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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Insulin is a known growth factor in nonneural tissue, and recent studies have shown that there are insulin receptors throughout the adult and fetal central nervous system. Since insulin has only limited access to the adult brain, this study was undertaken to determine if insulin has increased availability to the newborn brain where it may act as a neonatal brain growth promoter. In vivo brain uptake of 125I-insulin after a single-pass carotid injection was measured in newborn, 3-wk-old and 11-wk-old (adult) rabbits. The brain uptake index (BUI) relative to a 3HOH reference was 22.0 +/- 1.1% (mean +/- SEM) for newborn, 12.8 +/- 0.6% for 3-wk-old, and 6.5 +/- 0.1% for adults. Specific 125I-insulin binding to isolated cerebral microvessels was similarly increased in the newborn (60.6 +/- 3.3%/mg protein) compared with the 3-wk-old (23.8 +/- 1.7) and adult animals (13.6 +/- 1.9). Scatchard analysis revealed that the difference was due to an increase in receptor number with only minimal changes in the affinity. The increased availability of circulating insulin to the newborn brain was further corroborated by elevated CSF/serum and brain/serum insulin ratios in the newborn versus adult. These results suggest that insulin has increased access to the newborn brain where it may function as a growth factor.
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PMID:Enhanced insulin binding to blood-brain barrier in vivo and to brain microvessels in vitro in newborn rabbits. 389 16

Cerebrospinal fluid of 22 dogs with histologically confirmed granulomatous meningoencephalomyelitis was analyzed, retrospectively. Seventeen dogs had cisternal CSF analysis, 4 dogs had lumbar CSF analysis, and 1 dog had both. For cisternal CSF, the mean +/- SEM total WBC count was 800.8 +/- 300.9 cells/microliter. The WBC differential count was predominantly lymphoplasmacytic cells, but 13 of the 18 cisternal CSF had polymorphonuclear (PMN) cells, and the mean +/- SEM PMN cell percentage was 18.6 +/- 5.3%. The mean +/- SEM total protein content of cisternal CSF was 255.8 +/- 98 mg/dl. Of 5 cisternal CSF pressures measured, 4 were within the normal range. The mean +/- SEM total WBC count and total protein content of lumbar CSF were 533.4 +/- 256.5 cells/mu/microliter and 163.2 +/- 25 mg of protein/dl, respectively. As with cisternal CSF, the WBC differential count of lumbar CSF was predominantly lymphoplasmacytic cells. Of 5 lumbar CSF, 4 contained PMN cells, but the percentage was less than the PMN cell percentage of cisternal CSF. Although variable, the general pattern of CSF abnormality associated with granulomatous meningoencephalomyelitis was different from the CSF abnormalities commonly seen with viral, bacterial, or mycotic encephalitides.
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PMID:Characteristics of cerebrospinal fluid associated with canine granulomatous meningoencephalomyelitis: a retrospective study. 394 20

The anatomical organization of the tuberal area of th posterior hypothalamus in Salamandra was investigated by the Golgi methods, SEM and TEM techniques. The ependymal cells of this area are poor in cilia and often show morphological features of actively secreting or absorbing elements. Intermingled with ependymal cells, two kinds of CSF-contacting processes are seen, arising from neurons of the periventricular grey. Their contents and morphological characteristics allow them to be divided into two groups, A and B. In the neuropil different synaptic contacts are seen. The observation of unconventional synaptic contacts possibly of axo-axonic type suggests the occurrence of local circuits on the final neurosecretory pathway.
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PMID:Ultrastructural analysis of the posterior hypothalamus of salamander. 617 21

The serotonin metabolite 5-hydroxytryptophol was studied in human cerebrospinal fluid. A minor fraction (approximately 13%) was found in conjugated form from which it was liberated by treatment with sulphatase containing beta-glucuronidase activity. A concentration gradient of 5-hydroxytryptophol concentration was shown on lumbar tapping and the concentration in ventricular CSF was about 2.5 times higher than that in lumbar CSF. 5-Hydroxytryptophol and 5-hydroxyindoleacetic acid concentrations were significantly correlated in healthy, psychotic, and depressed subjects, but not in alcoholics. 5-Hydroxytryptophol concentrations in CSF of psychotic and depressed subjects were not different from those of healthy controls (4.22 pmol/ml +/- 0.15, SEM). In healthy subjects, hereditary factors seemed to have little influence on the CSF level of 5-hydroxytryptophol.
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PMID:5-hydroxytryptophol in human cerebrospinal fluid: conjugation, concentration gradient, relationship to 5-hydroxyindoleacetic acid, and influence of hereditary factors. 620 46

