Cerebrovascular and brain metabolism reviews最新文献

{"title":"Neuropeptides in the cerebral circulation.","authors":"R Uddman,&nbsp;L Edvinsson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The occurrence and distribution of peptide-containing nerve fibers to the cerebral circulation are described. Immunocytochemical studies have revealed that cerebral blood vessels are invested with nerve fibers containing neuropeptide Y (NPY), vasoactive intestinal peptide (VIP), peptide histidine isoleucine (PHI), substance P (SP), neurokinin A (NKA), and calcitonin gene-related peptide (CGRP). In addition, there are studies reporting the occurrence of putative neurotransmitters such as cholecystokinin, dynorphin B, galanin, gastrin releasing peptide, vasopressin, neurotensin, and somatostatin. The nerves occur as a longitudinally oriented network around large cerebral arteries. There is often a richer supply of nerve fibers around arteries than veins. The origin of these nerve fibers has been studied by retrograde tracing and denervation experiments. These techniques, in combination with immunocytochemistry, have revealed a rather extensive innervation pattern. Several ganglia, such as the superior cervical ganglion, the sphenopalatine ganglion, the otic ganglion, and small local ganglia at the base of the skull, contribute to the innervation. Sensory fibers seem to derive from the trigeminal ganglion, the jugular-nodose ganglionic complex, and from dorsal root ganglia at level C2. The noradrenergic and most of the NPY fibers derive from the superior cervical ganglion. A minor population of the NPY-containing fibers contains VIP instead of NA and emanates from the sphenopalatine ganglion. The cholinergic and the VIP-containing fibers derive from the sphenopalatine ganglion, the otic ganglion, and from small local ganglia at the base of the skull. Most of the SP-, NKA-, and CGRP-containing fibers derive from the trigeminal ganglion. Minor contributions may emanate from the jugular-nodose ganglionic complex and from the spinal dorsal root ganglia. NPY is a potent vasoconstrictor in vitro and in situ. VIP, PHI, SP, NKA, and CGRP act via different mechanisms to induce cerebrovascular dilatation. The sympathetic, the parasympathetic, and the sensory systems appear to be involved in modulating cerebrovascular tone in hypertension and in conditions of threatening vasoconstriction, e.g., subarachnoid hemorrhage and migraine.</p>","PeriodicalId":9739,"journal":{"name":"Cerebrovascular and brain metabolism reviews","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1989-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13841346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Double-label and conventional deoxyglucose methods: a practical guide for the user.","authors":"C Redies,&nbsp;A Gjedde","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The autoradiographic deoxyglucose method is widely used to map functional activity in mammalian brain. Whereas the method is simple to use, the underlying kinetic model is complex. This paper reviews the deoxyglucose kinetic model and the relevant implications for the user who does not have extensive knowledge of tracer kinetics. In generally understandable terms, single-label and double-label deoxyglucose approaches are discussed. Experimental procedures are described in detail. The calculations required for qualitative and quantitative experiments are explained. The deoxyglucose method is compared to other methods that map functional activity in mammalian brain.</p>","PeriodicalId":9739,"journal":{"name":"Cerebrovascular and brain metabolism reviews","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1989-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13841503","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cerebral acidosis in focal ischemia.","authors":"A M Hakim,&nbsp;E A Shoubridge","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The discovery in the 1970s that hyperglycemia accompanying cerebral ischemia adversely affected survival led to a significant research effort on the biochemical, histological, and clinical consequences of cerebral acidosis. In this article, we review the methods used currently to measure cerebral pH and discuss the means the cell has to control its pH environment. We then discuss the influence of both normoglycemic and hyperglycemic cerebral ischemia on pH and conversely the effect of acidosis on cerebral blood flow (CBF), glycolysis, mitochondrial function, the blood-brain barrier, cellular volume control, the formation of cerebral edema, and the histological damage resulting from ischemia. We conclude with a discussion of how acidosis could worsen the derangement in calcium homeostasis known to occur as a consequence of ischemia, and review methods now available to counteract cerebral acidosis.</p>","PeriodicalId":9739,"journal":{"name":"Cerebrovascular and brain metabolism reviews","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1989-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13843949","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Adenosine in the control of the cerebral circulation.","authors":"J W Phillis","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Adenosine has been proposed as a metabolic factor involved in the regulation of cerebral blood flow. The evidence in support of this hypothesis, presented in this review, includes information on the adenosine receptors associated with cerebral blood vessels, the synthesis and metabolism of adenosine, and the release of adenosine from the brain. Adenosine dilates cerebral blood vessels, acting at an A2 receptor. The critical evidence implicating an involvement of adenosine in cerebrovascular regulation is derived from experiments with adenosine antagonists and potentiators. The antagonists include methylxanthine adenosine receptor antagonists and the enzyme adenosine deaminase. Potentiators include transport inhibitors, enzyme inhibitors, and adenosine precursors. Adenosine has been implicated in vascular regulation during hypoxia/ischemia, hypercapnia, seizures, severe hypotension, and hypoglycemia. Adenosine possesses a number of properties that can be used to minimize neuronal degeneration during cerebral insults, such as ischemia, including vasodilatation, reduction of excitatory transmitter release, reduction of membrane calcium permeability, inhibition of platelets, and neutrophil aggregation. Several recent studies have demonstrated that manipulation of central adenosine tone can alter the extent of cerebral ischemic damage, indicating a potential new therapeutic approach for the treatment of stroke.