Inflammatory marker changes in a 24-month dietary and physical activity randomised intervention trial in postmenopausal women.

Chronic low-grade inflammation plays a role in the pathogenesis of several chronic diseases including cancer. Physical activity (PA) and diet have been supposed to modulate inflammatory markers. We evaluated the effects of a 24-month dietary and/or PA intervention on plasma levels of pro-inflammatory cytokines, a secondary analysis in the DAMA factorial trial. The 234 study participants (healthy postmenopausal women with high breast density, 50-69 years, non smokers, no hormone therapy) were randomised to four arms: (1) isocaloric dietary intervention mainly based on plant-foods; (2) moderate-intensity PA intervention with at least 1 h/week of supervised strenuous activity; (3) both interventions; (4) general recommendations on healthy dietary and PA patterns. Interleukins (IL)-1α, -1ß, -6, tumor necrosis factor-α and C-reactive protein were measured at baseline and at the end of the intervention. Intention-to-treat-analyses were carried out using Tobit regression. Although all cytokines tended to increase over time, after 24 months women in the PA intervention (arms 2 + 3) showed lower levels of IL-1α (exp(ß) = 0.66; p = 0.04) and IL-6 (exp(ß) = 0.70; p = 0.01) in comparison with women in the control group (arms 1 + 4). No effects of the dietary intervention emerged. In healthy postmenopausal women with high breast density a moderate-intensity PA appears to slow the age-related increase of pro-inflammatory cytokines.

Targeted Neonatal Echocardiography-Guided Therapy in Vein of Galen Aneurysmal Malformation: A Report of Two Cases with a Review of Physiology and Approach to Management.

Vein of Galen malformation results in predictable changes in physiology which exist on a continuum. Severe pulmonary hypertension may present as hypoxemia; however, excessive reduction in pulmonary vascular resistance may precipitate progressive pulmonary overcirculation and impaired systemic blood flow. Right ventricular performance and the patency and direction of the ductus arteriosus may play a crucial role in postductal organ perfusion. Physiological stabilization may be complex and variable over time. The utilization of targeted neonatal echocardiography to guide treatment decisions may improve the ability to provide therapy tailored to the specific disease pathophysiology and monitor serially as conditions change. An enhanced approach to physiological stabilization may reduce the risk of unexpected decompensation and allow for thoughtful, controlled endovascular embolization in appropriate candidates.

Assessment of deep dynamic mechanical sensitivity in individuals with tension-type headache: The dynamic pressure algometry.

BACKGROUND: To explore the validity of dynamic pressure algometry for evaluating deep dynamic mechanical sensitivity by assessing its association with headache features and widespread pressure sensitivity in tension-type headache (TTH). METHODS: One hundred and eighty-eight subjects with TTH (70% women) participated. Deep dynamic sensitivity was assessed with a dynamic pressure algometry set (Aalborg University, Denmark© ) consisting of 11 different rollers including fixed levels from 500 g to 5300 g. Each roller was moved at a speed of 0.5 cm/s over a 60-mm horizontal line covering the temporalis muscle. Dynamic pain threshold (DPT-level of the first painful roller) was determined and pain intensity during DPT was rated on a numerical pain rate scale (NPRS, 0-10). Headache clinical features were collected on a headache diary. As gold standard, static pressure pain thresholds (PPT) were assessed over temporalis, C5/C6 joint, second metacarpal, and tibialis anterior muscle. RESULTS: Side-to-side consistency between DPT (r = 0.843, p < 0.001) and pain evoked (r = 0.712; p < 0.001) by dynamic algometer was observed. DPT was moderately associated with widespread PPTs (0.526 > r > 0.656, all p < 0.001). Furthermore, pain during DPT was negatively associated with widespread PPTs (-0.370 < r < -0.162, all p < 0.05). DISCUSSION: Dynamic pressure algometry was a valid tool for assessing deep dynamic mechanical sensitivity in TTH. DPT was associated with widespread pressure sensitivity independently of the frequency of headaches supporting that deep dynamic pressure sensitivity within the trigeminal area is consistent with widespread pressure sensitivity. Assessing deep static and dynamic somatic tissue pain sensitivity may provide new opportunities for differentiated diagnostics and possibly a new tool for assessing treatment effects. SIGNIFICANCE: The current study found that dynamic pressure algometry in the temporalis muscle was associated with widespread pressure pain sensitivity in individuals with tension-type headache. The association was independent of the frequency of headaches. Assessing deep static and dynamic somatic tissue pain sensitivity may provide new opportunities for differentiated diagnostics and possibly a tool for assessing treatment effects.