In the subjects being prepared to neurosurgical treatment an i.v. injection of NaHCO3 (2 mEq/kg) elicited a significant increase in PCSFO2 from 69 +/- 6.4 (SEM) Torr to 75.5 +/- 3.9 (SEM) Torr. This change ws accompanied by a significant drop of PaO2 from 150.5 +/- 6.0 Torr to 138.0 +/- 5.8 Torr. Metabolic alkalosis (pH 7.54 +/- 0.02 SEM) elicited by bicarbonate administration was accompanied by arterial blood hyperoxia. Both these factors reduce the cerebral flow (CBF). We suppose that changes in the blood--CSF oxygen relationship reflect the presence of a mechanism which might protect the CNS against a decrease in CBF.
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PMID:Decrease of oxygen difference between arterial blood and cerebrospinal fluid after intravenous injection of sodium bicarbonate in hyperoxic patients, anaesthetized, paralyzed and artificially ventilated. 627 42

The association between central (cerebrospinal fluid [CSF]) and peripheral (plasma) levels of beta-endorphin-like immunoactivity (beta-ELI) in nonpregnant women (n = 8) and pregnant women (a) at 16 to 20 weeks of gestation (n = 6), (b) at term (n = 21), and (c) in labor (n = 15) was investigated. Umbilical arterial (n = 11) and venous (n = 11) samples were also obtained. In agreement with previous investigations, it was found that plasma levels of beta-ELI increased during labor (mean +/- SEM: nonpregnant women, 63.5 +/- 18.2; pregnant women at term, 64.0 +/- 12.2; women in labor, 110.8 +/- 30.3 pg/ml), and that levels of umbilical arterial plasma of beta-ELI exceeded those in umbilical venous plasma (132.5 +/- 34.0 versus 68.2 +/- 22.2). However, CSF levels of beta ELI did not change over the course of pregnancy or during labor (nonpregnant women, 36.5 +/- 15.8; pregnant women at 16 to 20 weeks of gestation, 60.1 +/- 10.3; pregnant women at term, 57.5 +/- 8.4; women in labor 48.5 +/- 8.3 pg/ml). This evidence that plasma and CSF levels of beta-ELI are dissociated during labor calls into question inferences regarding behavioral changes during parturition based on plasma beta-ELI measurements.
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PMID:Dissociation of plasma and cerebrospinal fluid beta-endorphin-like immunoactivity levels during pregnancy and parturition. 629 32

The cerebral microvasculature of rats rendered diabetic with streptozotocin (75 mg/kg) and vehicle-treated controls paired for age and sex were studied using in vivo and electron microscopic methods at intervals from two weeks to 12 months after induction of diabetes mellitus. By one month, the pial vessels of diabetics were dilated and tortuous; and, the vasoconstrictive responses of arterioles and venules to local increases of PO2 in the artificial CSF bathing these vessels was reduced as was the linear velocity of blood flow. Increased arterio-venous shunting also was observed. By five months the responsiveness to locally increased levels of PO2 was further reduced from control values of 49.9% +/- 5 (SEM) to 6.9% +/- 1.8 (SEM) in arterioles and from 11.5% +/- 2.1 (SEM) to 2.6% +/- 0.7 (SEM) in venules. No further significant change in responsiveness was measured from five to twelve months. At 5 months, the functional changes were no longer reversible; and focal changes were noted in the thickness and density of the vascular basement membrane. Astrocytic end feet were greatly swollen and contained mitochondria having longitudinal rearrangement of their cristae. Basement membranes contained nodules of electron-lucent material which impinged on degenerating smooth muscle cells, pericytes and astrocytes. In some sites these cells appeared to be replaced by an amorphous material laced with collagen fibrils. By 11 months, these focal lesions were more frequent and more pronounced. Additional cellular replacement had taken place which resulted in greatly widened basement membranes which varied in density and content. The ultrastructure of endothelial cells was not noticeably altered except for presence of numerous cytoplasmic vesicles. The tight interendothelial junctions appeared to be intact even though dramatic changes had taken place perivascularly. These architectural and functional changes in the microvasculature are suggested to result not only from metabolic defects in the vascular wall, but also as a response to a relative hypoxia of the brain during the diabetic state.
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PMID:In vivo and electron microscopic study of the development of cerebral diabetic microangiography. 654 44

