Dilatation Of Cerebral Blood Vessels Research Articles

Head injury case with blunt force traumatic: Case report

Child abuse has negative impact for children including emotional performance, mental dysfunction, and decrease intelligence. According to the 2014 Surveillance Report of Traumatic Brain Injury, in the United States, there are approximately 2.87 million head injury patients. Head injury, or so-called head trauma, is a blunt force/sharp force on the head or face that results in temporary cerebral dysfunction. It is one of the leading causes of death and disability in the productive age group, primarily traffic accidents. A boy went to the emergency room at Bhayangkara Kediri Hospital. There was swelling on the left head, expanding on the forehead and bruising on the left ear. Also found signs of sodomy marks in the form of abrasions around the anus. There are also bruises on the back and neck of the end. For a definitive diagnosis, the results of the CT scan were that the patient obtained extensive cerebral contusion and caused the deviation of the midline structure to the right as far as ± 0.9 cm with subgaleal hematoma and the dilation of cerebral blood vessels. In cases of head injury due to blunt trauma, blood infiltration will be found in the layers of the scalp and muscles in the direction of the trauma. The presence of blood infiltration is an intravital sign of evidence of extravasation of blood cells in the tissue. Another finding may be a skull base fracture in the posterior fossa caused by a direct blow to the occipital region. At the base of the skull, a fracture in the posterior fossa can cause symptoms such as bleeding from the nose, mouth, and ears, damage to the cranial nerves and cause raccoon eyes. In head injuries caused by blunt trauma can also cause subarachnoid hemorrhage and subdural hemorrhage due to rupture of the superior cerebral vein and “bridging vein” due to pressure/trauma it can cause death, to distinguish subarachnoid hemorrhage from subdural hemorrhage needs to be done sprinkling with water.

Incomplete circle of Willis and cerebrovascular reactivity in asymptomatic patients before and after carotid endarterectomy

Introduction/Objective. Circle of Willis (CoW) provides the most significant collateral flow in the presence of significant stenosis or occlusion of internal carotid artery. In terms of collateral flow ?incomplete? type and ?complete? type of CoW can be recognized. Patients with carotid artery disease with incomplete CoW have lower cerebrovascular reactivity and higher risk for stroke. Cerebrovascular reactivity refers to the residual capacity of dilatation of cerebral blood vessels in the condition of insufficient blood flow. In this study we analyzed changes in cerebrovascular reactivity after carotid endarterectomy in asymptomatic patients with respect to complete and incomplete CoW morphology. Methods. In this study in 97 patients with asymptomatic carotid artery disease we measured cerebrovascular reactivity before and after carotid endarterectomy by using method of ?apnea test? and ?breathholding index? (BHI). Patients were divided into two following groups: patients with ?complete? CoW and ?incomplete? CoW based on non-contrast magnetic resonance angio performed previously to the operation. Descriptive statistics, univariate analysis, and ANOVA for comparison of BHI values between groups were used. Results. The results showed significant increase in cerebrovascular reactivity at the side of stenosis in both groups of patients with complete CoW (BHI value increased from 0.897 to 1.090; F (1.65) = 30.788, p < 0.0005, parc. ?2 = 0.321) and incomplete CoW (BHI value increased from 0.690 to 1.010; F (1.27) = 62.318, p < 0.0005, parc. ?2 = 0.698) and the more significant increase in the group of incomplete CoW compared to the group with complete CoW (F (1.92) = 4.557, p = 0.035, parc. ?2 = 0.047) Conclusion. In most asymptomatic patients, cerebrovascular reactivity restores to normal following carotid endarterectomy. Parameters of cerebrovascular reactivity are lower in patients with incomplete CoW and the increase after carotid endarterectomy is more significant in such patients.

