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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is a need for new technical approaches whereby the cerebral microcirculation can be easily and continuously assessed. The objective of this study was to determine whether laser-Doppler (LD) flowmetry can be utilized to assess changes in cerebral cortical blood flow and to determine whether changes in blood perfusion measured by LD flowmetry correlate with simultaneously measured changes in flow measured by H2 clearance in cats or with changes in pial arteriolar diameter measured with a microscope in rabbits equipped with a closed cranial window. In the rabbit experiments a 0.84-mm-diam LD probe was inserted through a cranial window port, and in the cat experiments the probe was fixed adjacent to the H2 probe. The probe was fixed at a distance of 1-2 mm from the cortical surface, where it and its associated electronics detect changes in blood cell velocity and blood volume within a tissue volume of approximately 1 mm3. Volume and velocity are multiplied to provide a flow signal. When cerebral blood flow in cats was decreased by hyperventilation-induced hypocapnia and increased by norepinephrine-induced hypertension, the percent changes in LD flow and H2 clearance flow changed linearly (r = 0.94, slope = 0.97). When arterial PCO2 was increased from 28 to 48 mmHg in the rabbit experiments, the pial arterioles dilated 19 +/- 4% (mean +/- SE) and LD flow increased by 74 +/- 9%, LD flow changes which would be predicted by a third power relationship of diameter to flow.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Laser-Doppler assessment of brain microcirculation: effect of systemic alterations. 270 61

1. In systemic hypertension the pulmonary vessels show an excessive tone at rest and hyper-react to adrenoceptor stimulation. Alterations in Ca2+ handling by the vascular smooth muscle cells seem to underlie these disorders. Alveolar hypoxia also constricts pulmonary arteries, increasing the intracellular Ca2+ availability for smooth muscle contraction. This suggests the hypothesis that hypoxic pulmonary vasoconstriction depends on similar biochemical disorders, and that the response to the hypoxic stimulus may be emphasized in high blood pressure. 2. In 21 hypertensive and 10 normotensive men, pulmonary arterial pressure and arteriolar resistance have been evaluated during air respiration and after 15 min of breathing 17, 15 and 12% oxygen in nitrogen. Curves relating changes in pulmonary arterial pressure and arteriolar resistance to the oxygen content of inspired gas had a similar configuration in the two populations, but in hypertension were steeper and significantly shifted to the left of those in normotension, reflecting a lower threshold and an enhanced vasoconstrictor reactivity. 3. This pattern was not related to differences in severity of the hypoxic stimulus, degree of hypocapnia and respiratory alkalosis induced by hypoxia, and plasma catecholamines. 4. The association of high blood pressure with enhanced pulmonary vasoreactivity to alveolar hypoxia could have clinical implications in patients who are chronically hypoxic and have systemic hypertension.
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PMID:Enhancement of the pulmonary vasoconstriction reaction to alveolar hypoxia in systemic high blood pressure. 273 78

The effects of isoflurane (1 MAC) and enflurane (1 MAC) on cerebral blood flow and cerebral oxygen consumption were studied in 20 male patients without intracranial disease undergoing coronary artery bypass surgery (mean age 57 and 59 years respectively). The aim of the study was to investigate whether both agents diminish autoregulation of cerebral blood flow and CO2 reactivity of cerebral blood vessels. Patients were randomly assigned to one of two groups (10 patients each) receiving either isoflurane 1.15 vol.% or enflurane 1.68 vol.% endexpiratory. Measurements were performed and blood samples were taken in the awake state (I); 15 min after achievement of steady-state conditions with 1.68 vol.% enflurane or 1.5 vol.% isoflurane without blood pressure support (II); during norepinephrine-induced hypertension at a cerebral perfusion pressure of 110 mmHg (III); and during controlled hyperventilation at a PaCO2 of 27 mmHg and normotension (IV). Cerebral blood flow was measured by the argon wash-in technique. Isoflurane and enflurane produced a significant drop in cardiac index and cerebral perfusion pressure and reduced cerebral blood flow significantly by 35% and 39% respectively. Cerebral oxygen consumption was also significantly decreased by 49% (isoflurane) and 50% (enflurane). Induced hypertension with norepinephrine increased cerebral blood flow significantly by 32% (isoflurane) and 26% (enflurane), while hypocapnia reduced cerebral blood flow significantly by 26% (isoflurane) and 29% (enflurane).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effects of isoflurane and enflurane on cerebral hemodynamics and cerebral oxygen consumption in humans]. 326 82

