (ICP) take place. Parallel ultrastructural studies were performed upon cerebral arteries and their adjacent perivascular subarachnoid spaces. SAH was induced by a single intracisternal injection of autologous arterial blood. Serial measurements of regional cortical CBF by hydrogen clearance revealed that experimental SAH resulted in an immediate 50% global reduction in cortical flows that persisted for up to 3 h post SAH. At 24 h, flows were still significantly reduced at 85% of control values (p less than 0.05), but by 48 h had regained normal values and were maintained up to 5 days post SAH. ICP rose acutely after haemorrhage to nearly 50 mm Hg with C-type pressure waves being present. ICP then fell slowly, only fully returning to control levels at 72 h. Acute hydrocephalus was observed on autopsy examination of SAH animals but not in controls. Reductions in CPP occurred post SAH, but only in the order of 15%, which could not alone account for the fall in CBF that took place. At 48 and, to a lesser extent, 24 h post SAH, myonecrosis confined largely to smooth muscle cells of the immediately subintimal media was observed. No significant changes in the intima or perivascular nerve plexus were seen. Within 24 h of haemorrhage, a limited degree of phagocytosis of erythrocytes by pial lining cells took place. However, early on the second day post SAH, a dramatic increase in the numbers of subarachnoid macrophages arose from a transformation of cells of the pia-arachnoid. This period was characterised by intense phagocytic activity, erythrocytes, fibrin, and other debris being largely cleared over the next 24 h. At 5 days post SAH the subarachnoid macrophage population declined, cells losing their mobile active features to assume a more typical pia-arachnoid cell appearance once more. Our studies indicate that this increasingly utilised small animal model of SAH develops global cortical flow changes only acutely, and it is likely that early vasospasm, secondary to released blood products rather than pressure changes per se, is responsible for the initial cerebral ischaemia that develops. Interestingly, both cerebral arterial vasculopathy and perivascular macrophage phagocytic activity are most marked at approximately 48 h following SAH in the rat, a time at which a phase of delayed cerebral arterial narrowing has previously been documented.     

Correlation between intracranial pressure (ICP) and changes in CT images of cerebral hemorrhage

Abstract

The relationship between intracranial pressure and CT images was investigated in 80 cases of cerebral hemorrhage that occurred between 1984 and 1990. In traumatic intracerebral hematoma, positive correlation was found between intracranial pressure and both shift of midline structures and volume of hematoma except in the occipital lobe or at the base of the frontal lobe. In nontraumatic intracerebral hematoma, increased intracranial pressure was found to correlate with changes in the configuration of the lateral ventricles, intraventricular hemorrhage, and compression of the basal cisterns and cortical sulci. No correlation between intracranial pressure and hematoma volume was observed, most likely due to the number of elderly patients in the subject population. In nontraumatic subarachnoid hemorrhage, positive correlation existed between increased intracranial pressure and intraventricular hemorrhage as well as Evans' ratio calculated using repeat CT images that were obtained due to disturbances in cerebrospinal fluid circulation. These results suggest that the degree by which intracranial pressure increases in patients with cerebral hemorrhage can be estimated by the changes in CT images. [Neural Res 1998; 20: 225-230]     

Cerebral blood flow autoregulation during intracranial hypertension: a simple, purely hydraulic mechanism?

Objective  In this paper, we re-propose the role of a hydraulic mechanism, acting where the bridging veins enter the dural sinuses in cerebral blood flow (CBF) autoregulation. Materials and methods  We carried out an intraventricular infusion in ten albino rabbits and increased intracranial pressure (ICP) up to arterial blood pressure (ABP) levels. We measured CBF velocity by an ultrasound probe applied to a by-pass inserted in a carotid artery and recorded ICP by an intraventricular needle. Diastolic and pulsatile ICP and ABP values were analyzed from basal conditions up to brain tamponade and vice versa. Conclusions  A biphasic pattern of pulsatile intracranial pressure (pICP) was observed in all trials. Initially, until the CBF velocity remained constant, pICP increased (from 1.2 to 5.4 mmHg) following a rise in diastolic intracranial pressure (dICP); thereafter, in spite of a further rise in dICP, pICP decreased (2.87 mmHg) following CBF velocity reduction until intracranial circulation arrest (pICP = 1.2 mmHg). A specular pattern was observed when the intraventricular infusion was stopped and CBF velocity returned to basal levels. These findings can be interpreted as indicating a hydraulic mechanism. Initially, when CBF is still constant, pICP rise is due to an increase in venous outflow resistance; subsequently, when CBF decreases following a further increase in venous outflow resistance, the vascular engorgement produces an arteriolar vasodilation. This vasodilation determines an increase in vascular wall stiffness, thus reducing pulse transmission to surrounding subarachnoid spaces. Commentaries on this paper are available at doi: and doi: .     