Expression Analysis of Serotonin Receptors, Serotonin Transporter and l-Amino Acid Decarboxylase in the Mouse Sphenopalatine Ganglion by RT-PCR, Northern Blot Analysis and In Situ Hybridization

The sphenopalatine ganglion (SPG) is a gathering of the cell bodies of parasympathetic fibers that dominate the nasal gland, lacrimal gland and cerebral blood vessels. The SPG controls nasal secretions, tears, and the dilation of cerebral blood vessels. However, it is unclear how serotonin regulates SPG functions. In this study, we investigated the expression of genes involved in the serotonergic system in the mouse SPG. We examined the mRNA expression levels of 5-HT1A, 5-HT1B, 5-HT1D, 5-HT1F, 5-HT2A, 5-HT2B, 5-HT2C, 5-HT3A, 5-HT3B, 5-HT4, 5-HT5A, 5-HT5B, 5-HT6 and 5-HT7 receptors, as well as serotonin transporter, tryptophan hydroxylases 1 and 2, and L-amino acid decarboxylase (AADC) by RT-PCR. It revealed that the 5-HT3A and 5-HT3B ionotropic receptors and AADC were likely to be highly expressed in the SPG, as measured by RT-PCR. We next performed in situ hybridization on the SPG to examine the expression of these three genes at the cellular level after validating the specificity of each cRNA probe by northern blotting. The 5-HT3A receptor, 5-HT3B receptor, and AADC were expressed in 96.5% ± 1.0%, 29.7% ± 10.7%, and 57.4% ± 2.9% of neuronal cell bodies in the SPG, respectively, indicating that the 5-HT3A receptor was virtually expressed in all SPG neurons. Our results on the expression of these critical serotonin system genes in the parasympathetic SPG provide insight into the pathogenetics of rhinitis, conjunctivitis and headache. Furthermore, our findings suggest that targeting the 5-HT3A receptor might have therapeutic potential in the treatment of these ailments.

Homeopathy Impact on Physical Health Aspects of Quality of Life of Patients with Chronic Headache in Isfahan in 2015

Introduction In fact one of the most common physical side effects are headache, headache is a symptom, not a disease. Headaches can be a symptom of organic disease, stress responses, dilation of cerebral blood vessels, skeletal muscle tension or set of factors listed. (1) Headache is the most com

Recombinant erythropoietin administration reduces exercise‐induced deline in regional cerebral oxygenation at 4500 m

At high altitude, exercise‐induced arterial desaturation decreases regional cerebral oxygenation (rO2Hb). Erythropoietin (EPO) potentiates endothelium‐mediated dilation of isolated, perfused rat middle cerebral arteries. To determine if EPO administration in humans mitigated the decreased cerebral rO2Hb during exercise within the first 3 h at 4500 m eight healthy male lowlanders received a subcutaneous injection of either EPO (600 IU/Kg) or a placebo (PLA) (0.9% NaCl) ~12 hr prior to ascent in a hypobaric chamber in a double‐blind, cross‐over study. We measured frontal lobe rO2 Hb by NIRS, arterial saturation (SaO2) by pulse oximetry, and PetO2 and PetCO2 by metabolic cart during rest and 50 W cycling. At 4500 m, serum EPO levels were (mean ± SD) 6 ± 2 and 720 ± 273 mU/ml for PLA and EPO trials, respectively. From rest‐to‐ exercise SaO2 decreased similarly in both trials (PLA: −6 ± 4 and EPO: −8 ± 4%), but rSO2 declined less in EPO (PLA: −2.12 ± 1.93 and EPO: −1.47 ± 2.40 μM, p=0.027), while rest and exercise PetO2 and PetCO2 were similar for both trials.Conclusionsince PO2 and PCO2 were constant and not likely changing cerebral vasomotor activity, the smaller exercise‐induced decline in rO2Hb following EPO administration supports the hypothesis that increasing circulating EPO potentiates dilation of cerebral blood vessels at high altitude. Funding: USAMRMC. Authors’ views; not official U.S. Army or DoD policy.

