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At least 703 records · Page 39Linked to original sources
PubMed1978

Alkaline phosphatase activity in lymph and serum of bile duct-ligated rats.

To determine whether liver alkaline phosphatase (AP) reaches the circulation by crossing the space of Dissé and traversing lymphatic channels to the thoracic duct, AP was measured in lymph and serum hourly for 12 h after bile duct ligation in thoracic duct cannulated rats. AP did not rise at any time point in lymph, was markedly increased in serum by 7 h when compared with controls (p less than 0.05), and continued to rise for the next 5 h. However, AP in the thoracic duct lymph was increased 5-fold by corn oil feeding. Molecular weight for serum AP from bile duct-ligated rats was determined by gel chromatography and found to be approximately 125,000. Thus, hepatic AP molecules probably pass freely through the large openings in the sinusoidal endothelial lining and are transported out of the liver chiefly in sinusoidal blood, which flows more rapidly than liver lymph.

Alkaline Phosphatase↗
PubMed2004

Exogenous NADPH increases cerebral blood flow through NADPH oxidase-dependent and -independent mechanisms.

OBJECTIVE: NADPH, a substrate for the superoxide-producing enzyme NADPH oxidase, produces vasodilation in the cerebral circulation. However, the mechanisms of the effect have not been fully elucidated. We used a peptide inhibitor of NADPH oxidase (gp91ds-tat) and null mice lacking the gp91phox subunit of NADPH oxidase to examine the mechanisms of the cerebrovascular effects of exogenous NADPH. METHODS AND RESULTS: Cerebral blood flow (CBF) was assessed by laser-Doppler flowmetry in anesthetized mice equipped with a cranial window. Superfusion with NADPH increased CBF (27% at 100 micromol/L) without affecting the EEG. The CBF increase was attenuated by the free-radical scavenger MnTBAP (-54%, P<0.05) but not by the H2O2 scavenger catalase. The response was also attenuated by gp91ds-tat (-64%, P<0.05) and by the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine (-44%, P<0.05). The increase in CBF produced by NADPH was attenuated in gp91-null mice (-41%, P<0.05). NADPH increased production of reactive oxygen species, assessed by hydroethidine microfluorography, an effect blocked by MnTBAP or gp91ds-tat and not observed in gp91-null mice. CONCLUSIONS: These data suggest that the mechanisms of the CBF increases produced by exogenous NADPH are multifactorial and include NADPH oxidase-dependent and -independent factors.

Animals↗
PubMedDate not supplied

Augmentation of centrally induced alpha-adrenergic vasodepression in spontaneously hypertensive rats.

Central alpha-adrenergic mechanisms for cardiovascular regulation were studied by injecting phenylephrine into a recipient rat whose head was isolated from its body by cross perfusion with a donor rat. Blood pressure increases produced in the donor were accompanied by concurrent reduction of blood pressure and sympathetic nerve activity in the recipient rat's body. These effects were abolished when alpha-adrenergic receptors in the perfused head were blocked with phentolamine. By contrast, intracarotid injections of angiotensin increased blood pressure not only in donor but also in recipient rats. The magnitude of phenylephrine-induced vasodepression was significantly greater in spontaneously hypertensive rats (SHR) than in normotensive or DOCA-salt hypertensive ones. Distribution of radioactive microspheres indicated that carotid arterial blood went mainly to the cerebrum, midbrain, and hypothalamus, with almost negligible amounts going to the lower brainstem. Collectively, our results suggest that centrally administered phenylephrine reduces sympathetic vasomotor tone and blood pressure by acting on alpha-adrenergic receptors located in supramedullary brain areas (possibly in the hypothalamus). In SHR, augmented, vasodepressor responsiveness may be due to reduced brain levels of endogenous norepinephrine that could increase the alpha-adrenergic receptors available.

Animals↗
PubMed2002

Cardiac effects of clinically available Kampo medicine assessed with canine isolated, blood-perfused heart preparations.

