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At least 991 records · Page 55Linked to original sources
PubMed2005

The effect of i.v. L-NG methylarginine hydrochloride (L-NMMA: 546C88) on basal and acetazolamide (Diamox) induced changes of blood velocity in cerebral arteries and regional cerebral blood flow in man.

The aim of this study was to estimate the effect of Nitric Oxide synthase (NOS)-inhibition (L-NMMA) on the diameter of the middle cerebral artery (MCA) and on regional cerebral blood flow (rCBF). Furthermore, to assess the effect of L-NMMA on acetazolamide induced increases in MCA blood velocity (Vmean) and rCBF. In an open crossover design 12 healthy subjects attended the laboratory twice. The first day 6 mg/kg L-LNMMA i.v. over 15 min preceded 1 g acetazolamide i.v. over 5 min. Eight days later only acetazolamide was given. V(mean) in MCA was determined with transcranial Doppler (TCD) and rCBF with Xe-133 inhalation SPECT at baseline, after L-NMMA and 25 and 55 min after acetazolamide infusion. After L-NMMA the decrease in rCBF(MCA) was 6.8% (+/- 7.4) (P < 0.019, n = 12), whereas V(mean) was not affected (P = 0.83, n = 8). The change in MCA diameter was estimated to - 1.3% (P = 0.44, n = 8). L-NMMA did not affect acetazolamide increases in Vmean (P = 0.67, n = 8) nor rCBF (P = 0.29, n = 12). The percentage increase of V(mean) was 1.5 times that of rCBF (n = 8). Our data suggest that the basal tone of human cerebral arterioles but not of conduit arteries is NO-dependent. The action of acetazolamide in man is not NO-dependent.

Acetazolamide↗
PubMed2005

The effect of circulating adenosine on cerebral haemodynamics and headache generation in healthy subjects.

Adenosine is an endogenous neurotransmitter that is released from the brain during hypoxia and relaxes isolated human cerebral arteries. Many cerebral artery dilators cause migraine attacks. However, the effect of intravenous adenosine on headache and cerebral artery diameter has not previously been investigated in man and reports regarding the effect of intravenous adenosine on cerebral blood flow are conflicting. Twelve healthy participants received adenosine 80, 120 microg kg(-1) min(-1) and placebo intravenously for 20 min, in a double-blind, three-way, crossover, randomized design. Headache was rated on a verbal scale (0-10). Regional cerebral blood flow (rCBF) with 133Xe inhalation and single-photon emission computed tomography (SPECT) and MCA flow velocity (V(MCA)) with transcranial Doppler, were measured in direct sequence. Six participants developed headache during 80 microg kg(-1) min(-1) and six during 120 microg kg(-1) min(-1) compared with none on placebo (P = 0.006). The headache was very mild and predominantly described as a pressing sensation. When correcting data for adenosine-induced hyperventilation, no significant changes in rCBF (P = 0.22) or V(MCA) (P = 0.16) were found between treatments. A significant dilation of the superficial temporal artery (STA) was seen (P < 0.001). These results show that circulating adenosine has no effect on rCBF or V(MCA), while it dilates the STA and causes very mild headache.

Adenosine↗
PubMed2004

Non-invasive assessment of endothelial function - relation between vasodilatory responses in skin microcirculation and brachial artery.

OBJECTIVE: To compare different non-invasive methods for determination of human endothelial function in peripheral circulation. DESIGN: Observational, cross-sectional study in 39 healthy subjects (21 females, age 17-56 years). SETTING: Vascular research laboratory at university hospital. METHODS: Laser Doppler (LD) flowmetry was used to compare skin microvascular perfusion changes during postocclusive reactive hyperaemia with those induced by iontophoretic administration of acetylcholine (ACh), an endothelial-dependent vasodilator. LD measurements were compared with ultrasonographic measurements of postocclusive flow-mediated dilatation (FMD) in the brachial artery (n = 21). RESULTS: Local ACh induced a larger and more sustained skin perfusion increase than reactive hyperaemia after 4 min of regional arterial occlusion (P<0.001). A significant correlation was found between the magnitude of ACh-induced vasodilatation and peak reactive hyperaemia, both in absolute (r = 0.62, P<0.001) and relative terms (r = 0.58, P<0.001). A correlation was also found between brachial artery FMD and the magnitude of ACh-induced skin perfusion increase (r = 0.43, P<0.05) but not between FMD and reactive hyperaemia. CONCLUSION: Endothelial function, an early marker of cardiovascular risk, can be non-invasively assessed and graded by LD and FMD-measurements and despite inherent differences, both methods do correlate.