Beneficial Effects of Estrogen in a Mouse Model of Cerebrovascular Insufficiency

BackgroundThe M5 muscarinic acetylcholine receptor is known to play a crucial role in mediating acetylcholine dependent dilation of cerebral blood vessels. Previously, we reported that male M5 muscarinic acetylcholine knockout mice (M5R −/− mice) suffer from a constitutive constriction of cerebral arteries, reduced cerebral blood flow, dendritic atrophy, and short-term memory loss, without necrosis and/or inflammation in the brain.Methodology/Principal FindingsWe employed the Magnetic Resonance Angiography to study the area of the basilar artery in male and female M5R −/− mice. Here we show that female M5R −/− mice did not show the reduction in vascular area observed in male M5R −/− mice. However, ovariectomized female M5R −/− mice displayed phenotypic changes similar to male M5R −/− mice, strongly suggesting that estrogen plays a key role in the observed gender differences. We found that 17β-estradiol (E2) induced nitric oxide release and ERK activation in a conditional immortalized mouse brain cerebrovascular endothelial cell line. Agonists of ERα, ERβ, and GPR30 promoted ERK activation in this cell line. Moreover, in vivo magnetic resonance imaging studies showed that the cross section of the basilar artery was restored to normal in male M5R −/− mice treated with E2. Treatment with E2 also improved the performance of male M5R −/− mice in a cognitive test and reduced the atrophy of neural dendrites in the cerebral cortex and hippocampus. M5R −/− mice also showed astrocyte swelling in cortex and hippocampus using the three-dimensional reconstruction of electron microscope images. This phenotype was reversed by E2 treatment, similar to the observed deficits in dendrite morphology and the number of synapses.Conclusions/SignificanceOur findings indicate that M5R −/− mice represent an excellent novel model system to study the beneficial effects of estrogen on cerebrovascular function and cognition. E2 may offer new therapeutic perspectives for the treatment of cerebrovascular insufficiency related memory dysfunction.

Focal cerebral ischaemia induces corticotropin releasing factor (CRF) vascular immunoreactivity in rat occluded hemisphere

Corticotropin-releasing factor (CRF) induces the dilatation of cerebral blood vessels and increases cerebral blood flow (CBF). CRF receptor antagonists reduce ischaemic damage in the rat. In the present study, the expression of CRF around cerebral vessels has been investigated in the rat. No CRF immunoreactivity was identified around pial or intracerebral vessels in the absence of cerebral ischaemia. Four hours after middle cerebral artery occlusion (MCAo), intensely CRF-positive blood vessels were evident on the ischaemic cortical surface and in the peri-infarct and infarct zone. Increased CRF immunoreactivity was also detected in swollen axons in subcortical white matter, caudate nucleus and lateral olfactory tract of the ipsilateral hemisphere, consistent with the failure of axonal transport. These data provide morphologic support for a role of CRF in the pathophysiology of cerebral ischaemia.

Loss of M5 muscarinic acetylcholine receptors leads to cerebrovascular and neuronal abnormalities and cognitive deficits in mice

The M5 muscarinic acetylcholine receptor (M5R) has been shown to play a crucial role in mediating acetylcholine-dependent dilation of cerebral blood vessels. We show that male M5R-/- mice displayed constitutive constriction of cerebral arteries using magnetic resonance angiography in vivo. Male M5R-/- mice exhibited a significantly reduced cerebral blood flow (CBF) in the cerebral cortex, hippocampus, basal ganglia, and thalamus. Cortical and hippocampal pyramidal neurons from M5R-/- mice showed neuronal atrophy. Hippocampus-dependent spatial and nonspatial memory was also impaired in M5R-/- mice. In M5R-/- mice, CA3 pyramidal cells displayed a significantly attenuated frequency of the spontaneous postsynaptic current and long-term potentiation was significantly impaired at the mossy fiber-CA3 synapse. Our findings suggest that impaired M5R signaling may play a role in the pathophysiology of cerebrovascular deficits. The M5 receptor may represent an attractive novel therapeutic target to ameliorate memory deficits caused by impaired cerebrovascular function.

