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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Echocardiographic and systolic time intervals changes found after hemodyalisis in 16 patients with chronic renal failure are analysed and discussed. Echocardiogram shows: significant (p less than 0.05), no change statistically significant of end-systolic diameter, fractional shortening, mean velocity of circumferential shortening (VcF), and amplitude of septal motion. Systolic time intervals show: significant reduction (p less than 0.001) of total electromechanical systole (SEM), mechanical systole (SM) and left ventricular ejection time (LVET), and increase (p less than 0.05) of pre-ejection period (PEP) and the ratio PEP/LVET (p less than 0.005). The reason of these changes is the post-dialytic fluid's loss (2140 +/- 760 g) followed by left ventricular end-diastolic diameter and volume reduction which decreases stoke volume and LVET (according to Frank-Starling's law). It has not been possible to draw concordant and definitive conclusions on the post-dialytic left ventricular function. PEP lengthening would give evident for myocardial involvement (but pre-load and after-load changes modifies it), while the other data are slightly affected (VcF, fractional shortening, and amplitude of septal motion) or improved (amplitude and peak velocity of posterior wall motion).
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PMID:[The left ventricle in chronic renal failure patients. Ecocardiographic and poligraphic study before and after hemodialysis (author's transl)]. 16 34

Previous studies of the effect of angiotensin on myocardial contractility have yielded conflicting results. Possible reasons for the observed disparities include differences in techniques for measuring contractility, in species (dog, cat, and man), in myocardial state (normal or diseased), in preparation observed (heart-lung, isolated heart, papillary muscle, atrial myocardium, intact heart), and in dosage schedule. Moreover, there are no reported studies in the intact human heart, normal or diseased, in which contractility measurements are based on velocity-force relations. To resolve the conflict, left ventricular myocardial contractility was measured using the same expressions for the force-velocity relationship in all subjects. Studies were performed in five normal human subjects, six patients with cardiomyopathy, eight normal mongrel dogs, and six dogs with ischemic myocardial scarring, before and during angiotensin infusions in dosages producing 15--20-mm Hg increases of aortic diastolic pressure. Contractile element velocity at peak, dP/dt (Vce) and the Frank-Levinson contractility index (CyIx), which normalizes Vce for diastolic fiber length, decreased during angiotensin infusion in all groups. The mean decreases (11 to 19) per cent in Vce, 15 to 23 per cent in CyIx, SEM's 4-5 per cent) were significant (P values ranging from smaller than 0.05 to smaller 0.005) in the normal hearts of dogs and man and in the scarred canine hearts, in which preangiotensin Vce and CyIx were normal. In the cardiomyopathy group, in which contractility was depressed before angiotensin, the drug elicited a further decrease in Vce (mean fall 17 plus or minus 7 per cent, P smaller than 0.1) and CyIx (26 plus or minus 8 per cent, P smaller than 0.02). We conclude that, in the intact organism, with a normal myocardium or a diffuse or segmental myocardial disease, the administration of angiotensin results in a depression of contractility.
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PMID:The effect of angiotensin on myocardial contractility. 23 32

Relationship has been established between epicardial ST-segment elevation, considered a reliable estimate of ischemic injury in experimental myocardial damage, and ST changes by multiple-lead precordial electrocardiography. However, 35-lead precordial mapping is time-consuming and suitable only for anterior infarctions. An alternate, more rapid method for recording ST segments is an external 3-lead orthogonal vectorcardiographic (VCG) system which also can assess the entire ventricle. Accordingly, validity of VCG ST magnitude was evaluated by direct comparison with changes in epicardial ST magnitude (EST) induced by occlusion of major coronary arteries, reperfusion, and pharmacologic interventions in 15 closed-chest dogs. A total of 404 data points (average 27/dog), 20 epicardial grid and 3 Frank XYZ leds each, demonstrated close correlation (least squares linear regression) between VCG ST and EST changes (r = 0.921 +/- 0.02 SEM). These data document the accuracy of precordial VCG ST in noninvasive assessment of ischemic injury in various areas of myocardium and its practicality for clinical application.
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PMID:Evaluation of precordial orthogonal vectorcardiographic lead ST-segment magnitude in the assessment of myocardial ischemic injury. 84 31

In patients with isolated pulmonary valve stenosis, the right ventricular (RV) hypertrophy is related to the hemodynamic severity of their lesions. We estimated the peak RV pressure noninvasively in 112 patients with isolated pulmonary valve stenosis by a Frank lead vectorcardiogram (VCG), an orthogonal electrocardiogram (ECG), and a standard scalar ECG. In 78 randomly assigned patients, 10 ECG measurements and 13 VCG measurements were correlated with the peak RV pressure at cardiac catheterization; the best multiple linear regression equation used the R wave in standard lead 1 (ECG), maximal rightward voltage in the terminal part of the frontal vector loop (VCG), and the Q wave in the orthogonal Z lead, giving R = 0.66 (SEM 25). The equation was validated in the other 34 patients; correlation of estimated with actual peak RV pressure was r = 0.64. A nomogram for clinical use was devised from this regression equation.
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PMID:A simple method for ECG and VCG assessment of the severity of pulmonary valve stenosis. 90 52