Cardiac effects of 10 kinds of clinically available Kampo medicines were investigated: Kakkon-to (TJ-1), Dai-saiko-to (TJ-8), Boi-ogi-to (TJ-20), Chorei-to (TJ-40), Rokumi-gan (TJ-87), Tsu-do-san (TJ-105), Gosha-jinki-gan (TJ-107), San'o-shashin-to (TJ-113), Sairei-to (TJ-114) and Inchin-gorei-san (TJ-117). Chronotropic and inotropic effects were studied using canine isolated, blood-perfused heart preparations, while subcellular mechanisms were analyzed by measuring the drug-induced changes of the adenylate cyclase activity in the canine ventricular membrane preparation. Intracoronary injections of TJ-1, TJ-20, TJ-105 and TJ-113 increased the sinoatrial rate and developed tension of papillary muscle in a dose-related manner, which was significantly attenuated by the pretreatment of the preparations with beta-blocker propranolol. Meanwhile, the other extracts hardly affected these parameters. TJ-1, TJ-20 and TJ-113 increased the adenylate cyclase activity in a dose-related manner, but their potency was significantly less compared with that by an equivalent concentration of isoproterenol. Moreover, TJ-105 did not increase the adenylate cyclase activity. These results suggest that the positive chronotropic and inotropic effects of TJ-1, TJ-20, TJ- 105 and TJ-113 may be exerted through the direct stimulation of the beta-adrenoceptor and/or the norepinephrine release from the postganglionic nerve terminals in the heart.

Adenylyl Cyclases↗
PubMed2003

Emerging molecular targets in the treatment of bacterial meningitis.

The mortality and morbidity associated with bacterial meningitis have remained significant despite advances in antimicrobial chemotherapy and supportive care. A major contributing factor to this high mortality and morbidity is our incomplete understanding of the pathogenesis of this disease and its associated neurological sequelae. Most cases of bacterial meningitis develop as a result of haematogenous spread, but it is unclear how circulating bacteria cross the blood-brain barrier. Experimental animal studies indicate that two forms of neuronal injury, such as necrotic cortical injury and apoptotic hippocampal injury, are predominant in bacterial meningitis, but the mechanisms by which these two forms of injury occur are unclear. Recent studies have identified several bacteria-host determinants for bacterial translocation of the blood-brain barrier, and several host inflammatory markers that are associated with neuronal injury in animal models of experimental bacterial meningitis. These determinants/markers may provide important targets for the prevention and treatment of bacterial meningitis. This review focuses on representative steps in the pathogenesis of bacterial meningitis that are likely to be key targets in coming years, and summarises the status of current knowledge for each target.

ADAM Proteins↗
PubMed2005

Reducing cerebral microvascular amyloid-beta protein deposition diminishes regional neuroinflammation in vasculotropic mutant amyloid precursor protein transgenic mice.

Cerebral microvascular amyloid-beta (Abeta) protein deposition is emerging as an important contributory factor to neuroinflammation and dementia in Alzheimer's disease and related familial cerebral amyloid angiopathy disorders. In particular, cerebral microvascular amyloid deposition, but not parenchymal amyloid, is more often correlated with dementia. Recently, we generated transgenic mice (Tg-SwDI) expressing the vasculotropic Dutch (E693Q)/Iowa (D694N) mutant human Abeta precursor protein in brain that accumulate abundant cerebral microvascular fibrillar amyloid deposits. In the present study, our aim was to assess how the presence or absence of fibrillar Abeta deposition in the cerebral microvasculature affects neuroinflammation in Tg-SwDI mice. Using Tg-SwDI mice bred onto an apolipoprotein E gene knock-out background, we found a strong reduction of fibrillar cerebral microvascular Abeta deposition, which was accompanied by a sharp decrease in microvascular-associated neuroinflammatory cells and interleukin-1beta levels. Quantitative immunochemical measurements showed that this reduction of the neuroinflammation occurred in the absence of lowering the levels of total Abeta40/Abeta42 or soluble Abeta oligomers in brain. These findings suggest that specifically reducing cerebral microvascular fibrillar Abeta deposition, in the absence of lowering either the total amount of Abeta or soluble Abeta oligomers in brain, may be sufficient to ameliorate microvascular amyloid-associated neuroinflammation.

Alzheimer Disease↗
PubMed1989

Comparative study of cardiovascular effects of clonidine and alinidine in cross-perfused dog atrial preparations.