Cerebrovascular Effects of Sodium Nitroprusside in the Anaesthetized Baboon: A Positron Emission Tomographic Study

The effects of sodium nitroprusside (SNP), a potent hypotensive agent, on cerebral blood flow (CBF) have been extensively studied in clinical and experimental situations but the results remain controversial. Whereas its properties would predict a dilatation of cerebral blood vessels, most studies report either no change or a decrease in CBF. The aim of this study was to investigate the effects of SNP on CBF, cerebral blood volume (CBV), and cerebral oxygen metabolism (CMRO2), by means of positron emission tomography in the anaesthetized baboon. Measurements were performed during normotension (mean arterial pressure (MABP): 97+/-16 mm Hg) and repeated following SNP-induced hypotension (MABP: 44+/-9 mm Hg). Sodium nitroprusside led to an increase in CBF and CBV (+30% and +37%, respectively, P<0.05), whereas no change in CMRO2 was noted. Linear regression analysis of CBF values as a function of MABP confirmed that CBF increases when MABP is reduced by SNP. The comparison between these cerebrovascular changes and those found during trimetaphan-induced hypotension in our previously published studies further argues for a direct dilatatory effect of SNP on cerebral blood vessels.

Migraine: an ophthalmologist's perspective

Migraine is a common disorder with visual and neurologic manifestations. Many patients present to ophthalmologists without a previous diagnosis of migraine. It is therefore essential for the ophthalmologist to have a good understanding of migraine to appropriately help these patients. Neurologic syndromes with migraine and retinopathy are well known. Here again, the ophthalmologist may play a role in establishing the correct diagnosis. For long the initial changes during a migraine attack have been shown to occur in the occipital cortex. In the recent years, the understanding of migraine has advanced with the availability of functional neuroimaging. A possible role of brainstem structures in the initiation of migraine attacks has been proposed based on functional magnetic resonance imaging blood oxygenation level-dependent signals. Activation of brainstem structures preceded activation of occipital cortex. Our understanding of cortical spreading depression is also advancing. Using multiwavelength optical intrinsic imaging, cortical spreading depression has been shown to have a triphasic response in rats. For the first time it has been shown that the cortical spreading depression activated the trigeminovascular system, which is followed by a series of cortical meningeal and brainstem events that cause the migraine headache. Sildenafil has been shown to induce migraine attack without dilation of cerebral blood vessels, further confirming that Wolf's vasogenic theory may not be true. Several loci for migraine have been identified in recent years. A new locus for migraine with and without aura has been identified on chromosome 6, a locus for migraine without aura to chromosome 14, and a locus for migraine with aura on chromosome 4. Our understanding of migraine is rapidly evolving with functional neuroimaging. There are several unanswered questions. In this article, we will review the epidemiology, genetics, and clinical features of various forms of migraine with emphasis on ocular migraine, pathogenesis, and briefly the management of migraine.

Localization of the m5 muscarinic cholinergic receptor in rat circle of Willis and pial arteries

The expression and microanatomical localization of the muscarinic cholinergic m5 receptor subtype was investigated in rat circle of Willis and pial arteries by in situ hybridization, immunoblotting and immunohistochemistry. In situ hybridization histochemistry revealed a strong signal in the endothelium of circle of Willis and pial arteries and a moderate signal in the tunica media of the same arteries, within smooth muscle. Exposure of membranes of arteries to anti-m5 receptor protein antibodies caused the development of a band of approximately 81 kDa. Immunohistochemistry revealed the accumulation of m5 receptor protein immunoreactivity primarily within endothelium of circle of Willis and cerebral arteries and to a lesser extent in the tunica media, within smooth muscle. Medium (external diameter 200–100 μm) and small-sized (external diameter smaller than 100 μm) pial arteries displayed a significantly higher immune staining than large-sized pial arteries or circle of Willis arteries. The above data that are consistent with recent functional studies reporting cholinergic dilation of cerebral blood vessels mediated via a m5 receptor, have shown that both endothelial and muscular components of cerebral arteries synthesize and express a muscarinic m5 receptor. In view of the peculiar localization in cerebral vessels, handling of the muscarinic m5 receptor may be considered as an approach in the treatment of cerebrovascular disease.