A fast and easy strategy for protein purification using "teabags".

Protein purification often involves affinity capture of proteins on stationary resin, alternatively proteins are captured on free flowing resin for subsequent separation from bulk fluid. Both methods require labour and time intensive separation of particulate matter from fluid. We present a method where affinity resin is contained within porous-walled containers, supporting clarification, product recovery, and concentration in a single step with minimal hands-on processing time, without significant investments in equipment.

Treatment effects of R-appliance and Fränkel-2 in Class II division 1 malocclusions.

AIM: The purpose of this study was to compare the effects of a differently designed functional appliance (the R- appliance) with Fränkel-2. STUDY DESIGN: Twenty-seven patients (16 girls and 11 boys) with a mean age of 9.8 (SD 1.6) years were treated with the R-appliance for 15.4 (SD 0.4) months and twentyseven (15 girls and 12 boys) patients with a mean age of 9.1 (SD 1.1) years were treated with a Fränkel-2 appliance for 19 (SD 5.6) months. All patients had Class II division 1 malocclusions due to mandibular deficiency and all of them had prepubertal stages of skeletal development. Lateral cephalograms obtained at the beginning (T1) and at the end (T2) of the study were analysed. RESULTS: Paired t-tests showed that SNB significantly increased in both groups. The incisor mandibular plane angle (IMPA) was reduced in the R- appliance group by 2.2 (SD 4.9) degrees (P<0.03) but increased by 2.2 (SD 2.6) degrees (P<0.001) in the Fränkel-2 group. The SNA in the R-appliance group showed an increase of 0.2 (SD 2) degrees (P<0.6), while it was decreased by 0.4 (SD 0.5) degrees (P<0.6) in the Fränkel-2 group. CONCLUSIONS: Both treatment modalities were successful in moving the mandible forward. However, with the R-appliance, this was achieved without proclination of the lower incisors.

Evaluation of long-term effects in patients treated with Fränkel-2 appliance.

AIM: To evaluate the dentoskeletal effects produced by Fränkel-2 (FR-2) appliance during the treatment of patients with Class II malocclusion by mandibular retrusion and to verify the long-term stability of these changes. MATERIALS AND METHODS: Pre-treatment, post-treatment and long-term serial cephalograms (at least 10 years after the end of treatment) of patients treated with FR-2 were compared with data obtained from untreated controls. To be included in the study, patients and controls had to exhibit Class II malocclusion caused by short mandibular body. Lateral cephalograms were analysed with a specific tracing regimen in both groups. Summary measures for the initial cephalometric values and increments of changes between visits were calculated. RESULTS: Compared to controls, the FR-2 treatment produced a significant decrease in the ANB angle that improved the skeletal intermaxillary and occlusal relationship. At long-term follow- up, the FR-2 group showed further improvements of skeletal intermaxillary and occlusal relationship, therefore the changes observed during treatment showed no compensatory decline or rebound. CONCLUSION: FR-2 treatment, in conjunction with a period of post-functional fixed appliance therapy designed to perfect the occlusion, can produce a long-lasting improvement of the skeletal Class II malocclusions with little skeletal correction and significant incisor compensation.

Effects of simvastatin treatment on sICAM-1 and sE-selectin levels in hypercholesterolemic subjects.