Adolescent↗
PubMed1982

Chromosome analysis and sister chromatid exchange in encephalo-trigeminal angiodysplasia.

A female, aged 32, with facial birthmarks and suffering migraine headaches and a slight hemiparesis was examined with isotope scanning, CT and angiography. She was found to have a massive, unilateral angiodysplasia, transforming the right cerebral hemisphere into an expanding vascular sponge-like structure. There was a family history of red facial birthmarks. The patient and her father were analysed cytogenetically by estimating the frequency of chromosome aberrations and sister chromatid exchanges (SCE). The frequency of gaps and breaks was normal compared to healthy controls, but the patient showed a significantly higher level of spontaneous SCE's. The patient and her father also had a higher than normal number of SCE's after addition of mitomycin C (MMC) to the blood culture. Numerical and structural chromosome deviations markedly exceeded normal in both, possibly representing a genetic imbalance in this syndrome.

Adult↗
PubMed1993

Physostigmine and tetrahydroaminoacridine treatment of Alzheimer's disease.

The cholinergic hypothesis of Alzheimer's disease (AD) was tested in two doubleblind crossover studies. Physostigmine given intravenously to 10 AD patients for two hours caused improvement of reaction time and EEG and increased regional cerebral blood flow (rCBF) in the temporoparietal cortex. 17 AD patients (mean age 62.6 +/- 6.8 years) obtained three types of treatment: tetrahydroaminoacridine (THA), THA + lecithin and placebo in randomized order. Each treatment period was 6 weeks. The mean THA dose was 104 +/- 20 mg/day. There were differences in outcome between groups of patients over the total 26 weeks treatment period. The subclassification in responders, unchanged and deteriorated was supported by rCBF, EEG and psychometric testing.

Alzheimer Disease↗
PubMed1997

Psychopathological and SPECT findings in never-treated schizophrenia.

A total of 24 never-treated (i.e. drug-naive) actively psychotic schizophrenic patients, operationalized according to DSM-III-R, were examined in a pre-post-treatment design using the Positive and Negative Syndrome Scale for Schizophrenia (PANSS) and 99mTc-HMPAO-single photon emission computed tomography (SPECT) to assess regional cerebral blood flow (rCBF). The control subjects were 20 patients free of neurological and psychiatric symptoms. Before treatment there was only a slight hypofrontality, and hypoperfusion was observed in the left temporal superior region. After treatment, hypofrontality was reduced to one region and temporal hypoperfusion disappeared. Formal thought disorders were accompanied by increased rCBF in the bilateral frontal interior and left temporal superior regions. Delusions were associated with hypoperfusion in the anterior cingulate cortex. Negative symptoms showed no linkage to hypofrontality, either before or after treatment. Factor analysis showed delusions and hallucinations loading on different dimensions. The disorganized dimension correlated positively with all regions of interest, whereas these were negatively correlated with reality distortion.

Adult↗
PubMed1984

Involvement of the renin-angiotensin system in captopril-induced sodium appetite in the rat.

The angiotensin converting enzyme inhibitor, captopril, given to rats in their drinking water (about 40 mg/day) for 6 days caused an increase in intake of hypertonic NaCl solution which began 1-2 days after the captopril was started and reached a plateau after 4-5 days. Twice-daily subcutaneous injections of captopril (15 mg per injection) elicited a sodium appetite similar in pattern to that seen with oral administration. The rats remained in sodium and fluid balance during oral captopril treatment and the haematocrit did not alter. Captopril infused directly into the ventricles (12 micrograms/h), or captopril reaching the brain from the periphery across a leaky blood-brain barrier, suppressed the sodium appetite which normally follows oral captopril. Continuous intravenous infusion of captopril at rates high enough to block angiotensin converting enzyme in the brain (25, 50 or 500 mg/day) did not cause sodium appetite. As soon as the rate was reduced to a low value (5 mg/day), NaCl intake increased. In conclusion, moderate levels of circulating captopril which do not cross the blood-brain barrier in sufficient amounts to block cerebral angiotensin converting enzyme, result in an increase in circulating angiotensin I which stimulates sodium appetite when it is converted to angiotension II in the brain.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1979

Acetaminophen: potentially toxic metabolite formed by human fetal and adult liver microsomes and isolated fetal liver cells.