</p>","PeriodicalId":9739,"journal":{"name":"Cerebrovascular and brain metabolism reviews","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1989-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13843946","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"99mTc-D,L-hexamethylene-propyleneamine oxime (99mTc-HMPAO): basic kinetic studies of a tracer of cerebral blood flow.","authors":"A R Andersen","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The lipophilic 99mTc-D,L-hexamethylene-propyleneamine oxime (99mTc-HMPAO) has been developed for regional cerebral blood flow (rCBF) measurements by single photon emission computed tomography (SPECT). The molecule is unstable and converts rapidly from the lipophilic form, which passes the blood-brain barrier (BBB), to the hydrophilic form, which is unable to pass the BBB and is trapped in the brain. The rate-limiting step for this conversion is probably dependent on the reductant gluthathione. The lipophilic input to the brain can be estimated by rapid octanol extraction of lipophilic tracer from arterial blood. The input takes place during the first few minutes after tracer injection. The first-pass extraction from blood to brain E is high (0.72 at a CBF of 0.59 ml/g/min) in human studies as measured by the indicator dilution method. It is dependent on the CBF level and decreases when CBF increases. It is also dependent on binding to proteins and blood constituents. 99mTc-HMPAO is initially distributed like rCBF. In measuring the retention in the human brain after intravenous and intracarotid injection of 99mTc-HMPAO, an early back-diffusion (brain to blood) is seen. This lasts only 2-3 min. The back-diffusion is flow dependent, leading to a preferential loss of activity from the high flow regions of the brain. This can be corrected for by an algorithm. The effect of the algorithm is that the steady-state 99mTc-HMPAO distribution images obtained from 10 min to 2-3 h after injection of tracer agrees more closely with rCBF images as measured by reference CBF methods using SPECT and positron emission tomography (human studies) and quantitated autoradiography (rats). The retention in the brain is very stable when the early back-diffusion has ceased, and only a small loss of tracer amounting to 0.4%/h is observed in most human cases during the next 24 h. This review concludes that 99mTc-HMPAO is suitable for measurements of rCBF by SPECT. A few examples of clinical application are given.</p>","PeriodicalId":9739,"journal":{"name":"Cerebrovascular and brain metabolism reviews","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1989-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13843970","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Local cerebral blood flow by xenon-enhanced CT: current status, potential improvements, and future directions.","authors":"D Gur,&nbsp;H Yonas,&nbsp;W F Good","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>A noninvasive technique for measuring local cerebral blood flow (CBF) by xenon-enhanced x-ray transmission computed tomography (CT) was developed and reported on extensively in recent years. In this method, nonradioactive xenon gas in inhaled, and the temporal changes in radiographic enhancement produced by the inhalation are measured by sequential computed tomography. Time-dependent xenon concentration within various tissue segments in the brain is used to derive both the local partition coefficient (lambda) and CBF in each tissue volume (voxel) of the CT image. A comprehensive assessment of this method reveals that although it provides functional mapping of blood flow with excellent anatomic specificity and has several other significant advantages, there are distinct and important limitations. The assumptions underlying this methodology are examined and the advantages as well as the problems associated with applications of this technique are reviewed. Laboratory and clinical observations that have been made using this technique in recent years are summarized, and potential improvements as well as possible future directions are discussed.</p>","PeriodicalId":9739,"journal":{"name":"Cerebrovascular and brain metabolism reviews","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1989-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13843948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brain edema: a classification based on blood-brain barrier integrity.","authors":"A L Betz,&nbsp;F Iannotti,&nbsp;J T Hoff","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Brain edema is a frequent complication of a variety of brain injuries and disorders. Two primary types of brain edema can be distinguished depending upon the integrity of the blood-brain barrier. With intact-barrier edema, the permeability of the blood-brain barrier is normal and brain edema results from a disturbance in ionic homeostasis. This type of edema is typically associated with swelling of the brain cells and a contraction of the extracellular space. In open-barrier edema, the permeability of the blood-brain barrier is increased and brain edema results from the oncotic forces generated by an influx of serum proteins into brain. In this case, the edema fluid accumulates primarily in the extracellular space. To a greater or lesser extent, both types of edema occur simultaneously in the majority of clinical conditions; however, one form usually predominates and demands the attention of both the scientist and clinician. Furthermore, classification of brain edema based upon blood-brain barrier integrity is useful to focus research on common mechanisms for brain edema formation and to direct therapy. This review considers intact-barrier and open-barrier edema with regard to their (a) histological features, (b) biophysical forces, (c) possible biochemical mediators, (d) mechanisms of resolution, and (e) implications for therapy.</p>","PeriodicalId":9739,"journal":{"name":"Cerebrovascular and brain metabolism reviews","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"1989-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"13843950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}