1,720,972 research outputs found
[Nifedipine and essential arterial hypertension refractory to hypotensive therapy: results of a preliminary double-blind study]
No full text[Electrocardiographic changes in myocardial damage; effect of treatment with nifedipine]
No full textEffect of changes of posture, beta-blocking agents and the cold pressure test on the levels of plasma renin activity (PRA) in essential hypertension with low serum renin
No full textPlasma renin activity in hypertensive patients under basal conditions and in various postures: preliminary data
No full textWe have studied PRA levels in 10 healthy subjects compared with 10 patients affected with essential hypertension (with low PRA) on venous blood samples collected after 8 hours of rest and after 15-20 minutes of slow plain walk. Contemporarely we have taken up arterious pression levels in each class of subjects of these studies. No significant differences of PRA are demonstrable in healthy subjects and in patients affected with essential hypertension. Postural changes in hypertension produces significant rise of PRA, not related to arterial pressure
Chronic venous insufficiency, edema and the permeability of the microvascular barrier
No full textMany hypotheses have been proposed to explain the clinical features and laboratory findings during chronic venous insufficiency (CVI). Edema is known to occur primarily as a result of the increase in venous pressure, accompanied by increased capillary permeability (PerM) and decreased blood colloid osmotic pressure as contributing factors. Nevertheless, there are many clinical and experimental observations which are not consistent with this accepted suggestion. Therefore, the diagnosis of edema is formulated, when edema has already occurred, i.e. only when the collection of the fluid exceeds a certain threshold and becomes clinically or instrumentally evident. The aim of this review was to clarify the pathophysiology of venous edema studying two fundamental processes: filtration and absorption that oversee the balance of intra- and extracellular fluids. In particular, we have described the alterations between filtration and absorption. The mechanisms involved in the CVI are several, starting from the structural rearrangement of the vascular endothelium up to the changes in intra and extracellular fluid. Evaluating the previous studies, we hypothesize that the venous edema is produced by the hydrostatic pressure prevailing on blood oncotic pressure, while the "intermediary" system or transduction system must be able to transform the physical stimulus induced by hypertension in a biochemical message promoting the cellular responses. Moreover, the chronic increase in shear stress, characteristic in CVI, prevails on calcium dependent mechanism, resulting in either hypertension, a mechanical stress, abolishes the Ca++ linked mechanism inducing a stable disassembly of adherens junction, or in the long run, the same mechanisms are unable to preserve the barrier integrity with a profound alteration of the vessel wall PerM, accompanied by leakage of macromolecules and blood cells. In conclusion, it is possible to assume that the essential sign in the venous chronic insufficiencies is not the edema, and then an excess of filtration, but the vessel wall permeation is the key factor to clarify the pathophysiological cascade and the clinical signs
[Evaluation by the Minnesota Code of the electrocardiographic changes in patients over 70]
No full textOxoprenolol and plasmatic renin activity in essential hypertension: preliminary data
No full textWe have studied PRA levels in 10 healthy subjects compared with 10 patients affected with essential hypertension (with low PRA) on venous blood samples collected after 8 hours of rest and after 15-20 minutes of slow plain walk and 15 minutes after intravenous administration of oxoprenolol (mg 2). Contemporarely we have taken up arterious pression levels in each class of subjects of these studies. Postural changes produces significant rise of PRA in subjects affected with essential hypertension, that is significantly inhibited by pharmacologic interference produced by beta-blocking agents. This occurrence is independent of arterial pressure changes
Transcutaneous oxygen pressure in systemic sclerosis: evaluation at different sensor temperatures and relationship to skin perfusion
No full textTranscutaneous oxygen pressure (TcPO2) and skin blood flow (as evaluated by laser doppler) (LD) were investigated in 24 systemic sclerosis (SSc) patients in sclerotic skin (dorsal aspect of the hand) and non-sclerotic skin (interscapular region) and in 24 controls matched for sex and age for the same sites. The two parameters were evaluated at 44 degrees C (temperature of the two sensors) in 13 patients and 13 controls, and at 36-37 degrees C in the remaining 11. At 44 degrees C, TcPO2 was lower in SSc patients than in controls for both sclerotic and non-sclerotic skin. At 37 degrees C there was no significant difference. At 44 degrees C, LD values were decreased in patients with respect to controls for both sclerotic and and non-sclerotic skin. In contrast, at 37 degrees C the values were increased in patients only for the sclerotic skin. It can be hypothesized that the increased LD values at physiological temperature are at least in part balancing a decreased tissue oxygen tension, then a normal TcPO2 is ensured. On the other hand, the decreased LD values at 44 degrees C, when TcPO2 is also decreased, indicates that there is an inability of SSc vessels to significantly increase their flow under the stimulus of a maximal hyperaemia-inducing temperature
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