A reactive metabolite of acetaminophen is hepatotoxic in humans when the drug is ingested in large overdoses. The ability of the human fetal and adult liver to oxidize acetaminophen by trapping the potentially toxic metabolite as a glutathione conjugate has been measured. Oxidation by fetal liver was approximately ten times slower than by adult liver. However, there was a definite increase in acetaminophen oxidation with fetal age. Isolated human fetal liver cells conjugated acetaminophen with sulfate but not with glucuronic acid. The results indicate that the human fetal liver is able to detoxify acetaminophen by conjugation. However, it also catalyzes the formation of an active metabolite of acetaminophen through oxidation. Hence the fetus remains at risk should a large dose of the drug cross into the fetal circulation.

Acetaminophen↗
PubMed2006

Streptococcus pneumoniae Infection aggravates experimental autoimmune encephalomyelitis via Toll-like receptor 2.

The course of autoimmune inflammatory diseases of the central nervous system (CNS) can be influenced by infections. Here we assessed the disease-modulating effects of the most frequent respiratory pathogen Streptococcus pneumonia on the course of experimental autoimmune encephalomyelitis (EAE). Mice were immunized with myelin oligodendrocyte glycoprotein 35-55 (MOG(35-55)) peptide, challenged intraperitoneally with live S. pneumoniae type 3, and then treated with ceftriaxone. EAE was monitored by a clinical score for 35 days after immunization. EAE was unaltered in mice infected with S. pneumoniae 2 days before and 21 days after the first MOG(35-55) injection but was more severe in animals infected 7 days after the first MOG(35-55) injection. The antigen-driven systemic T-cell response was unaltered, and the intraspinal Th1 cytokine mRNA concentrations at the peak of disease were unchanged. The composition of CNS-infiltrating cells and subsequent tissue destruction were only slightly increased after S. pneumoniae infection. In contrast, the serum levels of tumor necrosis factor alpha and interleukin-6 and spinal interleukin-6 levels were elevated, and the expression of major histocompatibility complex class II molecules, CD80, and CD86 on splenic dendritic cells were enhanced early after infection. Serum cytokine concentrations were not elevated, and EAE was not aggravated by S. pneumoniae infection in Toll-like receptor 2 (TLR2)-deficient mice. In conclusion, infection with S. pneumoniae worsens EAE probably by elevation of proinflammatory cytokines and activation of dendritic cells in the systemic circulation via TLR2 and cross talk through the blood-brain barrier.

Animals↗
PubMedDate not supplied

Effect of rosary prayer and yoga mantras on autonomic cardiovascular rhythms: comparative study.

OBJECTIVE: To test whether rhythmic formulas such as the rosary and yoga mantras can synchronise and reinforce inherent cardiovascular rhythms and modify baroreflex sensitivity. DESIGN: Comparison of effects of recitation of the Ave Maria (in Latin) or of a mantra, during spontaneous and metronome controlled breathing, on breathing rate and on spontaneous oscillations in RR interval, and on blood pressure and cerebral circulation. SETTING: Florence and Pavia, Italy. PARTICIPANTS: 23 healthy adults. MAIN OUTCOME MEASURES: Breathing rate, regularity of breathing, baroreflex sensitivity, frequency of cardiovascular oscillations. RESULTS: Both prayer and mantra caused striking, powerful, and synchronous increases in existing cardiovascular rhythms when recited six times a minute. Baroreflex sensitivity also increased significantly, from 9.5 (SD 4.6) to 11.5 (4.9) ms/mm Hg, P<0.05. CONCLUSION: Rhythm formulas that involve breathing at six breaths per minute induce favourable psychological and possibly physiological effects.

Adult↗
PubMed2003

Effect of early targeted indomethacin on the ductus arteriosus and blood flow to the upper body and brain in the preterm infant.

