大鼠蛛网膜下腔出血脑微区血流量与血清一氧化氮变化

目的探讨蛛网膜下腔出血（ＳＡＨ）后继发性脑缺血损害及其一氧化氮（ＮＯ）的作用。方法应用非开颅性方法建立大鼠ＳＡＨ模型,检测２４ｈ内脑微区血流量和颅内血清ＮＯ的动态改变,并测量基底动脉（ＢＡ）管径。结果ＳＡＨ后脑微区血流量迅速降低,１ｈ达最低值,２４ｈ内无明显恢复趋势（Ｐ＜ ０．０１）。ＳＡＨ后１ｈ血清ＮＯ开始减低,井持续２４ｈ（Ｐ＜０．０１）。ＢＡ管径于ＳＡＨ后明显缩小（Ｐ＜０．０１）。结论ＳＡＨ时脑灌注压降低、脑血管痉挛及微循环异常均可能与脑血流量降低有关。ＮＯ减少是脑血管 痉挛和微循环异常发生的重要因素之一。     

Niravoline, a selective kappa-opioid receptor agonist effectively reduces elevated intracranial pressure

To ascertain the effects of niravoline (RU 51599, a selective kappa-opioid receptor agonist) on elevated intracranial pressure with mass lesion, the authors experimentally induced intracranial hypertension in cats by progressive inflation of an extradural balloon with physiological saline at the constant rate of 0.5 ml/h for 2.5 h. After 2.5 h, inflation was discontinued, but the balloon remained inflated for an additional 3 h. Immediately after cessation of balloon inflation and while the balloon remained expanded, the control group (n = 8) received ringer's lactate solution only. In the treatment group (n = 8), each cat was treated with an intravenous administration of niravoline at a dose of 1.0 mg/kg immediately after the cessation of balloon inflation and every hour for 3 h in post-inflation period (three injections total). Changes in intracranial pressure (ICP), mean arterial blood pressure (MAP), cerebral perfusion pressure (CPP), electroencephalogram (EEG), pupil size, blood gasses and pH, plasma osmolality and electrolytes, and brain water content were studied in both groups. Compared with the untreated group, niravoline treatment produced significant decreases in ICP and significant increases in CPP at 1, 2, and 3 h post-inflation in the presence of an extradural mass lesion. Brain water content was significantly reduced both in the compressed and contralateral hemispheres following niravoline treatment. No significant changes were observed in plasma osmolality and systemic arterial blood pressure following niravoline administration. The results from this present study provide further evidence that niravoline is effective in reducing elevated intracranial pressure, brain water content, and maintaining an adequate cerebral perfusion pressure even in the presence of an extradural mass lesion. Niravoline may offer a new therapeutic modality in head-injury patients with an acute intracranial, expanding mass lesion by providing a safer extended time-period until the mass can be surgically evacuated.     

A mathematical model of the relationship between cerebral blood volume and intracranial pressure changes: The generation of plateau waves

The relationship between intracranial pressure (ICP), cerebral blood volume (CBV), cerebrospinal fluid dynamics, and the action of cerebral blood-flow (CBF) regulatory mechanisms is examined in this work with the help of an original mathematical model. In building the model, particular emphasis is placed on reproducing the mechanical properties of proximal cerebral arteries and small pial arterioles, and their active regulatory response to perfusion pressure and cerebral blood flow changes. The model allows experimental results on cerebral vessel dilatation and cerebral blood-flow regulation, following cerebral perfusion pressure decrease, to be satisfactorily reproduced. Moreover, the effect of cerebral blood volume changes—induced by autoregulatory adjustments — on the intracranial pressure time pattern can be examined at different levels of arterial hypotension. The results obtained with normal parameter values demonstrate that, at the lower lumits of autoregulation, when dilatation of small arterioles becomes maximal, the increase in cerebral blood volume can cause a significant, transient increase in intracranial pressure. This antagonism between intracranial pressure and autoregulatory adjustments can lead to instability of the intracranial system in pathological conditions. In particular, analysis of the linearized system “in the small” demonstrates that an impairment in cerebrospinal fluid (CSF) reabsorption, a decrease in intracranial compliance and a high-regulatory capacity of the cerebrovascular bed are all conditions which can lead the system equilibrium to become unstable (i.e., the real part of at least one eigenvalue to turn out positive). Accordingly, mathematical simulation “in the large,” in the above-mentioned conditions, exhibits intracranial pressure periodic fluctuations which closely resemble, in amplitude, duration, frequency and shape, the well-known Lundberg A-waves (or plateau waves).     

