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

The change in left ventricular volume during a representative cardiac cycle was assessed in 19 patients with CAD and 8 control subjects before and after 10 mg isosorbiddinitrate sublingually. 15mCi99mTc-HSA were administered intravenously. After the tracer had equilibrated, the precordial changes of activity were measured with a gamma-camera connected to a computer. In order to determine the overall left-ventricular function from volume curves, the ejection fraction, the maximal systolic ejection rate and the maximal diastolic filling rate of the left ventricle were measured. For the assessment of regional wall motion abnormalities the volume changes were observed in a cinemode on a colour video display. In addition the relative changes of regional EF, regional stroke volume and the timing of endsystole were recorded as a functional scintigram. The results showed very clear differences between control subjects and patients with CAD. Furthermore differences existed between patients with hypokinesia and those with akinesia or aneurysm. The results emphasize that quantitative gated nuclear cardiography not only provides information concerning the left ventricular function but also allows the assessment of local wall motion as to reversible or irreversible asynergy.
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PMID:[Quantitative gated nuclear cardiography in coronary artery disease after administration of isosorbiddinitrate (author's transl)]. 54 1

Thirty-five non-selected, consenting patients were studied during induction of anesthesia before coronary artery bypass grafting. Anesthesia was induced with diazepam, thiopentone and fentanyl, followed by pancuronium. Before induction, 200 MBq Tc 99 m - HSA was given i.v. and ejection fraction (EF) of the left ventricle was measured with a collimated single-crystal probe. The patients were allocated to five groups (seven patients in each) treated with: Group A: nitroglycerin i.v. bolus 4 micrograms x kg-1 given 30-60 s before laryngoscopy; Group B: nitroglycerin i.v. in continuous infusion, 1 micrograms x kg-1 x min-1 started before induction; Group C: two-stage topical anesthesia of the vallecula region and larynx with lidocain; Group D: a combination of nitroglycerin and topical anesthesia (as in Group B and C); and Group E: propranolol i.v. 0.01 mg x kg-1 given 5 min before intubation. All groups reacted in the same way during induction of anesthesia up to the point of laryngoscopy. End-diastolic volume and systemic arterial pressure decreased while cardiac index remained unchanged and EF increased. During laryngoscopy and intubation, however, differences between the groups were evident. Nitroglycerin i.v. as a bolus effectively prevented a reduction in EF and an increase in left ventricular volume. In addition to these beneficial hemodynamic effects, there was a moderate increase in heart rate and a reduction of stroke index. Continuous infusion of nitroglycerin and propranolol i.v. had no effect, since EF fell and left ventricular volume increased. Patients receiving topical anesthesia demonstrated a blunted response to endotracheal intubation with a moderate decrease in EF and an unchanged (Group C) or slightly increased (Group D) left ventricular volume.
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PMID:A comparative study of five different techniques to reduce left ventricular dysfunction during endotracheal intubation. 178 39

Induction of anesthesia with isoflurane in combination with fentanyl, thiopentone, nitrous oxide and pancuronium was studied in nine patients scheduled for coronary artery bypass grafting. Ejection fraction (EF) of the left ventricle was monitored with a single crystal probe linked to a microcomputer, after injection of 200 MBq Tc 99m-HSA. Stroke volume index determined by thermodilution and EF were used to calculate left ventricular end-diastolic volume index (LVEDVI). The degree of ischemia was numerically scored as evaluated from the ECG (modified V5 lead). The study protocol covered seven periods from awake before induction to 5 min after intubation. EF decreased moderately during intubation (P less than 0.05). Systemic vascular resistance index (SVRI) was decreased (P less than 0.05) at all times except during intubation when it was unchanged compared to control. LVEDVI decreased during induction (P less than 0.05), while left ventricular filing pressure remained unchanged. Heart rate did not change. Systolic arterial pressure decreased from 147 mmHg (19.6 kPa) to about 100 mmHg (13.3 kPa) during induction (P less than 0.05). Two patients were given vasoconstrictors because of low arterial pressure. The mean ischemic score did not change. One patient, however, had signs of progressive ischemia. In this patient isoflurane administration was stopped after the last recording and the ECG normalized within 20 min.
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PMID:Isoflurane and intravenous anesthesia used for induction before coronary artery bypass grafting. 278 47