This study was performed to determine whether the levels of soluble intercellular adhesion molecule-1 (sICAM-l) and soluble endothelial molecule-1 (sE-selectin) were elevated in subjects with hypercholesterolemia who presented with no other risk factors or evidence of atherosclerosis. The effects of administration of an HMG-CoA reductase inhibitor on the serum levels of these molecules were also examined. Forty hypercholesterolemic subjects (HCh) (19 males and 21 females), without hypertension or cardiovascular disease, received placebo for 4 weeks. The patients were then randomized in two groups; 20 of them (simvastatin group) were treated with simvastatin (20 mg/day) and the other 20 (placebo group) continued placebo administration. After 12 and 24 weeks of either simvastatin or placebo treatment, sICAM-1 and sE-selectin levels were measured. The same parameters were measured in 20 control subjects (C) with normal cholesterol levels, matched for sex and age. HCh had sICAM-1 basal values higher than C (352.4+/-57.9 ng/ml versus 114.9+/-89.6 ng/ml; P<0.001); however, sE-selectin basal values were not different in the two groups. No correlation was observed between HCh sICAM-1 levels and cholesterol levels (total and low-density lipoprotein). Furthermore, cholesterol-lowering treatment with simvastatin did not significantly diminish sICAM-1 levels. Our findings would support the hypothesis that patients with isolated hypercholesterolemia and without clinical atherosclerosis may be silent carriers of arterial subendothelial inflammation, expressed as an increase of sICAM-1.

Detection of residual tissue viability within the infarct zone in patients with acute myocardial infarction: ultrasonic integrated backscatter analysis versus dobutamine stress echocardiography.

OBJECTIVES: The goals of this study were to analyze temporal changes in cardiac cyclic variation of integrated backscatter (CVIB) in acute myocardial infarction (AMI) and to investigate the predictive value of CVIB normalization compared with that of dobutamine stress echocardiography (DSE) in the assessment of functional recovery after revascularization. BACKGROUND: The normal CVIB is blunted by ischemia and recovers early after reperfusion, faster than wall motion improvement. Analysis of CVIB has been widely investigated for its potential to detect viable myocardium in the early stage of infarction. No studies have compared CVIB analysis with other techniques for viability assessment in patients with acute ischemic. METHODS AND RESULTS: Integrated backscatter images were obtained in 12 patients with AMI on days 1, 3, and 7 after admission and 1 month after revascularization. On day 7, DSE was performed in all patients. On admission, 22 of 144 segments were dyssynergic. On day 1, CVIB was abnormal in all 22 infarcted segments, on day 3, in 16, and on day 7, in only 10 infarcted segments. Eight of 10 segments nonviable by CVIB (CVIB-nonviable) were also nonrespondent by DSE; whereas 12 of 14 segments viable by DSE (DSE-viable) were also CVIB-viable. At follow-up, 10 CVIB-viable segments and 1 CVIB-nonviable segment showed functional recovery; whereas 10 of 14 DSE-viable segments showed functional recovery. Thus the positive predictive value of CVIB and DSE was 83% and 72%, respectively, with a diagnostic agreement between techniques in 77% of segments. CONCLUSIONS: Our data suggest that the normalization in CVIB in the first week after AMI accurately predicts residual tissue viability within the infarct zone. We also observed that the initial pattern of cyclic variation may be predictive of functional recovery. Finally, we found a good correlation between the recovery of a normal CVIB in segments that were still dysfunctional and a more validated method to assess tissue viability, such as the dobutamine test.

Effects of fluvastatin treatment on red blood cell Na+ transport systems in hypercholesterolemic subjects.