Metabolites from cerebrospinal fluid in aneurysmal subarachnoid haemorrhage correlate with vasospasm and clinical outcome: a pattern-recognition 1H NMR study

Following subarachnoid haemorrhage the most significant complication is sustained cerebral vascular contraction (vasospasm), which may result in terminal brain damage from cerebral infarction. Despite this, the biochemical cause of vasospasm remains poorly understood. In this study, the global high-concentration metabolite composition of CSF has been correlated with patient outcome after subarachnoid haemorrhage using multivariate statistics and 1H NMR spectroscopy. In total, 16 patients with aneurysmal subarachnoid haemorrhage (aSAH) were compared with 16 control patients who required a procedure where CSF was obtained but did not have aSAH. Multivariate statistics readily distinguished the aSAH group from the heterogeneous control group, even when only those controls with blood contamination in the CSF were used. Using principal components analysis and orthogonal signal correction, vasospasm was correlated to the concentrations of lactate, glucose and glutamine. These pattern recognition models of the NMR data also predicted Glasgow Coma Score (54% within +/- 1 of the actual score on a scale of 1-15 for the whole patient group), Hunt and Hess SAH severity score (88% within +/- 1 of the actual score on a scale of 1-5 for the aSAH group) and cognitive outcome scores (78% within +/- 3 of the actual score on a 100% scale for the whole patient group). Thus, the approach allowed the prediction of outcome as well as confirming the presence of aSAH.     

Brainstem control of cerebral blood flow and application to acute vasospasm following experimental subarachnoid hemorrhage

Symptomatic ischemia following aneurysmal subarachnoid hemorrhage (SAH) is common but poorly understood and inadequately treated. Severe constriction of the major arteries at the base of the brain, termed vasospasm, traditionally has been thought to be a proximal event underlying these ischemias, although microvascular changes also have been described. The vast majority of studies aimed at understanding the pathogenesis of ischemic deficits, and vasospasm have focused on the interaction of the “spasmogen” of the extravasated blood with the smooth muscle and endothelium of the arteries. This has led to a comparative neglect of the contribution of the CNS to the maintenance of cerebral perfusion. In the present study, we focused on the role of the rostral ventromedial medulla (RVM) in modulating cerebral perfusion at rest and following an experimental SAH in the rat. Changes in cerebral blood flow (CBF) were measured using laser-Doppler flowmetry and three-dimensional optical microangiography. Focal application of a GABA_A receptor agonist and antagonist was used to respectively inactivate and activate the RVM. We show here that the RVM modulates cerebral blood flow under resting conditions, and further, contributes to restoration of cerebral perfusion following a high-grade SAH. Failure of this brainstem compensatory mechanism could be significant for acute perfusion deficits seen in patients following subarachnoid hemorrhage.     

脑逆灌注血液动力学数学模型研究

脑逆灌注方法是指在脑梗塞患者发病后最短时间内从股动脉引出动脉血经血泵由颈内静脉逆行灌入大脑缺血部位从而缓解缺血程度 ,减轻缺血损伤 ,提高患者预后质量。目的是建立脑逆灌注血液动力学模型 ,研究逆灌注血流速度与颅内压、静脉窦压及脑血管床压的关系 ,从理论上验证脑逆灌注的可行性。     