111In-labelled platelets were used for analysing platelet dynamics in 43 patients with idiopathic thrombocytopenic purpura (ITP). The detected time-activity curves, recorded with a gamma camera, were analysed by three methods: two- and three-compartment models, and an open model in which only the splenic curve was analysed. In the two-compartment model the mean rate constant from blood to spleen was 0.328 +/- 0.028 min-1 (mean +/- SEM) and from spleen to blood 0.061 +/- 0.007 min-1, whereas in the three-compartment model the corresponding values were 0.236 +/- 0.020 and 0.044 +/- 0.007 min-1, respectively. The mean rate constant from blood to liver was 0.466 +/- 0.149 min-1 and from liver to blood 0.341 +/- 0.106 min-1 as derived from the three-compartment model. The rate constant from spleen to blood, as determined from the three-compartment model, was significantly higher in patients with a strongly positive result for platelet-associated auto-antibodies (platelet suspension immunofluorescence test (PSIFT] than in patients with a negative PSIFT. The mean hepatic net rate in patients with a high level of antibodies is into the liver, while in patients with little or no antibodies the net rate is into the blood pool. The mean half-life for the fast component of the inverted splenic curve was 2.5 +/- 0.2 min and for the slow component 16 +/- 2 min. In patients with a strongly positive PSIFT the half-life for the slow component was significantly longer than in patients with a negative PSIFT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Compartmental analysis of short-lived platelet dynamics. 224 74

Although immune mechanisms are known to be partially responsible for the thrombocytopenia of patients infected with HIV-1, an understanding of the mechanism underlying this disorder is incomplete. A casual observation that bone marrow biopsies of HIV-infected individuals seem to exhibit an unusually large number of denuded megakaryocyte nuclei (DN-MK) prompted a study comparing MK of 20 HIV-seropositive individuals with those of 10 patients with HIV-negative idiopathic thrombocytopenic purpura and 10 hematologically normal subjects. In normal marrows the number of DN-MK average 2.1 +/- 0.5 SE per 10 low power field. In patients with ITP the average number was 6.5 +/- 1.4 SEM, whereas HIV-ITP marrows had an average of 42.5 +/- 3.7 SEM. Electron microscopy of AIDS megakaryocytes exhibited ballooning of the peripheral zone to an extent not seen by us in any other myelodysplastic syndromes. These observations support the concept that the pathophysiology affecting MK/platelets in HIV-infection should not be equated with the destructive process underlying other immune thrombocytopenias.
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PMID:Structural changes in the megakaryocytes of patients infected with the human immune deficiency virus (HIV-1). 275 19

In the stage 24 chick embryo, a paced increase in heart rate reduces stroke volume, presumably by rate-dependent decrease in passive filling. We hypothesized that rate-dependent stroke volume reduction could be abolished by volume loading. Dorsal aortic blood velocity was measured with a 20 mHz pulsed-Doppler meter from a 0.75-mm piezoelectric crystal (eight embryos), and atri-oventricular velocity was simultaneously measured from the ventricular apex (six embryos). Sinus venosus pacing (stimuli of 1 ms duration and less than 4 mA) was performed at intrinsic rate (P:I) and at 150% of intrinsic rate (P:150%I). Volume loading was performed during P:150%I by intravenous injection of 7.5 microL of chick Ringer's solution. Using atrioventricular velocity profile, stroke volume was divided into the proportion due to passive (E-phase) and active (A-phase) filling. Stroke volume was compared during P:I, P:150%I, immediately (P:150%I') and 30 s after (P:150%I") volume loading. Data (mean +/- SEM) were compared by ANOVA. During pacing, stroke volume (mm2/cycle) decreased but increased after volume loading (I, 0.43 +/- 0.03; P:I, 0.37 +/- 0.03; P:150%I, 0.19 +/- 0.03; P:150%I', 0.24 +/- 0.05; P:150%I", 0.28 +/- 0.04 (p less than 0.005). During P:150%I, E-phase filing disappeared and was not restored by volume loading, whereas, A-phase filling diminished but was restored by volume loading. In stage 24 chick embryos, rate-dependent stroke volume decrease is reversed by volume loading that restores stroke volume due to an increase in active filling but not passive filling. Thus, even at rapid heart rate, the embryonic ventricle responds to volume loading, indicating that the Frank-Starling relationship functions during tachycardia in the embryonic heart.
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PMID:Effect of heart rate increase on dorsal aortic flow before and after volume loading in the stage 24 chick embryo. 281 94