This study was performed to ascertain the effects of short-term cholesterol-lowering therapy with fluvastatin on red blood cells Na+ transport systems. Forty familial hypercholesterolemic subjects (FH; 19 men and 21 women) without hypertension or cardiovascular disease were given a placebo for 4 weeks, and then randomized in two groups. Twenty (fluvastatin group) were given fluvastatin (40 mg/day), and the other 20 (placebo group) continued placebo administration. After the placebo period and after 4 and 12 weeks of placebo or fluvastatin treatment, we measured Na+/K+ pump activity, Na+/K+ cotransport (Na+/K+ Ct), Na+/Li+ countertransport (Na+/Li+ Cnt), passive Na+ permeability (Na+PP), and internal Na+ content (Na+i). The same parameters were measured in 23 control subjects (C) with normal cholesterolemic values, who were matched for sex and age. FH had higher Na+/Li+ Cnt values than C (193.2 +/- 59.4 vs. 139.8 +/- 48.7 microM cells/h; p < 0.01), an increase in Na(+)PP (0.034 +/- 0.012/h vs. 0.018 +/- 0.004/h; p < 0.001), and higher Na(+)i (7.5 +/- 1.5 vs. 6.2 +/- 0.9 mM cells; p < 0.001). In hypercholesterolemic subjects, Na(+)i values were correlated with cholesterol (total and LDL) and apo B levels, whereas an inverse correlation was found for HDL-c and apo AI levels. Reduced total and LDL cholesterol and apo B levels after fluvastatin treatment caused a decrease in both Na(+)/Li(+) Cnt (from 186.1 +/- 60.5 to 125.1 +/- 34.0 microM cells/h; p < 0.001) and Na(+) PP (from 0.035 +/- 0.013/h to 0.02 +/- 0.016/h; p < 0.01), and an increase in Na+/K+ pump activity (from 1,549.0 +/- 507.7 to 1,894.2 +/- 536.2 microM cells/h; p < 0.04), with a significant reduction in the internal Na+ content (from 7.5 +/- 1.6 to 5.8 +/- 2.4 mM cells; p < 0.001). Our findings show that hypercholesterolemia affects red blood cell Na+ transport systems, with an increase in Na+/Li+Cnt, Na+PP, and the internal Na+ content. Cholesterol-lowering treatment with fluvastatin influences Na+ transport systems and reduces the internal Na+ content. This might also be responsible for the greater vascular reactivity observed in hypercholesterolemic patients, and its amelioration after a reduction in cholesterol levels.

[Elevated levels of lipoprotein(a) are present in subjects with early ischemic cardiopathy and with a familial history of ischemic cardiopathy]. / Più elevati livelli di lipoproteina(a) sono presenti in soggetti con cardiopatia ischemica precoce e con storia familiare di cardiopatia ischemica.

BACKGROUND: Elevated levels of lipoprotein(a) are associated with a greater risk of atherothrombotic cardiovascular diseases. Since the Lp(a) levels are genetically determined and fairly stable in the course of life and a family history appears to be an independent risk factor of cardiovascular diseases, we evaluated the behavior of Lp(a) levels in patients with early events of coronary heart disease (CHD) and also in subjects with positive family history of ischemic heart diseases. METHODS: The levels of lipoprotein (a) [Lp(a)] were measured in 254 subjects, 138 males and 116 females with an average age of 48.6 +/- 13.8 years (range 20-76 years). Diabetic subjects, females submitted to oestrogen treatment and those already in treatment with hypolipidaemic drugs were excluded from the study. Forty of the 254 patients (15.7%), 27 males and 13 females, had CHD (29 a previous myocardial infarction and 11 a stable angina). A positive family history for CHD was considered present (102 of the 254 patients) if one or more first degree relatives had angina or myocardial infarction before the age of 60 years in men and 65 in women. RESULTS: The levels of Lp(a) were higher (p < 0.01) in women (25.1 +/- 28.3 mg/dl) compared to men (17.6 +/- 18.4 mg/dl), without differences in relation to age. The Lp(a) plasmatic levels were not correlated with age, body mass index, total cholesterol, LDL and HDL, triglycerides, apo B, apo AI, fibrinogen and there were no differences in Lp(a) levels in presence or absence of other known cardiovascular risk factors such as hypertension and smoking. The Lp(a) levels were not different between subjects with CHD (28.15 +/- 31.7 mg/dl) and controls (20.3 +/- 22.8 mg/dl). The subjects with CHD were older and had higher levels of fibrinogen and a significantly greater prevalence of hypertension and family history of CHD. Fifteen of the 40 subjects with CHD had an early onset of CHD (before 50 years of age) and only in such patients the Lp(a) levels were significantly greater compared to controls (35.8 +/- 33.2 mg/dl vs 20.3 +/- 22.8 of the controls, p < 0.01), independently of other variables (age, BMI, smoking, hypertension, cholesterol, triglycerides, HDL-c, LDL-c, fibrinogen). Furthermore the Lp(a) plasmatic levels were higher in subjects with a family history of CHD (28.3 +/- 27.6 mg/dl vs 16.3 +/- 18.6 mg/dl of the subjects without a family history of CHD, p < 0.01) even if they had or not had a previous coronary ischemic event. CONCLUSIONS: Such data confirm the importance of high levels of Lp(a) above all for the early events of CHD and for the subjects with a family history of CHD, which could be expression of a greater predisposition for cardiovascular events.