Cross-perfused canine atrial preparations were used to investigate the direct and indirect cardiac actions of clonidine and alinidine. Intravenous injections of clonidine (0.1-3 micrograms/kg) produced an initial brief pressor response and bradycardia followed by hypotension in the intact dog. Chronotropic and inotropic responses were absent in the isolated atrium perfused with the intact dog's blood. Intravenous clonidine (10-300 micrograms) also induced negative chronotropic and inotropic effects in isolated atria. On the other hand, alinidine, at doses which caused a depressor action and bradycardia in the intact dog, consistently produced negative chronotropic and inotropic effects in the isolated atrium. Therefore, it was confirmed that a relatively small dose of clonidine has a selective vascular action, while alinidine has direct cardiac depressant properties at all effective doses. Negative chronotropic and inotropic effects of peripheral vagal stimulation, carbachol and adenosine were not significantly modified by 100 or 300 micrograms doses of intraarterial clonidine. On the other hand, the effects of vagal stimulation and carbachol were significantly inhibited by 100 and 300 micrograms of alinidine, without affecting adenosine-induced cardiac actions. Therefore, it was demonstrated that alinidine has anti-muscarinic properties.

Animals↗
PubMed1990

Cardiovascular effects of 2-amino-N-(2,6-dimethylphenyl)-N-[3-(3-pyridyl)propyl]propionamide dihydrochloride (Ro 22-9194) in the isolated, cross-perfused atrium of the dog.

The cardiovascular effects of 2-amino-N-(2,6-dimethylphenyl)-N-[3- (3-pyridyl)propyl]propionamide dihydrochloride (Ro 22-9194) were investigated in the canine isolated atrial preparation perfused with arterial blood from another donor dog. Intravenous administration of Ro 22-9194 (0.3-3 mg/kg) reduced heart rate and systemic arterial blood pressure of the donor dog. Simultaneously, in the isolated atrium perfused with donor's blood, negative chronotropic and inotropic responses were induced in a dose-dependent manner. Direct administration of Ro 22-9194 (1-300 micrograms) into the sinus node artery of the isolated atrium induced negative chrono- and inotropic responses and a transient increase in coronary blood flow in a dose-related manner. Mexiletine (1-300 micrograms) also induced negative chrono- and inotropic responses. The potency of Ro 22-9194 for negative cardiac effects was similar to that of mexiletine. The negative cardiac effects of Ro 22-9194 were not modified by atropine in doses which significantly inhibited the cardiac effects of acetylcholine. Ro 22-9194 did not affect the cardiac responses to norepinephrine and to acetylcholine significantly. These results suggest that Ro 22-9194 has non-cholinergic cardiac depressant properties with its vasodilating action, and it has neither anti-adrenergic nor anti-cholinergic actions on the dog heart.

Acetylcholine↗
PubMed1987

Adrenal status during the first month of life in mature and premature human infants.

Measurements of 17-hydroxyprogesterone (17-OHP) in blood collected onto filter paper after heel puncture by lancet and steroid metabolites in random collections of urine, were made in human infants born from 25 weeks of gestation onwards. The concentration of 17-OHP in blood eluted from filter paper samples was inversely related to both gestational age and birth weight. In mature infants, 17-OHP concentrations fell rapidly soon after birth, whereas concentrations remained high over the first month of life in infants born earlier than 33 weeks of gestation. Sulphated urinary steroids were identified as having a 3 beta-hydroxy-5-ene structure and although the pattern of excretion was similar in mature and premature infants, significantly higher concentrations were found in the premature group. Steroid metabolites normally present when concentrations of circulating 17-OHP are increased due to 21-hydroxylase deficiency were not detectable in urine samples collected from infants born prematurely. Where direct comparison of 17-OHP in blood spots and urinary steroid metabolites was possible, the concentrations of 17-OHP in blood samples paralleled 3 beta-hydroxy-5-ene steroid metabolites in urine. The results suggest that a circulating cross-reacting 3 beta-hydroxy-5-ene steroid may be responsible for increased concentrations of 17-OHP in infants born prematurely. Increased concentrations of both 17-OHP in blood spots and steroid sulphates in urine were associated with stress in premature, but not in more mature, infants suggesting that in infants born prematurely postnatal stress may delay adrenal maturation.