The chemistry, pharmacology, pharmacokinetics, adverse effects, dosage, and availability of nimodipine are discussed, and the clinical use of nimodipine in preventing and treating cerebral arterial spasm in patients with subarachnoid hemorrhage is reviewed. Nimodipine is a highly lipid-soluble dihydropyridine derivative that readily crosses the blood-brain barrier. In animal studies, nimodipine has been shown to be effective in increasing cerebral blood flow; preventing vasoconstriction attributable to sympathetic stimulation, hypocapnia, and hypertension; and improving neurological outcome after cerebral ischemia. Nimodipine is reported to be 90% protein bound; its half-life is approximately 13 hours, with substantial interpatient variability. Nimodipine has been studied in the prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage. In four open trials, in which nimodipine was administered orally, intravenously, topically during surgery, or by intracarotid injection, and in two double-blind, placebo-controlled trials, neurological outcomes were improved in patients receiving the drug. However, in both sets of trials nimodipine had limited effects on cerebral arterial spasm. Although nimodipine can cause hypotension, no serious adverse reactions to the drug were reported in clinical trials in patients with subarachnoid hemorrhage. Based on limited data currently available, nimodipine appears to improve neurological outcome in patients with subarachnoid hemorrhage. However, its efficacy in preventing or treating cerebral arterial spasm in these patients seems to be limited.
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PMID:Use of nimodipine for prevention and treatment of cerebral arterial spasm in patients with subarachnoid hemorrhage. 332 39

It has been reported in exercising ponies that O2 supply to all regions of the brain increased primarily due to a large increment in CaO2 and it was implied that this may reflect a generalized increase in brain metabolism during strenuous exercise. Splenectomy ameliorates the rise in CaO2 observed with exercise in ponies. Thus, the objective of the present study was to examine changes in regional brain blood flow and O2 supply of splenectomized ponies with sub-maximal and maximal exercise and to compare these data with previous observations in normal ponies. It was reasoned that in the absence of a marked rise in CaO2, the brain blood flow of splenectomized ponies would have to increase markedly if brain metabolism also increased with severe exercise. Regional brain blood flow was studied using 15 micron diameter radionuclide labeled microspheres injected into the left atrium during rest (control) and sub-maximal as well as maximal exertion on a treadmill. It was observed that despite marked arterial hypocapnia and acute systemic hypertension which developed during exercise, blood flow as well as O2 supply in the cerebral cortex, caudate nuclei, cerebral white matter, cerebellar white matter, thalamus-hypothalamus, mid-brain, pons and medulla were not different from control values. In the cerebrellar cortex, however, blood flow and O2 supply increased with both work intensities. Thus, it was concluded that in exercising ponies, metabolic O2 requirement increased in the cerebellar cortex but was most likely not different from control (rest) in other regions of the brain.
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PMID:Regional distribution of brain blood flow during maximal exertion in splenectomized ponies. 360 13

The purpose of this study was to examine regional autoregulation of blood flow in the brain during acute hypertension. In anesthetized cats severe hypertension increased blood flow more in cerebrum (159%) and cerebellum (106%) than brain stem (58%). In contrast to the heterogeneous autoregulatory response, hypocapnia produced uniform vasoconstriction in the brain. We also compared vasodilatation during severe hypertension with vasodilatation during hypercapnia. During hypercapnia, blood flow increased as much in brain stem, as in cerebrum and cerebellum. Thus regional differences in autoregulation appear to be specific for autoregulatory stimulus and are not secondary to nonspecific differences in vasoconstrictor or vasodilator capacity. To determine whether the blood-brain barrier is more susceptible to hypertensive disruption in regions with less effective autoregulation, permeability of the barrier was quantitated with 125I-albumin. Severe hypertension produced disruption of the barrier in cerebrum but not in brain stem. Thus there are parallel differences in effectiveness of autoregulation and susceptibility to disruption of the blood-brain barrier in different regions of the brain.
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PMID:Heterogeneity of brain blood flow and permeability during acute hypertension. 392 26

The effects of topical application of agents which produce oxygen radicals on cerebral arterioles were studied in anesthetized cats. Xanthine oxidase plus xanthine, which produced superoxide anion radical, hydrogen peroxide, and hydrogen peroxide plus ferrous sulfate, which produced the free hydroxyl radical, induced sustained dilation, reduced responsiveness to the vasoconstrictor effect of hypocapnia, and destructive lesions of the endothelium and of the vascular smooth muscle. Similar effects were produced by arachidonate, 15-HPETE, and PGG2. The effect of arachidonate was inhibited by mannitol, a free hydroxyl radical scavenger, the effect of PGG2 was inhibited by SOD, the effect of 15-HPETE was inhibited by either catalase or SOD. These results suggest that these cerebral vascular abnormalities were produced by a single destructive free radical, probably the hydroxyl free radical, generated via interaction of superoxide and hydrogen peroxide. Cerebral vascular abnormalities similar to those produced by oxygen radicals were also seen after experimental concussive brain injury or after acute hypertension. After brain injury, activation of phospholipase C and increased brain prostaglandin concentration were demonstrated. The vascular effects of brain injury and acute hypertension were inhibited by free radical scavengers. The results suggest that, in these conditions, vascular damage is induced by oxygen radicals generated from arachidonate in association with increased prostaglandin synthesis.
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PMID:Oxygen radicals and vascular damage. 640 99