Effects of picotamide on release of endothelin-1, thromboxane and prostacycline after treadmill stress in patients with peripheral artery disease.

To assess the effects of picotamide, an antithromboxane receptor and antithromboxane synthase drug, on vascular function and endothelin-1 release, 20 patients with peripheral arterial disease, without hypertension or diabetes mellitus, receiving placebo and picotamide (900 mg/day) were studied. The modifications of vascular parameters were evaluated by arterial distensibility index and postischemic hyperemia test (postischemic perfusion index and recovery time). Endothelin-1, prostacycline, and thromboxane B2 were determined under resting conditions and after treadmill test. Picotamide treatment caused a decrease of resting thromboxane B2 and endothelin-1 concentrations, produced an improvement of the vascular function as seen by the increase of vascular parameters reported, and attenuated the ischemic treadmill-induced increase of thromboxane B2, but not of endothelin-1. These data confirm that the picotamide improved vascular flow by the reduction of thromboxane-mediated effects, reduced resting endothelin-1 levels, but did not attenuate endothelin-1 concentrations induced by the treadmill stress.

The complex relation between myocardial viability and functional recovery in chronic left ventricular dysfunction.

Preserved myocardial viability and recurrent symptomatic ischemia are the most widely accepted criteria indicating that coronary revascularization should take place in patients with postischemic left ventricular dysfunction. However, the presence of viable myocardium within the infarct zone does not necessarily imply recovery of function after coronary revascularization. The complex relation between the extent of transmural necrosis and the degree of residual perfusion within the infarct area plays an important role. However, independently of functional recovery, cell viability may have important clinical implications, since it may improve long-term prognosis by attenuating left ventricular remodeling processes. Several different methods are used to detect hibernating myocardium. Mounting evidence suggests that thallium-201 scintigraphy is most sensitive in identifying tissue viability, whereas dobutamine echocardiography is most specific in predicting functional recovery after revascularization. In between, myocardial contrast echocardiography is the only technique able to evaluate the microvascular integrity that is a condition sine qua non for both cell viability and later functional recovery. Combined information derived from these 3 different approaches might be considered as the best way to understand how the combination of contractile, viable but noncontractile, and dead tissue affect resultant function and prognosis.

Erythrocyte passive potassium flux is increased in patients with ischemic coronary disease (ICD) and in subjects with family history of ICD.

BACKGROUND: It has been proposed that ischemic coronary disease (ICD) associated potassium loss could be due to modifications of potassium permeability. We investigated whether a positive family history of ICD can influence this parameter. We have compared potassium permeability in erythrocytes from ICD patients and from positive family history subjects (FICD) with control subjects. METHODS: All patients and subjects were carefully selected for the absence of hypertension and dysmetabolic pathologies. ICD group: 24 patients (19 males, 5 females; ages 43 to 69) all affected by ischemic coronary disease, under no drug treatment; FICD group: 18 subjects (all males, ages 27 to 42) with a verified positive ICD family history, without hypertensive family history and cardiovascular pathology; control group: 16 subjects (11 males, 5 females; ages 28 to 48) without positive family history of ICD. Passive potassium efflux (PPE) was spectrophotometrically measured in K-free medium containing ouabain and bumetanide. The kinetic constant was calculated by dividing PPE by the erythrocyte potassium concentration. RESULTS: No statistically significant differences were noted between the intracellular potassium content of the three groups. However, (1) the passive potassium permeability of the ICD group was significantly higher (kK=0.055 +/- 0.021 h(-1), n=24) than that of the control group (kK=0.023 +/- 0.008 h(-1), n= 16; p<0.00001), (2) the FICD group was higher (kK=0.036 +/- 0.012 h(-1), n=18) than the control group (p<0.001), and (3) the ICD group was higher than the FICD group (p<0.001). CONCLUSIONS: Our results suggest an inheritability of ICD, paralleling the familial aggregation of the pathology. Erythrocyte potassium permeability could represent an early marker of ischemic coronary disease and be used as a prophylactic tool.