17-alpha-Hydroxyprogesterone↗
PubMed1994

Central hypoxic depression of respiration determined by perfusing a recipient cat's carotid bodies with blood from a donor cat.

The respiratory response to sustained hypoxia reflects the net effect of the peripheral chemoreceptor excitation and the central depression. To obtain a pure depressant effect of central hypoxia (alv. PO2, 35-75 mmHg) on respiration, the recipient cat's carotid bodies were vascularly isolated and bilaterally perfused with blood from a donor cat. Cats were anesthetized, vagotomized, paralyzed, and artificially ventilated. Alv. PCO2 was kept at a normal value (iso- and normocapnia) throughout the experiment. The minute integrated phrenic nerve activity (Min. PNA) was used as an indication of inspiratory activity. The Min. PNA at which the recipient and donor cats were both breathing room air (central normoxia and peripheral chemoreceptor normoxia) was taken as 100% (control), and Min. PNA expressed as a percentage of the control was measured in a series of three experiments (A, B, and C): experiment A (normoxia-hypoxia; central normoxia and peripheral chemoreceptor hypoxia), experiment B (hypoxia-hypoxia; central hypoxia and peripheral chemoreceptor hypoxia), and experiment C (hypoxia-normoxia; central hypoxia and peripheral chemoreceptor normoxia). At alv. PO2 of about 50 mmHg, Min. PNA was 169.7 +/- 23.6% (mean +/- SD) in experiment A, 127.3 +/- 22.0% in experiment B, and 71.6 +/- 17.3% in experiment C. Thus, a pure depressant effect of normocapnic hypoxia (alv. PO2 of 50 mmHg) was 42.4% (= 169.7-127.3) or 28.4% (= 100-71.6). At alv. PO2 of about 40 mmHg, Min. PNA was 185.2 +/- 16.8% in experiment A, 146.2 +/- 19.0% in experiment B, and 54.8 +/- 15.2% in experiment C. Thus, a pure depressant effect of normocapnic hypoxia (alv. PO2 of 40 mmHg) was 39.0% (= 185.2-146.2) or 45.2% (= 100-54.8). From these results, we concluded that a pure depressant effect of normocapnic central hypoxia (alv. PO2, 40-50 mmHg) was 28-45% and this was affected by a stimulating drive from the peripheral chemoreceptors.

Animals↗
PubMed1986

Experimental hypercupremia does not result in increases in copper in lens, iris, or ocular fluids.

Rabbits were continuously administered copper sulfate via subcutaneously implanted osmotic pumps. After one month, plasma, liver, ocular tissues and fluids were analyzed for copper by atomic absorption spectrophotometry. No elevation in copper content of the ocular fluids, lens or iris was noted although, dose-related increases were seen in the plasma and liver indicating that the copper was absorbed and disseminated systemically. It is likely that excess copper, like that which is normally ingested and absorbed, is largely protein-bound in the circulation, preventing crossing of the blood-ocular barrier.

Animals↗
PubMed1978

The relation of cerebral ischemia, hypoxia, and hypercarbia to the Cushing response.

A marked increase in intracranial pressure (ICP) produces a concomitant increase in systemic blood pressure (the Cushing response). In this study a comparison is made between this response of systemic blood pressure to increased ICP and the blood pressure responses produced by ischemia, hypoxia, and hypercarbia of the primate brain. A carotid-to-carotid cross-perfusion system was used to produce a purely cerebral hypoxia and hypercarbia. Each stimulus, except hypercarbia, produced a hypertensive response that was qualitatively and quantitatively similar. These responses were characterized by a short latent period, a rapid development, and an increase in mean arterial pressure of 60% or more. The similarity of the responses suggests that these stimuli act through a final common pathway independent of the purely mechanical effects of increased ICP upon the brain.

Animals↗
PubMed2000

Circulating immunoreactive proANP(1-30) and proANP(31-67) in sedentary subjects and athletes.