Two intravenous induction techniques were compared with respect to changes in ejection fraction (EF) and central hemodynamics in 30 patients scheduled for coronary artery surgery. Left ventricular EF was measured with a collimated single crystal probe linked to a microcomputer, after injection of 200 MBq Tc 99 m HSA. Stroke volume index (SI) determined by thermodilution and EF were used to calculate left ventricular volume in end-systole and end-diastole. In 20 patients (Group I), anesthesia was induced with diazepam (94 micrograms x kg-1), thiopentone (3 mg x kg-1) and fentanyl (3 micrograms x kg-1). In 10 patients (Group II), fentanyl (30 micrograms x kg-1) was used for induction. In Group I, EF decreased from 0.43 to 0.26 at intubation, while systemic vascular resistance index (SVRI) showed an increase. Left ventricular volume decreased during induction of anesthesia except during intubation. In Group II, EF and left ventricular volume remained unchanged during the study period. SVRI showed no increase at intubation. No change in contractility was indicated from the relation between the end-systolic pressure and volume, in any of the groups.
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PMID:Changes in ejection fraction during induction of anesthesia with two different i.v. techniques. 200 7

Nineteen studies on 18 subjects were performed by single photon emission computed tomography (SPECT) of the head after the successive intravenous administration of a plasma label (99mTc-human serum albumin [HSA]) and 99mTc-labeled autologous red blood cells (RBC). Two sets of cerebral tomographic sections were generated: for cerebral 99mTc-HSA alone and for combined 99mTc-HSA and 99mTc-RBC. By relating counts in regions of interest from the cerebral tomograms to counts from blood samples obtained during each tomographic acquisition, regional cerebral haematocrit (Hct) was calculated by the application of a simple formula. Results show 1) lower cerebral Hct than venous Hct (ratio of HCT brain/Hct venous 0.65-0.90) in all subjects, and 2) comparison between right and left hemisphere Hct in 3/3 normal subjects, 6/6 patients with transient ischaemic attacks and 3/8 patients with stroke showed no significant difference. However, in 3/8 patients with stroke (most recent strokes) significant differences were found, the higher Hct value corresponding to the affected side.
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PMID:Regional brain hematocrit in stroke by single photon emission computed tomography imaging. 350 27

We measured the clearance from blood to pulmonary edema fluid of a small molecular weight hydrophilic radiotracer, Indium-111-DTPA (In-DTPA) and a larger molecular weight radiotracer, Iodine-125-HSA (I-HSA), in patients with pulmonary edema on either a cardiac or noncardiac (permeability) basis. In previous investigations, we had noted an apparent relationship between the magnitude of clearance of I-HSA across the alveolocapillary membrane and the severity of noncardiac pulmonary edema. In this study, we were able to distinguish at least 2 distinct groups of patients with noncardiac pulmonary edema. Patients with the greatest damage to the alveolo-capillary exchanging membrane, defined by the flux of I-HSA from blood to edema fluid, were significantly differentiated from those with a lesser microvascular injury on the basis of higher mean heart rate (HR), temperature, cardiac index (CI), pulmonary artery pressures, right ventricular stroke work index (RVSWI), and a lower mean total white blood cell count (WBC), among others. Therefore, noncardiac pulmonary edema is characterized by a spectrum of permeability injury to the pulmonary microvasculature which seems to parallel other measurable indices of the severity of the systemic response to the illness.
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PMID:Clinical correlates of the spectrum of lung microvascular injury in human noncardiac edema. 682 83

A cerebral vasodilatory capacity map, consisting of a 99mTc-DTPA-HSA SPECT image obtained after acetazolamide injection minus the baseline image, was produced in a patient with moyamoya disease. The map demonstrated diminished capacity in the posterior region of the right cerebral hemisphere. Subsequently, cerebral infarction occurred in the corresponding area. This observation suggests that regions of low vasodilatory capacity identified by cerebral vasodilatory capacity mapping may be at high risk of ischemic stroke.
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PMID:Cerebral vasodilatory capacity mapping using technetium-99m-DTPA-HSA SPECT and acetazolamide in moyamoya disease. 822 45