Intracranial flow patterns at increasing intracranial pressure

Summary In the course of a pilot study, changes in intracranial pressure were compared with the transcranial Doppler findings of the middle cerebral artery. The cases of five patients were discussed who developed dissociated brain death in spite of intensive therapeutic measures. The studies showed that changes of the intracranial pressure influenced the flow patterns considerably: at increasing intracranial pressure (decreasing cerebral perfusion pressure) a progressive reduction of the systolic and above all diastolic flow velocities and finally a pendular flow occurred. These changes could be recorded quantitatively by means of the Pourcelot index and the mean flow velocity. Acute changes of the intracranial pressure can be detected at an early stage by noninvasive transcranial Doppler studies and can be followed by adequate intensive therapy.Abbreviations CPP Mean cerebral perfusion pressure - ICP Intracranial pressure - MAP Mean systemic arterial pressure - MCA Middle cerebral artery - MFV Mean flow velocity - pCO₂ Carbon dioxide tension - R Index de résistance=Pourcelot index - TCD Transcranial Doppler Supported by the DFG (SFB 330)     

蛛网膜下腔出血后继发性脑缺血的实验研究

目的探讨蛛网膜下腔出血（ＳＡＨ）后继发性脑缺血损伤和尼莫地平（ＮＤ）的保护作用。方法利用大鼠ＳＡＨ模型,对单纯ＳＡＨ组和ＮＤ处理组检测术前及ＳＡＨ后２４ｈ内脑微区血流量（ＣＢＦ）、体感诱发电位（ＳＥＰ）和脑组织一氧化氮（ＮＯ）含量,并于ＳＡＨ后３ｄ对海马组织行病理检查。结果单纯ＳＡＨ组大鼠在产生ＳＡＨ后ＣＢＦ立即降低,并持续２４ｈ,ＳＥＰ潜伏期从ＳＡＨ后１ｈ开始逐渐延长,３ｄ后海马ＣＡ１区神经元明显损伤;脑组织ＮＯ含量在ＳＡＨ后１ｈ至２４ｈ显著增加。ＮＤ处理组的上述改变均较单纯ＳＡＨ组明显减轻。结论ＳＡＨ可导致继发性脑缺血损伤,其原因之一为脑组织ＮＯ大量增加;ＮＤ通过拮抗脑组织ＮＯ的病理变化而减轻ＳＡＨ后继发性脑缺血性损伤。     

Ultra-Early Surgery for Poor-Grade Intracranial Aneurysmal Subarachnoid Hemorrhage: A Preliminary Study

Purpose

To describe the therapeutic effect and possibility of the ultra-early surgery for poor-grade aneurysmal subarachnoid hemorrhage (Hunt-Hess grades IV - V).

Materials and Methods

Nine cases with intracranial aneurysms, demonstrated by computed tomographic angiography (CTA), were treated by ultra-early surgery under general anesthesia within 24 hours from subarachnoid hemorrhage (SAH), 5 cases were treated within 6 hours and 4 cases in 6 - 24 hours. Preoperative Hunt-Hess grade: 6 cases were IV and 3 cases were V. The clinical outcome was evaluated by Glasgow Outcome Scores (GOS).

Results

In operation, difficult dissection occurred in 5 cases (55.6%), and rupture of aneurysm occurred and temporary obstructions were performed in 4 cases (44.4%). After clipping of aneurysm, 2 cases underwent V-P shunt because of hydrocephalus, pulmonary infection occurred in 3 cases, hypothalamus reaction accompanied with upper gastrointestinal hemorrhage in 2 cases. The clinical outcome were favorable (GOS 4 - 5) in 4 cases (44.4%), dissatisfied (GOS 2 - 3) in 3 cases (33.3%), and dead (GOS 1) in 2 cases (22.2%) when patients departed from our hospital.

Conclusion

The ultra-early surgery can avoid early rebleeding of intracranial aneurysm, therefore, should be considered in the treatment of Hunt-Hess grade IV-V intracranial aneurysms. The appliance of CTA can make it possible to use of ultra-early surgery and improve the therapeutic effect.     

Potentials of magnesium treatment in subarachnoid haemorrhage.

