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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Regional cerebral blood flow (rCBF) was determined in man by Xenon-133 intravenous bolus injection technique. This method is of value especially for patients with stroke. The measuring system constituted of a 16 channel cerebrograph (rCBF 1656, Meditronic, Denmark) and a minicomputer (AI Electronics, Japan). Then, for an estimation of rCBF, two compartment analysis was applied in which a special computer program was used for this purpose. Amount of Xenon-133 in expired air was used for calculation, since we confirmed that Xenon-133 clearance in expired air was similar to that in arterial blood except for those patients with obstructive lung disease and so on. In normal adults, rCBF of the gray matter was 67 +/- 13 ml/100 g brain/min. (95% confidence limits). Patients who had been TIA or RIND, revealed a decrease of rCBF of 33--49 ml/100 g brain/min. bilaterally, although they did not show any clinical signs at the time of measurement. Contrariwise, two cases of Moya-moya disease showed a normal value of rCBF at their silent periods.
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PMID:[A study of regional cerebral blood flow by intravenous injection method of Xenon-133 (author's transl)]. 52 61

Filling pressures of the heart and hemodynamic responses were studied before, during, and after administration of morphine, 2 mg/kg, intravenously (5 mg per minute) in eight patients with coronary-artery disease and normal ventricular contractility requiring myocardial revascularization. Left-heart filling pressure (LHFP) was estimated by measuring balloon-occluded pulmonary arterial pressure via a Swan-Ganz catheter, and right-heart filling pressure (RHFP) by right atrial pressure measurements. LHFP and RHFP were unchanged until 1.5 mg/kg morphine had been administered; after 2 mg/kg, LHFP had risen from a control level of 6.9 plus or minus 0.8 to 10.6 plus or minus 1.1 mm Hg (P less than .01) and RHFP from 2.9 plus or minus 0.4 to 4.9 plus or minus 0.8 mm Hg (P less than .05). Heart rate (P less than .02) and rate-pressure product (P less than .05), an indirect index of myocardial oxygen consumption, decreased throughout the study period. Systemic arterial pressure, cardiac index, and left ventricular stroke work decreased significantly only at the 0.5 mg/kg dose level, while systemic vascular resistance and stroke index remained unchanged. Mean pulmonary arterial pressure increased (P less than .05) after 1.5 mg/kg morphine, but pulmonary vascular resistance was unchanged. PaC02, pH, base excess, and hematocrit were constant throughout the study period. These data indicate that doses of morphine to 2 mg/kg, iv, are well tolerated by, and, presumably, decrease the myocardial oxygen consumption of, patients with coronary-artery disease. The hemodynamic response resembles that seen in man without hear or lung disease.
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PMID:Filling pressures of the heart and pulmonary circulation of the patient with coronary-artery disease after large intravenous doses of morphine. 111 63

Nitroprusside was infused intravenously (20, 40, 80 and 200 mug/min) in nine patients with pulmonary hypertension due to mitral stenosis (group I), nine with precapillary pulmonary hypertension associated with primary lung disease (group II) and nine with normal pulmonary-arterial pressures (group III). The mean pulmonary-arterial pressure was markedly reduced at a rate of 20 mug/min in group I and II, while higher doses were necessary in group III to produce a similar effect. Mean arterial pressure was decreased in all three groups and was dose-related. Heart rate rose, stroke volume fell during nitroprusside administration, while cardiac output remained unchanged. Pulmonary vascular resistance was reduced on 20 mug/min in group I, but only on 200 mug/min or more in group II, and unchanged at all dosages in group III. Peripheral vascular resistance declined in all three groups on nitroprusside infusion, which is apparently of value in the short-term lowering of pulmonary hypertension.
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PMID:[Lowering of pulmonary-arterial pressure with nitroprusside in mitral stenosis and cor pulmonale (author's transl)]. 126 32