BACKGROUND: Atrial natriuretic peptide (ANP) is synthesized and stored in myocytes as prohormone(1-126), which upon release is cleaved into proANP(1-98) and alpha-ANP(99-126). In addition, cleavage of proANP(1-98) produces proANP(1-30), proANP(31-67), and proANP(79-98) fragments. ProANP(1-30) and proANP(31-67) have roles in fluid and electrolyte homeostasis. The aim of the present study was to develop a plasma assay for proANP(1-30) and proANP(31-67) and to compare results in trained athletes and sedentary subjects. METHODS: Two competitive enzyme immunoassays were established with affinity-purified sheep antiserum against synthetic ANP fragments. The immunoreactivity (ir) of proANP(1-30) and proANP(31-67) was measured in 10-microL plasma samples without extraction in a microwell-based assay. Plasma concentrations in sedentary male subjects (n = 22) and male endurance athletes (n = 14) were examined. RESULTS: In the assay for ir-proANP(1-30) and ir-proANP(31-67), the concentrations at 95% B/B(0) were 4.7 and 14.2 pmol/L, respectively. Within-run CVs were 4-6% and 5-6%, and between-run CVs were 9% for both assays. Both assays were linear on dilution (y = 0.9945x - 0. 7291 and y = 1.0001x - 3.428), and the recoveries were 102-112% and 102-106%, respectively. In the sedentary and athletic groups, the ir-proANP(1-30) concentrations were similar: 318 +/- 38 pmol/L and 312 +/- 25 pmol/L (mean +/- SE), respectively, whereas the ir-proANP(31-67) was higher in the rowers (713 +/- 81 pmol/L) than in the sedentary subjects (387 +/- 71 pmol/L; P <0.005). CONCLUSIONS: The proANP fragment assays are precise (CV <10%) and exhibit nearly quantitative recovery (102-112%). Only ir-proANP(31-67) responds to physical training.

Animals↗
PubMed2000

Apolipoprotein E facilitates neuritic and cerebrovascular plaque formation in an Alzheimer's disease model.

The epsilon4 allele of apolipoprotein E (ApoE) is an important genetic risk factor for Alzheimer's disease (AD). Increasing evidence suggests that this association may be linked to the ability of ApoE to interact with the amyloid-beta (Abeta) peptide and influence its concentration and structure. To determine the effect of ApoE on Abeta and other AD pathology in vivo, we used APPsw transgenic mice and ApoE knockout (-/-) mice to generate APPsw animals that carried two (ApoE +/+), one (ApoE +/-), or no copies (ApoE -/-) of the normal mouse ApoE gene. At 12 months of age, Abeta deposition was present in the cortex and hippocampus and was also prominent within leptomeningeal and cortical blood vessels of all APPsw ApoE +/+ mice. Importantly, although Abeta deposition still occurred in APPsw ApoE -/- mice, no fibrillar Abeta deposits were detected in the brain parenchyma or cerebrovasculature. There was also no neuritic degeneration associated with Abeta deposition in the absence of ApoE. These data demonstrate that ApoE facilitates the formation of both neuritic and cerebrovascular plaques, which are pathological hallmarks of AD and cerebral amyloid angiopathy.

Alzheimer Disease↗
PubMed2000

Mice overexpressing rat heat shock protein 70 are protected against cerebral infarction.

Increased expression of heat shock protein 70 (HSP70) in the brain has been extensively documented in association with a variety of insults, including ischemia, and is suggested to play a role in cell survival and recovery after ischemic injury. To more directly assess the protective role of HSP70 during ischemic brain damage, we used transgenic mice overexpressing the rat HSP70 (HSP70tg mice). In contrast to wild-type (wt) littermates, high levels of HSP70 messenger RNA and protein were detected in brains of HSP70tg mice under normal conditions, and immunohistochemical analysis revealed primarily neuronal expression of HSP70. Heterozygous HSP70tg mice and their wt littermates were subjected to permanent focal cerebral ischemia by intraluminal blockade of the middle cerebral artery. Cerebral infarction after 6 hours of ischemia, as evaluated by Nissl staining, was significantly less in HSP70tg mice compared with wt mice. This reduction in infarction volume in HSP70tg mice was not attributable to an altered cardiovascular anatomy or to initial differences in body temperature or hemodynamic parameters. The HSP70tg mice were still protected against cerebral infarction 24 hours after permanent focal ischemia. The data suggest that HSP70 can markedly protect the brain against ischemic damage and that approaches aimed at inducing HSP70 may lead to new therapeutic interventions in cerebrovascular injuries.

Animals↗