Subarachnoid hemorrhage from a ruptured aneurysm is a subset of stroke. The young age (median 55 years) and poor outcome (50% of patients die; 30% of survivors remain dependent) explain why in the population the loss of productive life years from aneurysmal subarachnoid hemorrhage (SAH) is as large as that from brain infarcts, the most common type of stroke. Ischemia plays an important role in the pathophysiological process after SAH. A period of global cerebral ischemia firstly occurs in the acute phase, immediately after rupture of the aneurysm, due to acute vasoconstriction and elevated intracranial pressure, which leads to a drop in perfusion pressure. This is quite distinct from the secondly, delayed cerebral ischemia (DCI), which is focal or multi-focal. DCI usually occurs between 4 and 10 days after the initial bleeding, has a gradual onset and is multi-focal, and is an important cause of death and dependency after SAH. The interval between the bleeding and the onset of ischemia provides an opportunity for preventive treatment. Magnesium is readily available, inexpensive and has a well-established clinical profile in obstetrical and cardiovascular practice. It is beneficial in the treatment of eclampsia, a disease with a pathophysiology comparable to DCI after subarachnoid hemorrhage. Neuroprotective mechanisms of magnesium include inhibition of the release of excitatory amino-acids and blockade of the NMDA-glutamate receptor. Magnesium is also a non-competitive antagonist of voltage dependent calcium channels, has cerebrovascular dilatory activity and is an important co-factor of cellular ATPases, including the Na/K-ATPase. Magnesium can reverse delayed cerebral vasospasm and reduces the extent of acute ischemic cerebral lesions after experimental subarachnoid hemorrhage in rats. In this article we discuss the neuroprotective potency of magnesium in SAH by describing the pathophysiology of ischaemia after SAH and the many ways magnesium may interfere with this.     

Endothelial injury following experimental subarachnoid hemorrhage in rats: Effects on brain blood flow

Background: The leading cause of death and disability in patients suffering from aneurysmal subarachnoid hemorrhage (SAH) is cerebral vasospasm, a persistent, progressive, and often irreversible constriction of cerebral arteries. A wide array of pathological changes occur in cerebral arteries following SAH, with endothelial injury being the earliest and most consistent one. Since intact endothelium modulates many reflexes that influence vascular tone, damage to them may represent a significant contributor to cerebral vasospasm. Methods: Changes in local cerebellar blood flow (LCBF) and pathological alterations in major cerebral arteries were studied and compared in rats at various time intervals following SAH. SAH induced by the subarachnoid injection of 0.3 ml of whole blood. Sham rats received a subarachnoid injection of 0.3 ml of isotonic saline. Results: Except for an immediate but transient decrease, LCBF remained unchanged over a 3 day period following saline injection. Likewise, there were no pathological alterations in cerebral arteries of saline-injected rats. In contrast, the subarachnoid injection of whole blood produced significant changes in both LCBF and cerebral arteries. Within 30 minutes postblood injection, LCBF became significantly decreased and remained so for 4 hours. However, within 24 hours, LCBF had returned to control levels where it remained for 3 days. Endothelial injury was observed in the basilar and middle cerebral arteries from 30 minutes through 4 hours, the same periods in which LCBF was significantly reduced. Within 24 hours, the time period in which LCBF had rebounded to control ranges, cerebral arteries showed no evidence of endothelial damage and resembled control cells. Conclusion: The results indicate a direct correlation between changes in LCBF and the structural integrity of endothelial cells in the early stages following SAH. The lack of chronically depressed LCBF (after 1 day) may be related to the quick structural repair of endothelium. © 1994 Wiley-Liss, Inc.     