To assess the time-course of adaptive responses of the left ventricle to chronic volume overload, dogs were instrumented with a left ventricular (LV) micromanometer and pairs of ultrasonic crystals for the measurement of LV wall thickness (WTh), LV chamber diameter (D), and longitudinal segment length (L). Following a control study, mitral regurgitation (MR) was created by a transventricular section of the chordae tendineae. Heart rate was controlled during each study by atrial pacing. Plasma norepinephrine levels at rest were determined by high-performance liquid chromatography. Eight days (mean) after the onset of MR, enddiastolic (ED) D had increased by 9% from 34.2 +/- 2.4 mm (SEM) (P less than 0.001), with significant thinning of the wall thickness (from 8.2 to 7.7 mm, P less than 0.001). Consequently the calculated cross-sectional area (CSA) of the left ventricular wall remained the same. Peak wall stress (WSt) and EDWSt increased by 20% and 152%, respectively. During the subsequent 4 weeks, EDD progressively increased, averaging 11% above the control at 4 weeks, while EDWTh returned to the control level. Thus, the development of hypertrophy was clearly evidenced by an increase in CSA (by 8% over the control, P less than 0.001). These changes were accompanied by a consistent reduction in both peak WSt and EDWSt. Mean velocity of circumferential fiber shortening (meanVcf) and percentage shortening were significantly augmented following the onset of MR and remained at the same level thereafter, indicating no further use of the Frank-Starling mechanisms during chronic ventricular dilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adaptations of the left ventricle to chronic volume overload induced by mitral regurgitation in conscious dogs. 293 15

Immunoglobulins (Igs) and serum albumin were eluted from normal platelets and platelets from patients with idiopathic thrombocytopenic purpura (ITP) with a quantitative acid elution procedure followed by solid-phase radioimmunoassay (SPRIA). Acid elution was shown to release a reproducible fraction of platelet-associated Igs, and the amounts released per platelet were independent of the platelet concentration over a wide range of concentrations. This procedure is suitable for sensitive, reproducible, and specific quantitation of large numbers of samples. Washed platelets from 13 normal donors contained the following components (expressed in femtograms per platelet, mean +/- 2 SEM): IgG, 1.40 +/- 0.26; IgA, 0.72 +/- 0.36; IgM 0.078 +/- 0.036; albumin 7.7 +/- 1.5. Immunoglobulins and albumin eluted from the platelets of ten ITP patients (two in remission), expressed as femtograms per platelet, mean (range), were: IgG 104 (0.3 to 750); IgA 90 (0.9 to 715); IgM 162 (1.2 to 1,300); and albumin 34 (6.8 to 199). All platelet-associated Igs from thrombocytopenic ITP patients were found to be elevated twofold to 2,300-fold with one Ig class occasionally elevated 50-fold to 100-fold higher than the others. A similar group of ten thrombocytopenic ITP patients was found to have twofold to 26-fold elevations of platelet-associated albumin. This demonstration of increases in multiple classes of Igs as well as serum albumin associated with platelets from ITP patients suggests that some nonimmune process may be contributing to the phenomenon of increased platelet-associated proteins in ITP.
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PMID:Evaluation by quantitative acid elution and radioimmunoassay of multiple classes of immunoglobulins and serum albumin associated with platelets in idiopathic thrombocytopenic purpura. 395 31

A cell-free system prepared from rat liver containing cytosol and mitochondria as well as a number of cofactors at near physiological concentrations was shown to form glucose 6-phosphate from malate + 3-phosphoglycerate at a rate of 1.11 +/- 0.09 mumol . min-1 . g liver-1 (mean +/- SEM, n = 9, 30 degrees C). At least 70% of glucose 6-phosphate formed was derived from malate as calculated from experiments with [U-14C]malate. The indicated rates were measured between 10 min and 30 min incubation time when the system was near steady state with respect to the lactate/pyruvate ratio and to most of the gluconeogenic intermediates. In the absence of mitochondria, the rate of formation of glucose 6-phosphate from malate was about seven times lower than in their presence. A comparison between incubations carried out in presence or absence of mitochondria revealed that mitochondria decreased the lactate/pyruvate ratio and increased the ratio of (ATP + ITP)/(ADP + IDP). It could be shown that under the present incubation conditions, formation of glucose 6-phosphate was closely linked to the ratio of (ATP + ITP)/(ADP + IDP) whereas changing redox ratios had little influence on the gluconeogenic rate.
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PMID:Gluconeogenesis in vitro. Formation of glucose 6-phosphate from malate by a cell-free rat-liver system consisting of cytosol and mitochondria. 710 24


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