OBJECTIVE: To determine if indomethacin given to preterm infants with a large ductus arteriosus (DA) in the first hours of life results in maintained or improved brain and upper body blood (superior vena cava (SVC)) flow. STUDY DESIGN: A randomised, double blind trial of indomethacin v placebo. Echocardiography was performed on 111 infants born at < 30 weeks gestation at 3 and/or 10 hours after birth. Infants were eligible if the DA diameter was > 1.6 mm. Infants were randomised to receive indomethacin 0.2 mg/kg or placebo. Crossover occurred if the DA was still > 1.6 mm. Echocardiography was performed one hour after each treatment. RESULTS: Seventy (63%) infants had a DA > 1.6 mm, with 35 randomised to receive indomethacin and 35 to receive placebo. At one hour there was no difference in DA constriction (indomethacin -20% v placebo -15%), change in SVC flow (-1% v -9%), for right ventricular output (RVO). Two hours after indomethacin, 62 infants had uncontrolled observations, at which time significant ductal constriction had occurred. At this time, infants of > or = 27 weeks gestation had significantly greater increases in SVC flow and RVO than infants of < 27 weeks gestation. Infants with failed ductal constriction had significantly lower initial SVC flow and developed more late grade 3/4 peri/intraventricular haemorrhage (P/IVH). Initial SVC flow, but not ductal constriction, was a significant predictor of late grade 3/4 P/IVH in adjusted analysis. CONCLUSIONS: Indomethacin had minimal effect on ductal constriction and blood flow at one hour compared with placebo. Failure of ductal constriction is associated with low SVC flow and subsequent late severe P/IVH.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed2002

Cerebral haemodynamics and depression in the elderly.

BACKGROUND: Evidence from epidemiological and neuroimaging studies suggests that cerebrovascular disease is associated with depressive disorders in the elderly, but the extent to which it contributes to the pathogenesis of late life depression is unclear. OBJECTIVE: To investigate the relation between cerebral haemodynamics and depression in a population based study, using transcranial Doppler ultrasonography. METHODS: Cerebral blood flow velocity and CO2 induced vasomotor reactivity in the middle cerebral artery were measured in 2093 men and women who participated in the Rotterdam study. All subjects were screened for depressive symptoms using the Center of Epidemiological Studies Depression scale, and those with a score of 16 or over had a psychiatric work up. In a semistructured interview, diagnoses of depressive disorders according to the DSM-IV and subthreshold depressive disorder were established. Analyses of covariance controlled for age, sex, stroke, cognitive score, and cardiovascular risk factors were used to compare means of haemodynamic variables. RESULTS: Subjects with depressive symptoms had reduced blood flow velocities (mean difference, -2.9 cm/s; 95% confidence interval (CI), -5.0 to -0.8; p = 0.008) and lower vasomotor reactivity (mean difference -0.5%/kPa; 95% CI, -1.0 to -0.05; p = 0.03). Blood flow velocity was reduced most in subjects suffering from a DSM-IV depressive disorder (mean difference, -4.9 cm/s; 95% CI, -8.5 to -1.4; p = 0.006). The overall reduction in vasomotor reactivity was accounted for by subjects with subthreshold depressive disorder. CONCLUSIONS: Depression in late life is associated with cerebral haemodynamic changes that can be assessed by transcranial Doppler ultrasonography. The observed reduction in cerebral blood flow velocity could be a result of reduced demand in more seriously depressed cases with a DSM-IV disorder, whereas reduced CO2 induced cerebral vasomotor reactivity is a possible causal factor for subthreshold depressive disorder.

Aged↗
PubMed1999

Effects of exposure to low concentrations of carbon monoxide on exercise performance and myocardial perfusion in young healthy men.