一氧化氮与脑血管痉挛性神经元损伤和L-精氨酸的作用

目的:探讨一氧化氮(NO)与蛛网膜下腔出血(SAH)后脑血管痉挛(CVS)所致神经元损伤的关系及L-精氨酸(L-Arg)的保护作用。方法: 应用血管内穿刺法建立大鼠SAH模型,将动物随机分为假手术组(SO组)、SAH组和SAH+L-Arg组。动态检测24 h内大脑顶叶皮层局部脑血流量(rCBF),测量基底动脉(BA)管径变化,测定不同时点血清NO(NO^-₂/NO^-₃)水平和血浆ET-1含量,并行海马神经元形态学观察。 结果: 假手术对各项指标无显著影响。SAH组术后rCBF迅速降低,1 h达最低值,并持续24 h;SAH后BA管径明显缩小;血清NO^-₂／NO^-₃含量明显减少,血浆ET-1含量逐渐增加,海马神经元显著损伤。与SAH组比较,SAH+L-Arg组rCBF下降的速度减慢、程度减轻;BA管径缩小的程度减轻;血清NO^-₂／NO^-₃水平降低和血浆ET-1含量增高的变化减轻;海马神经元损伤的程度减轻。结论: 血清NO浓度的降低参与了CVS性神经元损伤,L-Arg对之具有一定减轻作用。     

Intracranial mechanisms for preserving brain blood flow in health and disease

The brain is an exceptionally energetically demanding organ with little metabolic reserve, and multiple systems operate to protect and preserve the brain blood supply. But how does the brain sense its own perfusion? In this review, we discuss how the brain may harness the cardiovascular system to counter threats to cerebral perfusion sensed via intracranial pressure (ICP), cerebral oxygenation and ischaemia. Since the work of Cushing over 100 years ago, the existence of brain baroreceptors capable of eliciting increases in sympathetic outflow and blood pressure has been hypothesized. In the clinic, this response has generally been thought to occur only in extremis, to perfuse the severely ischaemic brain as cerebral autoregulation fails. We review evidence that pressor responses may also occur with smaller, physiologically relevant increases in ICP. The incoming brain oxygen supply is closely monitored by the carotid chemoreceptors; however, hypoxia and other markers of ischaemia are also sensed intrinsically by astrocytes or other support cells within brain tissue itself and elicit reactive hyperaemia. Recent studies suggest that astrocytic oxygen signalling within the brainstem may directly affect sympathetic nerve activity and blood pressure. We speculate that local cerebral oxygen tension is a major determinant of the mean level of arterial pressure and discuss recent evidence that this may be the case. We conclude that intrinsic intra‐ and extra‐cranial mechanisms sense and integrate information about hypoxia/ischaemia and ICP and play a major role in determining the long‐term level of sympathetic outflow and arterial pressure, to optimize cerebral perfusion.     

增强型体外反搏增加心脏骤停犬颈总动脉血流量

目的: 探讨增强型体外反搏(EECP)干预对心脏骤停(SCA)犬颅内压(ICP)、脑灌注压(CPP)和右颈总动脉平均流量(MQ)的影响。方法: 12只犬制成SCA模型,经心肺复苏至自主循环恢复(ROSC)后随机分成对照组(4只)和EECP组(6只),2只建模未成功。EECP组分别行2次1 h EECP干预,观察致颤前后、ROSC后(每1 h)ICP、CPP和MQ的变化,ROSC 6 h后停止监测。结果: 平均动脉压(MBP)、收缩期血压峰值(MSP)、ICP、平均脑灌注压(MCPP)和收缩期脑灌注压峰值(SCPP)组间比较差异无统计学意义(P＞0.05);EECP时舒张期血压峰值(MDP)和舒张期脑灌注压峰值(DCPP)明显高于对照组(P<0.05)。EECP组颈总动脉血流阻力在EECP时明显低于对照组(P<0.05)。EECP时MQ明显高于对照组(P<0.05)。结论: EECP并不影响SCA-ROSC模型MBP、MSP、ICP、MCPP和SCPP而是通过增加MDP、DCPP和降低血流阻力等机制来增加颈总动脉的平均血流量。     