Restriction endonuclease analysis was used to detect alpha-gene deletions and to determine the haplotypes in the DNA of the beta S-gene-cluster [Benin, Central African Republic (CAR), and Senegal] in 221 patients with sickle cell anemia (SS). The clinical expression of SS was modified by the beta S-gene-cluster polymorphisms and the alpha-gene status (alpha-thalassemia-2). The overall risk of soft tissue organ failure caused by the obliterative sickle vasculopathy (including stroke, renal failure, chronic lung disease with cor pulmonale, leg ulcers, and young adult death) was increased threefold in those with a CAR haplotype and was decreased in those with a Senegalese chromosome (p = 0.003). In the presence of a Senegalese haplotype, the patient's health is better, and with the CAR haplotype it is always worse. With the Benin, it is intermediate. Acute recurrent clinical events including hospitalized sickle cell crisis, bone infarction, and infection are decreased in frequency in those with a Senegalese haplotype. The risk of most acute events including acute chest syndrome is equivalent in those with Benin or CAR haplotypes. In the United States, alpha-thalassemia-2 is co-inherited randomly among the beta S-gene-cluster haplotypes. Acute events occurring during childhood are minimally effected by this co-inheritance. The risk of soft tissue organ failure is decreased. After the age of 20 years, painful episodes of the lumbar dorsal area are increased in patients who had alpha-thalassemia-2 in association with degenerative bone disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Beta S-gene-cluster haplotypes in sickle cell anemia: clinical implications. 170 Jun 39

Identification of the beta s-gene-cluster haplotype and alpha-gene status provide a useful tool to improve the possibility for early detection in high-risk SS patients. The DNA polymorphisms of the beta s-gene-cluster modify the clinical course in sickle cell anemia especially as it involves the risk of end-stage organ failure of the kidney, lung, and brain. In both Africa and America, the CAR beta s haplotype increases the risk of developing irreversible complications at an early age. The degree of anemia, the Hb F concentration, and the preservation (or lack thereof) of G gamma Hb F is haplotype dependent and correlates with the overall clinical course of the patient. Further modulation of the clinical course by the coinheritance of alpha-thalassemia-2 tends to decrease the risk of soft tissue organ failure but increases the risk of osteonecrosis. A single individual can be expected to fit into the overall pattern. Some sickle related illness will eventually occur in all patients. In the presence of a Senegal haplotype, the patient's health is better, with the CAR haplotype it is always worse; severity is intermediate in the Benin. These genetic markers can be used to identify the endangered patient before the onset of irreversible major organ failure. The high risk SS patient with a CAR chromosome or one who is homozygous Ben without alpha-thalassemia-2 should be monitored closely for evidence of vasculopathy-induced microinfarction of the brain, kidneys, or lungs. Such a patient needs preventive therapy before suffering a major hemisphere stroke, losing kidney function, or developing cor pulmonale secondary to restrictive lung disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sickle cell anemia: beta s-gene-cluster haplotypes as prognostic indicators of vital organ failure. 188 45

We describe a patient with inherited plasminogen deficiency who developed extensive cerebral venous thrombosis. Several other conditions that might have contributed to a hypercoagulable state, including mild thrombocytosis, thyrotoxicosis, and a chronic inflammatory lung disorder, were present. We also discuss the evidence linking plasminogen deficiency with a thrombophilic state. The diagnosis of cerebral venous thrombosis in this case was readily established by nuclear magnetic resonance imaging, a technique that is ideally suited for the evaluation and follow-up of patients with this condition.
Stroke 1991 Mar
PMID:Cerebral venous thrombosis with plasminogen deficiency. 200 11

Cluster analysis was used to examine the nature and magnitude of changes in left ventricular pump function in relation to the severity of primary bronchial obstruction in patients with non-atopic bronchial asthma (n = 45) and chronic obstructive bronchitis (n = 45). In the patients with obstructive lung disease, central hemodynamic changes were found to be determined by the bronchial patency and independent of the pathogenesis of the obstruction. During a remission there was a significant reduction in total peripheral resistance as compared to the values seen in healthy subjects, whereas in moderate or severe obstruction there was a marked increase in total peripheral resistance and a decrease in stroke volume and cardiac output. A drastic bronchial obstruction was followed not only by central hemodynamic changes, but a fall in ejection fraction and a rise in left ventricular end-systolic and end-diastolic volumes.
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PMID:[Pump function of the left ventricle during the stages of cor pulmonale development]. 227 42

