PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “CEREBROVASCULAR CIRCULATION”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources
PubMed2000

A new method to estimate rCBF using IMP and SPECT without any blood sampling.

We developed and evaluated a method to measure rCBF without any blood sampling by using iodine- 123 IMP and SPECT. An integral of arterial input function, the integral taken from the value 0 to T of the variable Ca(t)dt, can be expressed as TC(T)/CO, where TC(T) is radioactivity delivered to the body in T minutes and CO is cardiac output. If T is acceptably small, rCBF can be determined by means of a microsphere model analysis with IMP as Cb(T)/(TC(T)/CO), where Cb(T) is cerebral radioactivity at T minutes. We derived TC(T) and CO from a chest dynamic scan. The method was applied to 45 patients who underwent rCBF studies (58 studies) with arterial blood sampling (ABS). Data from the chest scan were analyzed in comparison with ABS data in the first 28 studies, and equations for correction yielding an accurate TC(T)/CO were derived. The validity of the proposed method was evaluated in the subsequent 30 studies. The method yielded rCBF (rCBF-test) which agreed well with rCBF obtained by a two-compartment model analysis of dynamic SPECT and ABS data (rCBF-ref) with the mean and SD of differences between rCBF-test and rCBF-ref being 1.0 and 2.7 ml/100 g/min, respectively. In eleven subjects who underwent more than two studies, a percentage change in rCBF-test between the studies also closely approximated that of rCBF-ref (y = 1.11 x + 2.63, r = 0.92). The method can be used with acceptable reliability to measure rCBF without any blood sampling.

Adult↗
PubMed2003

Hyperglycaemia and its relation to cardiovascular morbidity and mortality: has it been resolved?

Type 2 diabetes is preceded by long-standing asymptomatic hyperglycaemia. This prediabetic state is characterised by elevated post-prandial hyperglycaemia and yet normal fasting plasma glucose (FPG). The relationship between abnormal circulating glucose levels and the development of long-term diabetic complications became apparent 70 years ago, soon after the introduction of insulin and the prevention of early death due to ketoacidosis. The main issues regarding diabetes and the various target organs throughout the cardiovascular system, including coronary artery disease (CAD), peripheral vascular disease (PVD), increased intima-media thickness (IMT) and stroke, are as follows: CAD causes much of the serious morbidity and mortality in patients with diabetes, who have a 2- to 4-fold increased risk of CAD; epidemiological evidence confirms an association between diabetes and increased prevalence of PVD; and diabetes induces increased IMT and stroke by adversely affecting cerebrovascular circulation including the carotid artery, akin to its effects in the coronary and lower extremity vasculature. In diabetes, FPG and HbA(1C) are the main parameters of glucose metabolism used to monitor and control hyperglycaemia. Recently, particular emphasis has been placed on post-prandial plasma glucose as a parameter in the metabolic assessment of diabetic patients. Therefore, while addressing the question of hyperglycaemia and its relation to cardiovascular morbidity and mortality, we have to look for the possible mechanisms by which diabetic hyperglycaemia causes these complications. Then, we must examine the evidence on how the main parameters of glucose metabolism correlate with cardiovascular complications. This review addresses these issues.

Blood Glucose↗
PubMed1994

Stent placement for arterial and venous cerebrovascular disease: preliminary experience.

PURPOSE: To report initial clinical experience with stent placement in the cerebrovascular circulation. MATERIALS AND METHODS: Four patients underwent arterial or venous stent placement. Two patients had cervical internal carotid artery dissections, with aneurysms and stenoses of the distal cervical carotid artery. Two patients had venous occlusive disease involving the major dural sinuses, with substantial pressure gradients across the stenoses. RESULTS: Immediately after stent placement, the true arterial lumina returned to normal diameter and both carotid aneurysms were more than 90% occluded. Follow-up angiography demonstrated continued improvement in the arterial aneurysms. Both patients with dural sinus venous occlusive disease showed substantial improvement of the sinus stenoses and substantial reversal of the pressure gradients after venous stent placement. At follow-up, these patients have done well. CONCLUSION: This preliminary experience suggests there may be a role for stents in the management of arterial and venous cerebrovascular disease, including carotid artery dissection and venous occlusive disease.

Adult↗
PubMed1998

Two-kidney, two clip renovascular hypertensive rats can be used as stroke-prone rats.

BACKGROUND AND PURPOSE: The cerebrovascular lesions in stroke-prone spontaneously hypertensive rats are not only dependent on high blood pressure but partly related to pressure-independent genetic factors. The aim of the present study was to observe whether spontaneous stroke occurred in renovascular hypertensive rats without a genetic deficiency. METHODS: The 1-kidney, 1 clip (1k1c); 2-kidney, 1 clip (2k1c); and 2-kidney, 2 clip (2k2c) methods were used to induce hypertension in male Sprague-Dawley rats with a ring-shaped silver clip. Sham-operated rats were used as controls. Blood pressure and neurological symptoms were observed in the rats without any artificial inducement. Brain sections stained with hematoxylin-eosin and phosphotungstic acid-hematoxylin were examined under a microscope to determine stroke foci. RESULTS: The attack rate of stable hypertension was 100% (55/55) in the 2k2c group, which was significantly higher than that in the 1k1c (23/30, 76.7%) and 2k1c (21/30, 70%) groups (P<0.01). None of the rats in the 2k2c group died of acute renal failure or suffered from diffuse cerebral lesions postoperatively. Forty weeks after renal artery constriction, the incidence of spontaneous stroke in the 2k2c group was 61.8% (34/55), which was significant higher than that in the 1k1c (7/30, 23.3%) and 2k1c (5/30,16.7%) groups (P<0.01). Stroke foci were not observed in normotensive controls. CONCLUSIONS: We conclude that 2k2c renovascular hypertensive rats with proper renal artery constriction can be used as stroke-prone renovascular hypertensive rats independent of a genetic deficiency.