血一氧化氮和内皮素含量变化在大鼠急性脑血管痉挛中的作用

目的：探讨一氧化氮（ＮＯ）,内皮素（ＥＴ）在蛛网膜下腔出血（ＳＡＨ）后急性脑血管痉挛（ＣＶＳ）中的作用。方法：应用非开颅大鼠ＳＡＨ模型,检测ＳＡＨ前后基底动脉（ＢＡ）管径改变,２４ｈ内大鼠顶叶皮层局部脑血流量,血中ＮＯ,ＥＴ含量动态变化。     

TNF-α and sICAM-1 in intracranial aneurismal rupture

Introduction  Subarachnoidal hemorrhage (SAH) occurring after aneurismal rupture produces an inflammatory response in the cerebral circulation. Tumor necrosis factor (TNF)-α is a major cytokine in this process. Adhesion molecules provide information on inflammatory reactions taking place in the walls of blood vessels. Clinical evidence suggests a role of soluble intercellular adhesion molecule (sICAM)-1 in early hemorrhagic events. This study aimed to evaluate the implementation of early TNF-α and sICAM-1 serum measurement for the prognosis of patient outcome after intracranial aneurismal rupture. Materials and Methods  The study consisted of 27 patients with a diagnosis of intracranial aneurysm. SAH was evaluated on admission according to the Fisher scale, patients’ consciousness with the Glasgow Coma Scale, clinical grading with the Hunt and Hess scale, and clinical outcome with the Glasgow Outcome Scale (GOS). Blood samples were drawn within 72 h after arrival at the emergency room. Serum concentrations of TNF-α and sICAM-1 were assayed with the ELISA method. Results  The initial serum TNF-α concentration in the aneurismal patients was low and did not correlate with radiological and clinical scores. The serum sICAM-1 level positively correlated with the severity of bleeding assessed by the Fisher scale and negatively with the patient’s scoring in the GOS. Conclusions  This study demonstrated the absence of a systemic TNF-α-mediated inflammatory response at the onset of subarachnoid hemorrhage. Early measurement of serum sICAM-1 levels offers a potential prognostic value in the assessment of patients’ outcome after brain aneurismal rupture.     

Anatibant,a selective non-peptide bradykinin B2 receptor antagonist,reduces intracranial hypertension and histopathological damage after experimental traumatic brain injury

Bradykinin, the main metabolite of the kallikrein-kinin system and one of the first mediators released during inflammation, is well known to increase the permeability of the blood brain barrier (BBB) by activation of kinin B₂ receptors and hence promote brain edema formation following traumatic brain injury (TBI). Anatibant^® (LF 16-0687), a selective non-peptide bradykinin B₂ receptor antagonist, reduces brain edema after experimental TBI, however, so far no data are available if Anatibant^® reduces also the sequels of brain edema formation, i.e. morphological brain damage. Therefore, we investigated the effect of Anatibant (3.0 mg/kg b.w.) on intracranial pressure (ICP) and contusion volume after experimental TBI. Male C57/Bl6 mice (25–28 g) were subjected to Controlled Cortical Impact trauma (CCI). Anatibant^® was administrated as a subcutaneous bolus 15 min and 8 h after TBI. ICP was measured 3, 6, and 10 h after injury and contusion volume was quantified 24 h after trauma. Our data demonstrate a significant reduction of ICP (16.6 ± 1.67 mmHg vs. 24.40 ± 3.58 mmHg; n = 6; p = 0.002) and of contusion volume 24 h after trauma (28.28 ± 5.18 mm³ vs. 35.0 ± 3.32 mm³n = 7; p = 0.003) in treated mice. Therefore we conclude, that inhibition of bradykinin B₂ receptors seems to be a promising treatment option, and might therefore be investigated in clinical trails for the treatment of TBI.     