[Effects of adrenergic stimulation on transmembrane transport of Na+ in patients with essential hypertension]. / Effetti della stimolazione adrenergica sui sistemi di trasporto transmembrana del Na+ in pazienti con ipertensione essenziale.

BACKGROUND: It has been studied whether an adrenergic stimulation induced by the cold pressor test (CPT) could influence the behaviour of the transmembrane transport systems of sodium in hypertensive subjects compared to a normotensive control population. MATERIALS AND METHODS: Twenty-two hypertensive subjects (average age 43.2 +/- 5.7 years), with normal weight, without signs of cardiovascular and metabolic diseases, underwent the cold pressor test. The dynamic behaviour of sodium erythrocytic transport systems and plasmatic norepinephrine was evaluated basally, at the third minute during the cold pressor test and 20 minutes after the end of the test. The same test was carried out in a control population made up of 20 normotensive subjects (average age 41.9 +/- 4.8 years), selected on the basis of the absence of any cardiovascular or metabolic pathology and without family history of arterial hypertension. RESULTS: The cold pressor test did not cause significant changes in the sodium transmembrane transport systems in normotensive subjects, while in the hypertensive subjects a significant reduction was observed, during the test, in the total efflux of sodium and in the sodium/potassium pump, respectively from 2636 +/- 296 mumol/l/red blood cells/hr to 2032 +/- 178 mumol/l/red blood cells/hr (p < 0.0001) and from 2156 +/- 149 mumol/l/red blood cells/hr to 1610 +/- 101 mumol/l/red blood cells/hr (p < 0.0001); the intraerythrocytic sodium increased from 6.5 +/- 1.0 mmol/l/cells to 7.2 +/- 1.1 mmol/l/cells (p < 0.04) and the passive permeability decreased from 0.039 +/- 0.004 hr-1 to 0.018 +/- 0.006 hr-1 (p < 0.0001). During cold pressor test the increase in the plasma norepinephrine levels was correlated to the reduction in the total efflux of sodium (r = -0.60; p < 0.003) and in the sodium/potassium pump (r = -0.59; p < 0.003) only in hypertensive subjects. CONCLUSIONS: Our data show that an adrenergic stimulation, induced by the cold pressor test, is able to significantly influence the behaviour of transmembrane fluxes of sodium in hypertensive subjects, and it causes an inhibitory effect on the sodium/potassium pump and an increase in the intraerythrocytic sodium. Such data show the existence in hypertensive subjects of an interrelationship between adrenergic activity and sodium transport systems that could cooperate in causing and/or in maintaining the hypertensive syndrome.

[Effect of beta blockade on the erythrocyte transport of Na+: evaluation during stimulation by cold pressure test in patients with essential hypertension]. / Effetti del beta-blocco sui sistemi di trasporto eritrocitario del Na+: valutazione durante stimolo con cold pressor test in pazienti con ipertensione essenziale.