Dilation of rat brain arterioles by hypercapnia in vivo can occur even after blockade of guanylate cyclase by ODQ

1 H-[1,2,4]oxadiazolo[4,3,-a]quinoxalin-1-one (ODQ) is an inhibitor of guanylate cyclase and has been reported to inhibit dilation of cerebral blood vessels by hypercapnia. This supports the hypothesis that this dilation is dependent upon guanylate cyclase, activated by nitric oxide (NO) released from neural tissue. However, there are conflicting reports concerning the role of guanylate cyclase in response to hypercapnia. Therefore, we tested the effect of topically applied ODQ (10 μM) on rat pial arterioles observed with a microscope through a closed cranial window. In one study, we tested ODQ ability to inhibit both the dilation produced by hypercapnia (3% and 5% inspired CO 2) and, in the same rats, the dilation produced by N-methyl- d-aspartate (NMDA). In another experiment, we tested the ability of ODQ to inhibit dilation produced by hypercapnia and the dilation produced by 3-morpholinosydnonimine (SIN-1), a donor of NO. The responses to NMDA and to NO are known to depend upon activation of guanylate cyclase and were both blocked in the present study. However, the response to hypercapnia was not affected. These findings provide evidence that hypercapnic dilation can occur independently of guanylate cyclase activation.

Cholinergic dilation of cerebral blood vessels is abolished in M(5) muscarinic acetylcholine receptor knockout mice.

The M(5) muscarinic receptor is the most recent member of the muscarinic acetylcholine receptor family (M(1)-M(5)) to be cloned. At present, the physiological relevance of this receptor subtype remains unknown, primarily because of its low expression levels and the lack of M(5) receptor-selective ligands. To circumvent these difficulties, we used gene targeting technology to generate M(5) receptor-deficient mice (M5R(-/-) mice). M5R(-/-) mice did not differ from their wild-type littermates in various behavioral and pharmacologic tests. However, in vitro neurotransmitter release experiments showed that M(5) receptors play a role in facilitating muscarinic agonist-induced dopamine release in the striatum. Because M(5) receptor mRNA has been detected in several blood vessels, we also investigated whether the lack of M(5) receptors led to changes in vascular tone by using several in vivo and in vitro vascular preparations. Strikingly, acetylcholine, a powerful dilator of most vascular beds, virtually lost the ability to dilate cerebral arteries and arterioles in M5R(-/-) mice. This effect was specific for cerebral blood vessels, because acetylcholine-mediated dilation of extra-cerebral arteries remained fully intact in M5R(-/-) mice. Our findings provide direct evidence that M(5) muscarinic receptors are physiologically relevant. Because it has been suggested that impaired cholinergic dilation of cerebral blood vessels may play a role in the pathophysiology of Alzheimer's disease and focal cerebral ischemia, cerebrovascular M(5) receptors may represent an attractive therapeutic target.

The biology of serotonin receptors: focus on migraine pathophysiology and treatment.

Serotonin receptors are highly heterogeneous and they have been regrouped within seven different families (5-HT1-5-HT7). With the exception of the 5-HT3 which is a ligand-gated ion channel, all others are G-protein coupled receptors with each family sharing structural, pharmacological and transductional characteristics. 5-HT receptors have been implicated in the regulation of several psychiatric and neurological disorders related to serotonergic neurotransmission, and specific receptor subtypes have recently been associated with either the pathogenesis or the treatment of migraine headache. In this respect, activation of vascular 5-HT2B and/or 5-HT7 receptors, possibly as a consequence of the sudden rise in 5-HT levels reported at the onset of a migraine attack, would hypothetically result in dilation of cerebral blood vessels and concomitant activation of sensory trigeminovascular afferents, hence initiating the manifestation of head pain. At this stage in the migraine process, activation of specific subtypes of 5-HT1 receptors has proven clinically effective in relieving migraine pain. Neural 5-HT1D and/or 5-HT1F receptors localized pre-junctionally on trigeminovascular afferents appear to mediate the triptan-induced inhibition of the neurogenic inflammatory response, with possible additional sites of action for brain penetrant 5-HT1 receptor agonists in inhibiting the transmission of pain centrally. In contrast, activation of vascular 5-HT1B receptors would constrict meningeal vessels hence recovering their pre-migraine diameter. The recent availability of subtype selective 5-HT1D and 5-HT1F receptor agonists should allow a further test of the neural/vascular hypothesis and could possibly lead to antimigraine drugs with a safer cardiovascular profile.