The influence of subarachnoid hemorrhage on neurons: an animal model

Subarachnoid hemorrhage (SAH) has considerable mortality and morbidity, but the pathophysiologic mechanism is not entirely clear. Following SAH, blood or its lysate enters the subarachnoid space. This study examined how blood lysate influences the vulnerable brain following SAH. Heparinized hemolysate was slowly injected into the cisterna magna of 10 female rabbits, while a control group of 10 rabbits received a similar injection of heparinized isotonic sodium chloride solution without hemolysate. The basilar artery and brain tissue were excised after perfusion fixation. The degree of cerebral vasospasm was evaluated by measuring the cross-sectional area of the basilar artery, and brain damage was investigated by TUNEL staining. In the SAH group, the apoptosis index of neuronal cells located at the base of the temporal lobe averaged 26% (range = 3 to 56%), which was significantly higher than the corresponding apoptosis index in the control group (mean 0.5%, range = 0 to 4%, p <0.001). The mean cross-sectional area of the basilar artery in the SAH group did not differ significantly from that in the control group. These results suggest that SAH induces apoptosis of neuronal cells by a mechanism that is independent of cerebral vasospasm.     

Prostacyclin and thromboxane in cerebral vasospasm: effects of prostacyclin on experimentally-induced cerebral vasospasm

The basilar artery was exposed transclivally , and a vascular spasm was produced by topical application of a lysed erythrocyte solution. The maximum fall in the mean arterial blood pressure (MABP) after administering of 2 micrograms/ kgBW and 15 micrograms/ kgBW of PGI2, ranged from 35 to 45 mmHg and from 65 to 85 mmHg, respectively. The drop in MABP after an injection of papaverine hydrochloride (1.5 mg/ kgBW ) was between 30 and 40 mmHg. If MABP did not fall, the vessel diameter did not change. Although papaverine elicited marked dilation of both normal and spastic basilar arteries, PGI2 did not dilate normal basilar arteries and produced only a slight dilation of spastic basilar arteries. Subarachnoid hemorrhage (SAH) was simulated by an intracisternal injection of fresh autologous arterial blood 3 days prior to experimentation. Changes in regional cerebral blood flow (rCBF) were measured by the heat clearance method, before and after an intravenous administration of either PGI2 or papaverine hydrochloride. Changes in rCBF fell into 3 categories: Type A, no change; Type B, a change which varied with the arterial blood pressure, and Type C, an increase rCBF despite systemic hypotension. Type A or B was observed in 17 out of 19 cats with SAH in which PGI2 was administered intravenously, and Type C was observed in only 2 cats. Thirteen untreated control cats produced a Type A or B response in 12, and Type C response in only one cat. There were no significant differences between the control and SAH groups. When 15-hydroperoxy-5, 8, 11, 13-eicosatetraenoic acid (15-HPETE) was infused, the same results prevailed. Papaverine hydrochloride increased rCBF either transiently or continuously in all cats. These results suggest that PGI2 dilates extracranial rather than intracranial vessels regardless of the presence or absence of cerebral vasospasm.     

Splenic blood flow and intrasplenic flow distribution in rats

Summary In 75 rats, anesthetized with pentobarbital and breathing spontaneously, regional splenic blood flow (rSBF) was measured by means of the⁸⁵Kr(β)-clearance technique after an intraaortic slug injection of the dissolved indicator. In the normal and undisturbed spleen in situ rSBF is linearly related to the mean arterial blood pressure (MABP) within the range of 30–140 mm Hg. Mean rSBF is 0.71 ml/g/min, the mean arterial blood pressure being 105 mm Hg. In normal rats rSBF decreases significantly with increasing body weight or age. After total obstruction of the open circulation by application of rigid spherocytes, mean rSBF is reduced to 0.26 ml/g/min and is independent of the mean arterial blood pressure within the same range. In splenomegaly, due to enhanced reticuloendothelial activity and intensified immunological responses after tumor implantation, an increase in total splenic blood flow is found. However, related to 1 g of splenic wet weight, rSBF is diminished. In splenomegaly, rSBF also linearly depends on MABP within a wide range. Mean rSBF is 0.51 ml/g/min, the mean arterial blood pressure being 91 mm Hg. The distribution of intrasplenic blood flow between open and closed circulation depends on the size of the mean arterial blood pressure. The perfusion rate of the open circulation, compared with rSBF amounts to 72–93% (MABP=80–130 mm Hg).