Several studies have shown in essential hypertension alterations of the transmembrane red blood cells sodium fluxes, as an involvement, especially in the early phases, also of the adrenergic system. In this study we evaluated the behaviour of red blood cells fluxes of sodium before, during and after the cold pressor test, a method used also to evoke an adrenergic stimulation, in twenty hypertensive subjects, 14 males and 6 females, with an average age of 43.2 +/- 5.7 years, with normal weight and without cardiovascular complications and metabolic diseases. The behaviour of the Na+ total efflux (Na+ TE), of the Na+/K+ pump, of the Na+K+ cotransport (Na+/K+ CT), of the Na+/Li+ counter transport (Na+/Li+ Cnt), of the Na+ passive permeability (Na+ PP), of the intracellular Na+ (I Na+) and of the plasmatic noradrenaline (NE) was evaluated basally, at the third minute during cold pressor test (CPT) and 20 minutes after the end of the test. The test, which the same method, was repeated after a 30 day treatment with propranolol at the dose of 240 mg/day in three daily administrations. The beta-blockade caused, besides the reduction of both the systolic and diastolic pressure values, a significant increase in the Na+/K+ CT (from 248 +/- 41 to 314 +/- 71 mmol/l/cells/h, p < 0.001) and a decrease in the Na+ PP (from 0.039 +/- 0.004 to 0.023 +/- 0.007 hr-1, p < 0.00001), probably directed towards the reduction of the accumulation of intracellular Na+, that could compete, among the other mechanisms, with the anti-hypertensive action of the beta-blockers. The CPT caused, before the beta-blockade, a significant depression of the Na+/K+ pump (from 2057 +/- 149 to 1610 +/- 101 mmol/l/cells/h, p < 0.00001) and of the Na+ TE (from 2640 +/- 397 to 2032 +/- 179 mmol/l/cells/h, p < 0.00001) inversely correlated to the levels of NE (r = -0.60, p < 0.003), with a consequent increase in I Na+ (from 6.2 +/- 0.6 to 7.5 +/- 1.5 mmol/l/cells, p < 0.001), showing how the adrenergic activation in hypertensive subjects is able to interfere with the systems of transmembrane transport with an inhibitory attitude, that is expressed by an increase in the levels of I Na+. The beta-blockade was able to outweigh the depression of the Na+/K+ pump (from 1843 +/- 584 to 1728 +/- 640 mmol/l/cells/h, p: ns) and the reduction of the Na+ TE, preventing the accumulation of I Na+ (from 6.3 +/- 1.6 to 6.6 +/- 1.3 mmol/l/cells, p: ns). Such data show an increased susceptibility of the Na+ transport systems to the adrenergic stimuli in hypertensive subjects with a tendency to favor the accumulation of I Na+ and that the beta-blockade is able to antagonize the effects, with a maintenance of the intracellular levels of Na+.

[Transmembrane sodium transport systems in various forms of hyperlipoproteinemia]. / Sistemi di trasporto transmembrana del Na+ in forme diverse di iperlipoproteinemia.

The possible interrelationships between the erythrocytic transport systems of Na+ (Na+/K+ pump, Na+/K+ cotransport, Na+/Li+ countertransport, Na+ passive permeability) and the plasmatic lipids (cholesterol, triglycerides, HDL, LDL, apoprotein A1, apoprotein B) were studied in 42 normotensive subjects with different forms of hyperlipoproteinaemia and with a negative familiarity for arterial hypertension. In subjects with hypercholesterolaemia (hyperlipoproteinaemia II A and II B) an elevated activity of the Na+/K+ pump was noticed, while in subjects with hypertriglyceridaemia (type IV) an increase in Na+ passive permeability and Na+/Li+ countertransport with a lower level of intraerythrocytic Na+ was shown. A negative correlation was observed between the total efflux of Na+ and Na+/K+ pump and the levels of cholesterol (r = -0.43, p < 0.04 and r = -0.41, p < 0.05) and the apoprotein B/A ratio (r = 0.42, p < 0.05 and r = -0.50, p < 0.01). A negative correlation was also noticed between the Na+/K+ pump and the levels of apoprotein B (r = -0.41, p < 0.05). The Na+/K+ cotransport appeared inversely correlated with the levels of HDL cholesterol (r = -0.42, p < 0.05), while the Na+ passive permeability was negatively correlated with the levels of LDL (r = -0.43, p < 0.04) and positively correlated with the plasmatic triglycerides (r = +0.54, p < 0.01). Such data show that the plasmatic lipids can influence the systems of transmembrane ionic transport of Na+ and play an important role also this way, in cardiovascular pathology.