Fifteen patients undergoing thoracotomy were given 0.25 or 0.50 mg morphine intrathecally (L2-L3 or L3-L4) for an analgetic and pharmacokinetic study. Administration of morphine at the end of the operation resulted in a highly variable duration of analgesia ranging from 1-20.5 and 1-40 h for the 0.25 and 0.50 mg groups, respectively. Calculation of cumulative consumption pattern of additional analgesics given im indicated a dose-related analgesia lasting around 12 h. Morphine concentrations in the CSF were high and dose dependent. Thus, at 1 h, CSF concentrations (means +/- SEM) were 4,228 +/- 361 ng/ml and 10,447 +/- 1,538 ng/ml for the 0.25 and 0.50-mg groups, respectively. The plasma concentrations generally were very low, i.e., under 1 ng/ml. For the 0.50 and 0.25 mg groups, the terminal elimination half-life in CSF was 175 +/- 9 min and 196 +/- 13 min, respectively: the volume of CSF distribution was 0.88 +/- 0.16 ml X kg-1 and 1.06 +/- 0.17 ml X kg-1, respectively: and the clearance from CSF was 2.81 +/- 0.41 microliter X kg-1 X min-1 and 3.41 +/- 0.55 microliter X kg-1 X min-1, respectively (means +/- SEM). The study indicates that the significant pharmacokinetic parameter related to the long duration of analgesia after intrathecal morphine administration probably is the high CSF concentrations found, since the rate of elimination from CSF is similar to what is reported for morphine in plasma. Furthermore, modulation of nociceptive input in the thoracic region also may be achieved by lumbar administration, but a slower onset should be anticipated.
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PMID:Pharmacokinetic aspects of intrathecal morphine analgesia. 654 39

Epidural (E.D.) and intrathecal (I.T.) morphine (M) analgesia were studied in patients with pain after thoracotomy. The role of the pharmacokinetic properties of M. for the associated analgesia was also evaluated. M. concentrations in CSF and plasma were assayed using gas chromatography with EC detection. Analgesia was evaluated as the time postoperative until the patients again required analgetics and were given meperidine intramuscularly (I.M.) for thoracic pain. A lumbar site of E.D. and I.T. injection of M. resulted in a variable but in general longlasting postoperative analgesia although delayed after I.T. administration. The mean duration of analgesia after E.D. administration was dose-related (8.6 +/- 2.0 h, 13.0 +/- 3.5 h, and 15.6 +/- 2.6 h; means +/- SEM for the 2, 4 and 6 mg groups, respectively), which was comparable to that achieved after I.T. administration of 0.25 to 0.50 mg M. M. concentrations in plasma after E.D. administration were comparable in variability and magnitude to those found after I.M. administration. The concentrations of M. in plasma were not related to the long duration of analgesia and may only contribute to analgesia shortly after the E.D. administration. The reported time course of analgesia after E.D. injection with a delayed onset corresponded with the appearance of M. in the CSF. Fifteen min after E.D. administration, M. was found in higher concentrations in CSF than in plasma, but peak levels were not seen until 2 h after the injection. Both the high content of M. in CSF as expressed by AUC, as well as peak concentrations in CSF, were related to the longlasting analgesia after E.D. administration. A protracted clearance of M. from the CSF as a cause of longlasting analgesia was not found, M. was eliminated with a similar half-life from CSF and plasma. The high CSF concentrations of M. seen after E.D. administration were the result of a direct uptake across the dura. In contrast, the appearance of M. in CSF after I.M. administration of 10 mg was slower. Maximal concentration of M. in the CSF was reached after 3 h and the peak levels were on average about 100 times less than those found after E.D. injection of 6 mg morphine. CSF and plasma reached pseudoeliquilibrium at a ratio around 0.9 after I.M. administration. This is to be compared with a CSF/plasma concentration ratio around 100 after E.D. administration. A comparison of M. concentrations in the CSF after thoracic and lumbar E.D. injection showed that spinal CSF rapidly yielded comparable concentrations at the lumbar level.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pharmacokinetic aspects of spinal morphine analgesia. 658 39

In 16 patients with primary degenerative dementia mean CSF vasopressin concentration was lower (0.9 +/- 0.1 pg/ml (mean +/- SEM)) than in 28 control patients (1.3 +/- 0.1 (mean +/- SEM)) (p less than 0.01). In 18 patients with normal pressure hydrocephalus and potentially reversible dementia mean CSF vasopressin concentration (1.2 pg/ml +/- 0.1 (mean +/- SEM)) was not different from that found in controls. Several of the demented patients had inappropriate plasma vasopressin concentrations suggesting a defect in osmoregulation. These findings encourage further clinical trials of vasopressin in patients with primary degenerative dementia, but it is emphasised that the low CSF vasopressin concentration in these patients might be only a nonspecific phenomenon due to the diffuse loss of cells within the central nervous system.
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PMID:CSF and plasma vasopressin concentrations in dementia. 664 15


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