OBJECTIVE: To assess the effects of exposure to low concentrations of carbon monoxide (CO), as commonly measured in atmospheric urban air pollution and certain occupational environments, on exercise performance and myocardial perfusion in young healthy men, and the possible need for tighter restrictions on ambient concentrations of CO. METHODS: 15 young, healthy non-smoking men, 18-35 years old, were exposed blindly and randomly to air or to a mixture of CO and air, followed by an exercise treadmill test with thallium heart scintigraphy. Blood was drawn for determination of carboxyhaemoglobin before and at the end of the exposure, and for lactic and pyruvic acid at the beginning and the end of the exercise test. The main outcome measures include the duration of the exercise test, the maximal effort expressed in metabolic equivalent units (METs), the mean plasma lactic to pyruvic acid ratio at the end of the ergometry, ECG changes in the exercise test, and perfusion deficits in thallium heart scintigraphy. RESULTS: At the end of exposure to CO, the mean (SD) blood carboxyhaemoglobin concentration rose from 0.59% (0.08%) to 5.12% (0.65%) (p < 0.0001). At the end of the exercise period, the mean (SD) plasma lactate/pyruvate ratio, which reflects the level of anaerobic metabolism (69.9 (5.9) after air and 75.9 (7.0) after CO), was not significantly different between the two experimental groups. Exercise induced electrocardiographic changes were noted in only one subject after exposure to CO. No arrhythmias were detected in any of the subjects. Significant differences were found in the mean duration of the exercise test (p = 0.0012) and the METs (p = 0.0001). The mean adjusted difference of exercise duration between exposure to air and CO was 1.52 minutes 95% confidence interval (95% CI) 0.73 to 2.32 minutes. The mean adjusted difference of METs between exposure to air and CO was 2.04 95% CI 1.33 to 2.76. The models for duration of exercise and METs showed no significant sequence and period effects. Thallium myocardial perfusion imaging disclosed normal perfusion in all regions of the heart, with no significant differences in perfusion between the two exercise tests (after air or CO). CONCLUSION: Acute exposure to a low concentration of CO which produces blood carboxyhaemoglobin concentrations of 4%-6% significantly decreases exercise performance in young healthy men. No ischaemic electrocardiographic changes or disturbances in myocardial perfusion were found by graded exercise with thallium scintigraphy. Our findings suggest that pollution of atmospheric air by CO at concentrations which are commonly found in urban and industrial environments may exert an adverse effect on skeletal muscles, manifesting as decreased exercise performance.

Adolescent↗
PubMed2004

COOH-terminal 26-amino acid residues of progastrin are sufficient for stimulation of mitosis in murine colonic epithelium in vivo.

Transgenic mice (hGAS) that overexpress human progastrin are more susceptible than wild-type mice (FVB/N) to the induction of colonic aberrant crypt foci (ACF) and adenomas by the chemical carcinogen azoxymethane. We have previously shown significantly increased levels of colonic mitosis in hGAS compared with FVB/N mice after gamma-radiation. To investigate whether the effects of progastrin observed in hGAS colon require the presence of other forms of circulating gastrin, we have crossed hGAS (hg(+/+)) with gastrin knockout (G(-/-)) mice to generate mice that express progastrin and no murine gastrin (G(-/-)hg(+/+)). After azoxymethane, G(-/-)hg(+/+) mice developed significantly more ACF than control G(-/-)hg(-/-) mice (which do not express any forms of gastrin). G(-/-)hg(+/+) mice also exhibited significantly increased colonic mitosis both before and after exposure to 8 Gray Gy gamma-radiation or 50 mg/kg azoxymethane compared with G(-/-)hg(-/-). Treatment of G(-/-)hg(-/-) mice with synthetic progastrin (residues 21-101 of human preprogastrin) or G17 extended at its COOH terminus corresponding to the COOH-terminal 26-amino-acid residues of human preprogastrin (residues 76-101, G17-CFP) resulted in continued colonic epithelial mitosis after gamma-radiation, whereas glycine-extended gastrin-17 and the COOH-terminal tryptic fragment of progastrin [human preprogastrin-(96-101)] had no effect. Immunoneutralization with an antibody against G17-CFP before gamma-radiation significantly decreased colonic mitosis in G(-/-)hg(+/+) mice to levels similar to G(-/-)hg(-/-). We conclude that progastrin does not require the presence of other forms of gastrin to exert proliferative effects on colonic epithelia and that the portion of the peptide responsible for these effects is contained within amino acid residues 76-101 of human preprogastrin.

Amino Acid Sequence↗
PubMed1989

Lack of effect of vasopressin replacement on renin hypersecretion in Brattleboro rats.