The purpose of this study was to examine effects of nimodipine (Bay e 9736), a calcium blocker, on constrictor responses of cerebral vessels in vivo. Pial artery diameter was measured in anesthetized cats. In the control state, sympathetic nerve stimulation, acute hypertension, and hypocapnia produced maximal decreases in pial artery diameter of 13.7 +/- 1.4, 12.1 +/- 2.7, and 13.3 +/- 2.7% (SE), respectively. Low doses of nimodipine (0.1-0.25 microgram X kg-1 X min-1) decreased the vasoconstrictor response to all three stimuli, and higher doses (0.5-1.0) virtually abolished the response (P less than 0.05 vs. control). In other experiments in cats and monkeys, cerebral blood flow (CBF) was measured with microspheres during acute increases in arterial pressure. Elevation of arterial pressure by approximately 40 mmHg in cats produced only a modest increase in CBF from 48 +/- 3 to 57 +/- 3 ml X min-1 X 100 g-1 in the control state and a larger increase in CBF from 53 +/- 6 to 87 +/- 9 ml X min-1 X 100 g-1 during nimodipine (P less than 0.05, control vs. nimodipine). Nimodipine also inhibited autoregulatory vasoconstriction in monkeys. Nimodipine, in the doses used, had only modest effects on resting vessel diameter, CBF, or arterial pressure. We conclude that nimodipine inhibits cerebral vasoconstrictor responses to several physiological stimuli in vivo.
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PMID:Effects of nimodipine on cerebral vasoconstrictor responses. 643 30

Recurrent pulmonary embolism sometimes (3% of hospital autopsies) determines a progressive obstruction of the pulmonary vascular bed, which in turn causes pulmonary arterial hypertension and in time right ventricular hypertrophy and failure. The first stages of this process are characterized by slight pulmonary arterial hypertension at rest and by few and deceiving symptoms which make the diagnosis very difficult. Regarding anatomy, in most cases recurrent thromboembolism obstructs one of the main branches of the pulmonary artery. At the beginning pulmonary embolism usually manifests itself in a spontaneous and atypical manner: paroxysmal dyspnea, tachycardia, lateral chest pain, mild hemoptysis and recurrent fever. The clinical signs of peripheral thrombophlebitis are not very frequent. The chest roentgenogram supplies diagnostic information in 20% of cases, the electrocardiogram in 10%. Very important is the contribution of the analysis of arterial blood gases: hyperventilation, moderate hypoxia associated with shunting, hypocapnia with a widened difference between alveolar and arterial CO2. Pulmonary perfusion scintiphotography shows vast unperfused areas, different to the "plexogenic" appearance in primitive pulmonary arterial hypertension, in about 50% of cases. Pulmonary angiography discloses the exact site and extension of the obstruction in 80-90% of cases. On catheterization pulmonary arterial hypertension results to be inconstant and may appear only during stress. Regarding the evolution of pulmonary embolism, the forms associated with pulmonary arterial hypertension may last several years, although recurrent embolism may shorten its course. When the stage of right ventricular hypertrophy is reached, the evolution is generally rapid (from 1 to 4 years).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic pulmonary thromboembolism. 653 60

A patient with pronounced dyspnoea and cyanosis was found to have severe hypoxaemia with normal spirographic values. His past history included arterial hypertension, myocardial infarction and phlebitis of the lower limb. Airways resistance was normal, but maximal expiratory flow rates at low lung volume (Flow-volume curves) were reduced, suggesting "peripheral" airways obstruction. This was confirmed by the presence of pulmonary hyperinflation and mechanical non-homogeneity accompanied by unevenly distributed ventilation, as shown by alveolar nitrogen gradient. There was marked hyperventilation with hypocapnia. Since transfer values (measured by the CO single-breath method) and lung distensibility values were normal, emphysema could be ruled out as a cause of obstruction. Analysis of pressure-flow relationship confirmed that the obstruction of peripheral airways was "intrinsic" in character. It could be due to an increase in lung extravascular fluid (interstitial oedema due to left cardiac failure), or to repeated micro-emboli in the lungs, or to hypocapnia, these three mechanisms possibly being associated.
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PMID:[Peripheral airway obstruction involving cardiovascular factors. A case report (author's transl)]. 677 51


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