In an effort to better understand the cardiac contribution to exercise limitation in chronic lung disease, 21 patients with advanced chronic pulmonary parenchymal disease and 10 normal control subjects were evaluated for changes in right ventricular (RV) pressure, volume and function during incremental, symptom-limited supine bicycle exercise. Patients underwent sequential exercise tests with Doppler echocardiography and ultrafast cine computed tomography (CT). RV systolic pressure during exercise was determined by saline-enhanced Doppler of tricuspid regurgitation. RV ejection fraction, end-diastolic volume, stroke volume and cardiac index were obtained by CT at rest and peak exercise. Sixteen of the 21 study patients also exercised on high-flow oxygen. In the control subjects RV systolic pressure increased from 21 +/- 6 mm Hg (mean +/- standard deviation) at rest to 32 +/- 8 mm Hg at peak exercise, whereas in patients with lung disease, RV systolic pressure increased from 42 +/- 17 to 81 +/- 26 mm Hg (both p less than 0.01). Compared with the control subjects, the patients with lung disease had significantly lower mean values for RV ejection fraction at rest (47 +/- 7 vs 55 +/- 7%) and at peak exercise (47 +/- 9 vs 57 +/- 3%, respectively, both p less than 0.05). The patients who demonstrated oxyhemoglobin desaturation during exercise showed the most abnormal cardiac responses, with marked increases in mean RV systolic pressure, decreases in mean RV ejection fraction and blunted increases in cardiac index and RV stroke volume. Although acute oxygen supplementation was associated with a slight decrease in RV systolic pressure at peak exercise and a longer duration of exercise, there was no significant improvement in RV function. Doppler echocardiography and CT provide complementary and potentially useful information about right-sided heart pressures and RV ejection fraction during exercise in patients with advanced chronic lung disease. Oxyhemoglobin desaturation during exercise is a marker for the most abnormal pulmonary vascular reserve, as indicated by RV contractile dysfunction and limited ability to increase cardiac index.
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PMID:Doppler echocardiography and ultrafast cine computed tomography during dynamic exercise in chronic parenchymal pulmonary disease. 277 97

The cardiorespiratory incremental maximal exercise test is being used increasingly for clinical evaluation. It is based on the fact that during physical effort the output of the cardiovascular and respiratory systems increase to maintain a higher metabolic rate and stroke volume. Cardiac output increases by increase in both heart rate and stroke volume. Ventilation increases by increase in respiratory rate and tidal volume. All changes are synchronous, so that blood composition and gas partial pressures are constant over a wide range of work intensities. The response of a normal sedentary subject to incremental exercise is presented, as well as the improvement in an athlete's physical performance as a result of training. An obese subject, despite normal maximal oxygen uptake, felt compromised due to the high energy cost of moving his heavy torso. The large normal breathing reserve during exercise was demonstrated in 2 subjects who, despite lung disease, responded normally to the test. It is likely that this test will be widely used for evaluation of patients with heart and lung disease.
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PMID:[The integrative cardiorespiratory exercise test]. 279 24

The acute cardiovascular effects of a new xanthine, enprofylline, were studied in patients with chronic lung disease. The studies were done during cardiac catheterization (n = 12) and by radionuclide ventriculography (n = 6). Enprofylline was given intravenously, 2 mg/kg, and measurements were done after ten and 30 min. Enprofylline reduced the mean pulmonary artery pressure from 30 +/- 10 to 26 +/- 7 mm Hg (p less than 0.05) and the mean systemic arterial pressure from 92 +/- 17 to 83 +/- 15 mm Hg (p less than 0.01), increased the heart rate from 89 +/- 15 to 100 +/- 18 beats/min (p less than 0.01) and reduced the stroke volume from 55 +/- 12 to 48 +/- 12 ml (p less than 0.05) after 30 min. Radionuclide ventriculography revealed unchanged ejection fraction of left and right ventricles after enprofylline. None of the patients experienced serious side effects of the drug. Thus, enprofylline induced modest acute cardiovascular effects with a chronotropic response together with a small vasodilation in pulmonary and systemic circulation.
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PMID:Cardiopulmonary effects of enprofylline. A xanthine with weak adenosine receptor antagonism in patients with severe chronic lung disease. 339 15


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