Effects of cloricromene on the levels of endothelin and on the microcirculatory function in peripheral atherosclerotic arteriopathies.

The effects of cloricromene on plasma endothelin-1 (ET-1) levels and on microcirculatory function in 9 patients with peripheral atherosclerotic arteriopathy (PAA) and in healthy control subjects were studied. ET-1 levels and microcirculatory function were evaluated both under basal conditions and 30, 60, and 90 min after acute administration of cloricromene (30 mg i.v.). PAA patients had significantly increased levels of ET-1 and impaired vascular parameters (studied by means of Winsor's Index, Gosling's Index, postischemic perfusion index and recovery time) when compared to control subjects. The acute administration of cloricromene (30 mg i.v.) did not change plasma ET-1 both in control subjects and in patients with PAA. In contrast, cloricromene produced a significant improvement in the postischemic perfusion index and in recovery time in arteriopathic patients. Control subjects and patients with PAA also underwent a cold pressor test (CPT) under basal conditions and (72 h later) 30 min after an acute intravenous administration of cloricromene (30 mg i.v.). CPT caused a higher increase in ET-1 in the patients with PAA compared to the control group, and a reduction in the vascular flow at the femoral level, while the pretreatment with cloricromene prevented both the increase in the levels of ET-1 and the reduction of the femoral vascular flow observed after the cold stimulus in patients with PAA. Our data show that cloricromene, besides ameliorating the microcirculatory function, is able to interfere with dynamic mechanisms, such as those induced by the CPT, capable of stimulating the release of ET-1 at the vascular level.

Clinical study of the effects of latissimus dorsi muscle flap stimulation after cardiomyoplasty.

BACKGROUND: Beneficial hemodynamic effects after dynamic cardiomyoplasty have been inconsistently demonstrated, and the effects seen may be due to the wrap itself, to flap stimulation, or both. The aim of this study was to determine whether flap stimulation per se acts as a systolic active process after cardiomyoplasty. METHODS AND RESULTS: Catheterizations were performed in 13 patients 14.4 +/- 7 months after cardiomyoplasty. New York Heart Association functional class decreased from 3.3 to 2.1 after the procedure (P = .0005). Hemodynamic evaluations were first performed with the stimulator on in the 2:1 mode and then after the stimulator had been off for at least 24 hours. Left ventricular (LV) ejection fraction increased from 25.1 +/- 6% before surgery to 28.2 +/- 6.7% with the stimulator on after cardiomyoplasty (P = .04). When stimulation was stopped, there was no change (P > .05) in indexes of systolic or diastolic LV function (peak systolic LV pressure, LV ejection fraction, peak positive dP/dt, peak negative dP/dt, or tau). Pulmonary capillary wedge pressure and cardiac index were unchanged when stimulated and nonstimulated settings were compared (P > .05). However, a remarkable heterogeneity of individual responses was observed. Ejection fraction and cardiac index decreased with the stimulator off in 3 patients, but peak positive dP/dt decreased in 6 patients; diastolic function deteriorated in 2 patients, but a slight improvement was noted in 3 patients. Cardiothoracic ratio, echocardiographic LV end-diastolic dimension, and fractional shortening remained unchanged between immediate (< 1 month) and long-term (36.7 +/- 25.9 months) postoperative evaluations. CONCLUSIONS: In the majority of our patients, there was no short-term hemodynamic benefit of flap stimulation; therefore, we conclude that the efficacy of cardiomyoplasty may be a consequence of a passive "girdling effect," which limits the progression of ventricular enlargement and further deterioration of ejection fraction.

[Struma cordis: right intraventricular ectopic thyroid]. / Struma cordis: Thyroïde ectopique intraventriculaire droite.

The authors report the case of a benign tumour composed of hyperplasic thyroid tissue in the right ventricle, diagnosed in a 43 year old woman by echocardiography after a syncopal episode. The outcome was favourable with a 13 year follow-up after surgery.