Carbon dioxide and the cerebral circulation.

Carbon dioxide and the cerebral circulation.

Role of P-450 arachidonic acid epoxygenase in the response of cerebral blood flow to glutamate in rats.

Glutamate, a major excitatory neurotransmitter in the brain, has been implicated in the hyperemic response to increases in the activity of neurons, but the mechanism of glutamate-induced dilation of cerebral blood vessels is unknown. Glutamate has been shown to enhance the release of arachidonic acid (AA) in brain tissue and cultured astrocytes. We have previously shown that astrocytes metabolize AA to vasodilator products, epoxyeicostrienoic acids (EETs), and express a P-450 AA epoxygenase, P-450 2C11. We tested the hypothesis that glutamate-induced dilation of cerebral arterioles is mediated in part by changes in the formation and release of EETs by perivascular astrocytes. Primary astrocyte cultures were prepared from 3-day-old rat pups. The cells were labeled with [14C]AA, and the effect of glutamate on the formation of EETs from [14C]AA by cultured astrocytes was studied. The expression of P-450 2C11 protein in the microsomal fractions of cultured astrocytes was assessed by Western blot. In vivo cerebral blood flow measurements were made in adult rats by laser-Doppler flowmetry after administration of glutamate into the subdural space of the rat before and after treatment with miconazole. Glutamate treatment (100 mumol/L for 30 minutes) induced a threefold increase in the formation of EETs from [14C]AA by cultured astrocytes, and the increase was inhibited by miconazole (20 mumol/L), an inhibitor of P-450 AA epoxygenase. Treatment with glutamate (100 mumol/L) for 12 hours increased the expression of P-450 2C11 protein in the microsomal fraction of cultured astrocytes. The response of laser-Doppler cerebral blood flow to administration of glutamate (500 mumol/L) into the subdural space of the rat was significantly attenuated after treatment with miconazole (20 mumol/L for 30 minutes). These findings suggest a role for a P-450 AA epoxygenase in astrocytes in the coupling between the metabolic activity of neurons and regional blood flow in the brain.

Recent insights into the regulation of cerebral circulation.

1. Mechanisms that regulate the cerebral circulation have been intensively investigated in recent years. The role of several vasodilator mechanisms has been examined in the cerebral circulation, including nitric oxide (NO), trigeminal peptides and potassium channels, as well as the potent vasoconstrictor endothelin. These mediators appear to play a role in physiological and pathophysiological responses of the cerebral circulation. In the present review, we will focus on some recent developments in each of these areas. 2. Nitric oxide is an important regulator of cerebral vascular tone. Tonic production of NO maintains the cerebral vasculature in a dilated state. NO appears to be an important vasodilator during activation of neurons by excitatory amino acids, somatosensory stimulation and cortical spreading depression. Tonic production of NO appears to be critical in vasodilatation during hypercapnia, although NO may not directly mediate vasodilatation. NO produced by immunological NO-synthase appears to be important in dilatation following exposure to bacterial endotoxin. 3. Calcitonin gene-related peptide (CGRP), released from trigeminal perivascular sensory nerves in the brain, is an extremely potent dilator of brain vessels. CGRP may limit noradrenaline-induced constriction of cerebral vessels and contribute to dilatation during hypotension (autoregulation), reactive hyperaemia, seizures and cortical spreading depression. 4. Activation of potassium channels leads to hyperpolarization of cerebral vascular smooth muscle and appears to be a major mechanism for dilatation of cerebral arteries. Agents that increase the intracellular concentration of cyclic 3' 5'-adenosine monophosphate (cAMP) produce vasodilatation in part by activation of large conductance calcium-activated potassium channels (BKCa) and ATP-sensitive potassium channels (KATP). Activation of both KATP and BKCa channels also appears to contribute to vasodilatation during hypoxia. In contrast to KATP channels, BKCa channels appears to be active under basal conditions, contributing to tonic dilatation of cerebral blood vessels. 5. Endothelin is produced in the brain, but its role in the physiological regulation of cerebral blood flow is not known. Endothelin may contribute to the spasm of cerebral arteries following subarachnoid haemorrhage.