Spasm index in subarachnoid haemorrhage: consequences of vasospasm upon cerebral blood flow and oxygen extraction

A spasm index, defined as transcranial Doppler detected flow velocity in the middle cerebral artery divided by regional cortical cerebral blood flow (CBF), was used on 24 patients with subarachnoid haemorrhage (SAH). The aim was to estimate degree and time course of vasospasm, even in cases with great day-to-day variation in CBF, and correlate to CBF and oxygen extraction. All patients showed increase in spasm indices with peak index in the second or third week. The index seemed stable in spite of day-to-day fluctuations in CBF. Severe vasospasm were associated with poor clinical condition, reduced CBF (less than 30) and high AVDO2. The same picture could be seen with minor degree of vasospasm, probably, in some cases, due to high intracranial pressure. The results suggest that the spasm index is useful in monitoring patients with subarachnoid haemorrhage, and that severe vasospasm has a negative influence on clinical condition, CBF and oxygen extraction.     

高血压脑出血术后动态经颅多普勒超声与颅内压监护仪监测的临床意义

目的 探讨高血压脑出血手术方式以及术后如何控制血压.方法 对与96例高血压脑出血患者分别行开颅血肿清除术和血肿腔钻孔引流术,同时对每例患者行颅内压和平均动脉压连续监测7 d,同时监测术后1、3、7、14 d行双侧大脑中动脉平均血流速度和搏动指数值.结果 开颅术对于血肿量>50 ml的患者远期生存质量(6月后ADL分级)与血肿腔钻孔引流术比较有显著差异;另外术后1 d、3 d、7 d、14 d的TCD参数结果分析,开颅术对于缓解颅内压力、改善脑血流优于钻孔引流组.对所有患者术后ICP、MAP监测能有效控制血压防止再出血.结论 对于血肿量>50 ml患者应选择开颅手术.对所有高血压脑出血患者术后应常规进行ICP、MAP监测.     

Effects of elevated ICP on brain function: Can the multiparametric monitoring system detect the 'Cushing Response'?

Abstract

The 'Cushing Response' is a significant phenomenon associated with elevated ICP. The purpose of our study was to examine the effects of the intracranial hypertension level and duration on the cerebral tissue physiology, using a Multiprobe assembly (MPA). The parameters monitored simultaneously included ICP, CBF, mitochondrial NADH redox state, extracellular K⁺ and H⁺ levels, DC potential and ECoG, calculated CPP and blood pressure. Two groups of rats were used. In one group, ICP was elevated to 50–60 mmHg for 13–15 min and, in the second group, ICP was elevated to 20 mmHg for 30 min. The results show that ICP of 50–60 mmHg led to CPP reduction below the lower limits of autoregulation. However, ICP of 20 mmHg, even for a prolonged period of time is completely tolerated. Additionally, we found that the 'Cushing Response', developed in the moderate treatment (ICP = 20 mmHg) is beneficial, assuring high CBF levels under intracranial hypertension. Furthermore, CBF and CPP monitoring, apparently, are not sufficient for autoregulation assessment; more parameters are needed.     

PET and CBF Studies of Chronic Hydrocephalus: A Contribution to Surgical Indication and Prognosis

The authors investigate whether measurement of cerebral blood flow (CBF) in chronic hydrocephalus is a reliable indicator in selecting patients to undergo ventriculoperitoneal shunting. Global and regional CBF is quantified (Kety-Schmidt one-compartment model) by positron emission tomography in 21 patients. CBF is determined following inJection of 15 0-H2O at three time points 1 week before, 7 days after, and 7 months after shunting. The neurological status of these patients is classified, and cerebrospinal fluid (CSF) dynamics (continuous intracranial pressure [ICP] monitoring and CSF infusion tests) were assessed prior to surgery. Preoperative global CBF values correlate well with clinical outcome. Patients with a significantly lower global CBF value show clinical improvement after 7 months, whereas patients with higher CBF values do not (mean, 33 vs. 45 ml/1 00 ml per minute; p < 0 05). In contrast to conventional methods, including long-term ICP measurement and CSF infusion tests, preoperative global CBF values are discriminating in terms of clinical outcome. Thus, measurement of CBF may be helpful in evaluating the ultimate utility of shunt therapy in chronic hydrocephalus.