Animals↗
PubMed2006

Carbon monoxide contributes to hypotension-induced cerebrovascular vasodilation in piglets.

The gaseous compound carbon monoxide (CO) has been identified as an important endogenous biological messenger in brain and is a major component in regulation of cerebrovascular circulation in newborns. CO is produced endogenously by catabolism of heme to CO, free iron, and biliverdin during enzymatic degradation of heme by heme oxygenase (HO). The present study was designed to test the hypothesis that endogenously produced CO contributes to hypotension-induced vasodilation of cerebral arterioles. Experiments used anesthetized piglets with implanted, closed cranial windows. Topical application of the HO substrate heme-l-lysinate caused dilation of pial arterioles that was blocked by a metal porphyrin inhibitor of HO, chromium mesoporphyrin (CrMP). In normotensive piglets (arterial pressure 64 +/- 4 mmHg), CrMP did not cause vasoconstriction of pial arterioles but rather a transient dilation. Hypotension (50% of basal blood pressure) increased cerebral CO production and dilated pial arterioles from 66 +/- 2 to 92 +/- 7 microm. In hypotensive piglets, topical CrMP or intravenous tin protoporphyrin decreased cerebral CO production and produced pial arteriolar constriction to normotensive diameters. In additional experiments, because prostacyclin and nitric oxide (NO) are also key dilators that can contribute to cerebrovascular dilation, we held their levels constant. NO/prostacyclin clamp was accomplished with continuous, simultaneous application of indomethacin, N(omega)-nitro-l-arginine, and minimal dilatory concentrations of iloprost and sodium nitroprusside. With constant NO and prostacyclin, the transient dilator and prolonged constrictor responses to CrMP of normotensive and hypotensive piglets, respectively, were the same as when NO and prostaglandins were not held constant. These data suggest that endogenously produced CO contributes to cerebrovascular dilation in response to reduced perfusion pressure.

Animals↗
PubMed1993

Disordered methionine/homocysteine metabolism in premature vascular disease. Its occurrence, cofactor therapy, and enzymology.

Mild homocysteinemia occurs surprisingly often in patients with premature vascular disease. We studied the possible enzymatic sources of this mild hyperhomocysteinemia and the control of homocysteine levels in plasma by treatment of patients with the cofactors and cosubstrates of homocysteine catabolism. We assessed homocysteine metabolism in 131 patients who had premature disease in their coronary, peripheral, or cerebrovascular circulation by using a standard oral methionine-load test. Impaired homocysteine metabolism occurred in 28 patients. We assayed levels of the primary enzymes of homocysteine catabolism in cultured skin fibroblast extracts from 15 of these 28 patients. The patients' cystathionine beta-synthase levels (3.68 +/- 2.52 nmol/h per milligram of cell protein, mean +/- SD) were markedly depressed compared with those from 31 healthy adult control subjects (7.61 +/- 4.49, P < .001). The patients' levels of 5-methyltetrahydrofolate: homocysteine methyltransferase were normal. While betaine: homocysteine methyltransferase was not expressed in skin fibroblasts, 24-hour urinary betaine and N,N-dimethylglycine measurements were consistent with normal or enhanced remethylation of homocysteine by betaine: homocysteine methyltransferase in the 13 patients tested. When treated daily with choline and betaine, pyridoxine, or folic acid, there was a normalization of the postmethionine plasma homocysteine level in 16 of 19 patients. Our results indicate that mild homocysteinemia in premature vascular disease may be caused by either a folate deficiency or deficiencies in cystathionine beta-synthase activity. It does not necessarily involve deficiencies of either 5-methyltetrahydrofolate:homocysteine methyltransferase or betaine:homocysteine methyltransferase. Effective treatment regimens are also defined.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed1976

Cortical neuronal function during ischemia. Effects of occlusion of one middle cerebral artery on single-unit activity in cats.

To assess the effects of ischemia on neuronal function, the action potentials of 261 individual cortical neurons were recorded extracellulary and related to regional cerebral blood flow (CBF) measured by hydrogen clearance in 19 cats, seven of which had the left middle cerebral artery occluded during a recording. The onset of ischemia could be associated with transient increases of activity, including "seizure discharges," as well as cessation of activity. No activity was noted at CBF less than 0.18 ml/gm/min; at higher (but ischemic) values for CBF, abnormal patterns of activity frequently were recorded. One neuron recovered function after cessation in association with an increase of CBF, indicating a potential for the restoration of function of ischemic neurons by effective therapeutic measures.

Action Potentials↗