31P and 23Na nuclear magnetic resonance study on forebrain ischemia in rats with shift reagent Dy(TTHA).

31P and 23Na nuclear magnetic resonance (NMR) spectroscopy was employed to study the dynamic changes in intracellular high-energy phosphates and sodium during 15 min of forebrain ischemia and recirculation in in vivo rat brain. In the presence of the shift reagent Dysprosium triethylenetetramine-N,N,N",N",N"',N"'-hexaacetic and [Dy(TTHA)], the sodium peak separated into two peaks, unshifted and shifted. During 15 min of ischemia, the unshifted sodium peak decreased and the shifted sodium peak increased. With recirculation, the unshifted and the shifted sodium peaks returned to the preischemia level within 10 min, but the shifted one increased during 30-60 min. Intracellular high-energy phosphates and intracellular pH (pHi) decreased during 15 min of ischemia and returned to the preischemia levels within 20 min of recirculation. We conclude that the decrease in unshifted sodium peak during ischemia is due to the decrease in subarachnoid sodium and the cellular influx of interstitial sodium would be minimum. The increase in shifted sodium peak during ischemia is considered to be due to the dilatation of cerebral blood vessels and the increase in interstitial sodium which was transported from subarachnoid space.

Does kallikrein improve the brain function in dementia?

Forty biological units of Kallikrein were administered intramuscularly to nine persons suffering from multi-infarct dementia. With automatic analysis equipment, the wave-form recognition method was used to analyze EEG before injection, immediately after injection, and 30, 60, 90, and 120 minutes after injection. The results of analysis done the five times after injection were then compared with the analysis results before injection. With the passage of time after injection, delta and theta waves showed a gradually decreasing tendency, while alpha and beta waves showed a gradual increase. It was inferred that these changes in the EEG were caused by an increase in the flow of cerebral blood, which in turn was the effect of the dilatation of cerebral blood vessels resulting from the action of the Kallikrein.

Cerebral circulation in chronic arterial hypertension.

Several new concepts have emerged recently regarding the effects of chronic hypertension on cerebral blood vessels. First, hypertrophy of large cerebral arteries in chronic hypertension attenuates increases in pressure of downstream vessels and protects the cerebral microvasculature. Second, in contrast to large cerebral arteries, which become less distensible during chronic hypertension, distensibility of cerebral arterioles increases during chronic hypertension despite hypertrophy of the arteriolar wall. Third, dilatation of cerebral blood vessels with disruption of the blood-brain barrier, and not vasospasm, appears to be the critical factor in the pathogenesis of hypertensive encephalopathy. This concept is supported by the finding that cerebral edema in stroke-prone spontaneously hypertensive rats is preceded by vasodilatation and disruption of the barrier. Fourth, alterations of endothelium-mediated dilatation may impair vasodilator responses in chronic hypertension and predispose to ischemia. Finally, chronic hypertension impairs dilatation of collateral blood vessels in the cerebral circulation. The implication of this finding is that increased susceptibility to cerebral infarction in chronic hypertension may be related in part to compromised responses of the collateral circulation.