The authors examined the effect of delayed high-concentration albumin therapy on ischemic injury in a highly reproducible model of middle cerebral artery (MCA) occlusion in rats. Male Sprague-Dawley rats weighing 270 to 320 g were anesthetized with halothane and subjected to 120 minutes of temporary MCA occlusion induced by means of a poly-L-lysine-coated intraluminal nylon suture inserted retrograde via the external carotid artery into the internal carotid artery and MCA. The agent (20% human serum albumin [HSA]) or control solution (sodium chloride 0.9%) was administered intravenously at a dosage of 1% of body weight immediately after suture removal following a 2-hour period of MCA occlusion. The animals' neurological status was evaluated during MCA occlusion (at 60 minutes) and daily for 3 days thereafter. The brains were perfusion-fixed, and infarct volumes and brain edema were determined. The HSA significantly improved the neurological score compared with saline at 24 hours after MCA occlusion. The rats treated with HSA also had significantly reduced total infarct volume (by 34%) and brain edema (by 81%) compared with saline-treated rats. There was a strong correlation between hematocrit level and brain edema (p < 0.01), and between total infarct volume or brain edema and neurological score at 24, 48, and 72 hours postinjury (p < 0.0002). These results strongly support the beneficial effect of delayed albumin therapy in transient focal ischemia and indicate its possible usefulness in treating patients with acute ischemic stroke.
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PMID:Effect of delayed albumin hemodilution on infarction volume and brain edema after transient middle cerebral artery occlusion in rats. 932 48

Serum and peripheral blood leukocytes from the chimpanzees (Pan troglodytes) of the colony of the Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, NIH, were tested for the presence of STLV-I-specific antibodies and proviral DNA. Antibodies were determined by gelatin particle agglutination and Western blot (WB) assays utilizing HTLV-I antigens. Proviral DNA was detected by four PCR assays targeting three different regions of STLV-I genome: the fragments of the env and pol genes and LTR. Twenty of twenty-two DNA samples from WB-positive animals were PCR positive. None of the DNA samples from WB-negative (n = 5) and WB-indeterminate (n = 4) animals was PCR positive. The results of the nested and double nested env PCR tests were fully concordant; the seminested LTR PCR test was much less sensitive. The DNA sequences from the env (483 bp) and the pol (200 bp) genes and LTR (705 bp) were determined for six, two, and two chimpanzee STLV-I isolates, respectively. Phylogenetic analysis revealed that chimpanzee STLV-I isolates can be attributed to three clades. The first of these clades (SS-PTR1/CSA) included STLV-I isolates from the chimpanzees and West African subspecies of African green monkeys (Cercopithecus a. sabaeus). The other clades (S-PTR2 and S-PTR3) included STLV-I isolates only from chimpanzees. However, both S-PTR2 and S-PTR3 clustered together with Central African HTLV-I comprising the human/simian clade (HS-HSA/PTR). This pattern of phylogenetic clustering suggests that interspecies transmission of STLV-I occurred between chimpanzees and African green monkey subspecies as well between chimpanzees and human populations in Central Africa.
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PMID:Phylogenetic analysis of simian T-lymphotropic virus Type I (STLV-I) in common chimpanzees (Pan troglodytes): evidence for interspecies transmission of the virus between chimpanzees and humans in Central Africa. 940 May 94

Zinc (Zn) is a co-factor for a vast number of enzymes, and functions as a regulator for immune mechanism and protein synthesis. However, excessive Zn release induced in pathological situations such as stroke or transient global ischemia is toxic. Previously, we demonstrated that the interaction of Zn and copper (Cu) is involved in the pathogenesis of Alzheimer's disease and vascular dementia. Furthermore, oxidative stress has been shown to play a significant role in the pathogenesis of various metal ions induced neuronal death. Thioredoxin-Albumin fusion (HSA-Trx) is a derivative of thioredoxin (Trx), an antioxidative protein, with improved plasma retention and stability of Trx. In this study, we examined the effect of HSA-Trx on Cu2+/Zn2+-induced neurotoxicity. Firstly, HSA-Trx was found to clearly suppress Cu2+/Zn2+-induced neuronal cell death in mouse hypothalamic neuronal cells (GT1-7 cells). Moreover, HSA-Trx markedly suppressed Cu2+/Zn2+-induced ROS production and the expression of oxidative stress related genes, such as heme oxygenase-1. In contrast, HSA-Trx did not affect the intracellular levels of both Cu2+ and Zn2+ after Cu2+/Zn2+ treatment. Finally, HSA-Trx was found to significantly suppress endoplasmic reticulum (ER) stress response induced by Cu2+/Zn2+ treatment in a dose dependent manner. These results suggest that HSA-Trx counteracted Cu2+/Zn2+-induced neurotoxicity by suppressing the production of ROS via interfering the related gene expressions, in addition to the highly possible radical scavenging activity of the fusion protein. Based on these findings, HSA-Trx has great potential as a promising therapeutic agent for the treatment of refractory neurological diseases.
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PMID:Thioredoxin-albumin fusion protein prevents copper enhanced zinc-induced neurotoxicity via its antioxidative activity. 2912 8


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