To determine how the vasopressin deficiency in homozygous Brattleboro rats with diabetes insipidus produces increased renin secretion, homozygous and heterozygous Brattleboro rats were infused through subcutaneously implanted Alzet minipumps for 1 wk with a dose of arginine vasopressin that restored plasma vasopressin to normal in the homozygous animals. In the homozygous animals, plasma renin activity (PRA) and the PRA response to immobilization remained elevated compared with Long-Evans controls. Propranolol reduced PRA to normal and markedly reduced the PRA response to immobilization. PRA was normal in heterozygous Brattleboro rats. The data indicate that the increased renin secretion in homozygous rats is a result of increased sympathetic activity, and because circulating vasopressin does not cross the blood-brain barrier, it seems likely that the increased sympathetic activity is central in origin.

Animals↗
PubMed1997

Role of NO in the O2 and CO2 responsiveness of cerebral and ocular circulation in humans.

It is well known that changes in PCO2 or PO2 strongly influence cerebral and ocular blood flow. However, the mediators of these changes have not yet been completely identified. There is evidence from animal studies that NO may play a role in hypercapnia-induced vasodilation and that NO synthase inhibition modulates the response to hyperoxia in the choroid. Hence we have studied the effect of NO synthase inhibition by NG-monomethyl-L-arginine (L-NMMA, 3 mg/kg over 5 min as a bolus followed by a continuous infusion of 30 micrograms.kg-1.min-1) on the changes of cerebral and ocular hemodynamic parameters elicited by hypercapnia and hyperoxia in healthy young subjects. Mean flow velocities in the middle cerebral artery and the ophthalmic artery were measured with Doppler ultrasound, and ocular fundus pulsation amplitude, which estimates pulsatile choroidal blood flow, was measured with laser interferometry Administration of L-NMMA reduced ocular fundus pulsation. (-19%, P < 0.005) but only slightly reduced mean flow velocities in the larger arteries. Hypercapnia (PCO2 = 48 mmHg) significantly increased mean flow velocities in the middle cerebral artery (+26%, P < 0.01) and fundus pulsation amplitude (+16%, P < 0.005) but did not change mean flow velocity in the ophthalmic artery. The response to hypercapnia in the middle cerebral artery (P < 0.05) and in the choroid (P < 0.05) was significantly blunted by L-NMMA. On the contrary, L-NMMA did not affect hyperoxia-induced (PO2 = 530 mmHg) hemodynamic changes. The hemodynamic effects of L-NMMA (at baseline and during hypercapnia) were reversed by coadministration of L-arginine. The present study supports the concept that NO has a role in hypercapnia induced vasodilation in humans.

Adult↗
PubMed1999

Acetazolamide-induced cerebral and ocular vasodilation in humans is independent of nitric oxide.

Acetazolamide, a carbonic anhydrase inhibitor, is used orally in the treatment of primary and secondary open-angle glaucoma and induces ocular and cerebral vasodilation. Several in vitro studies have shown that carbonic anhydrase pharmacology and the L-arginine-nitric oxide (NO) pathway are closely related. We investigated the role of NO in acetazolamide-induced vasodilation on cerebral and ocular vessels in 12 healthy subjects in the presence or absence of NG-monomethyl-L-arginine (L-NMMA), a NO synthase inhibitor, and in the presence or absence of L-arginine, the precursor of NO. Acetazolamide was administered after pretreatment with either L-NMMA or placebo and either L-arginine or placebo. Pulsatile choroidal blood flow was assessed with laser interferometric measurement of fundus pulsation. In addition, mean blood flow velocity (MFV) in the middle cerebral artery (MCA) and ophthalmic artery (OA) was measured with Doppler sonography. Acetazolamide increased ocular fundus pulsation amplitude (FPA; +27%, P < 0.001) and MFV in the MCA (+38%, P < 0.001) and in the OA (+19%, P = 0.003). Administration of L-NMMA alone reduced FPA (-21%, P < 0.001) and MFV in the MCA (-11%, P = 0. 030) but did not change MFV in the OA. All hemodynamic effects of L-NMMA were reversed by L-arginine. However, neither L-NMMA nor L-arginine altered acetazolamide-induced changes in cerebral or ocular hemodynamic parameters. The present data indicate that acetazolamide-induced hemodynamic changes are not mediated by NO. Which mediators other than NO are involved in the hemodynamic effects as induced by carbonic anhydrase inhibitors remains to be elucidated.

Acetazolamide↗