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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clinical reports have suggested that therapy with fresh frozen plasma is a useful adjunct in the management of the hemolytic-uremic syndrome (HUS). We reviewed the charts of 36 children with severe HUS who were treated at the Izaac Walton Killam Hospital for Children, Halifax, over 10 years to assess the effectiveness of plasma therapy. All children who required specific supportive therapy for renal dysfunction, hemolysis or serious extrarenal complications were included. We compared the outcome of 18 children who received plasma therapy from 1982 to 1987 with that of 18 children who did not. The two groups were similar with regard to the severity of HUS, the length of hospital stay, the duration of renal dysfunction and the incidence of disease-related complications, such as seizures, enterocolitis and cardiomyopathy. At discharge the prevalence of hypertension was higher in the plasma therapy group than in the control group. Plasma therapy did not demonstrate any benefit that would outweigh the risk of fluid overload, hyperproteinemia and transmission of viral infection.
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PMID:Plasma therapy for severe hemolytic-uremic syndrome in children in Atlantic Canada. 225 39

Combination therapy of (1) hypervolemia with albumin (1 g/kg/day), (2) artificial blood substitute (Fluosol-DA 20%, 10 ml/kg/day) and (3) induced hypertension was performed for the treatment of symptomatic vasospasm. Outcome was compared between thus treated patients (Treated group) and those without specific treatment (Non-treated group) in (1) 30 patients presenting with vasospasm who were planned to undergo delayed operation (Delayed operation group), (2) 23 patients undergoing early operation whose subarachnoid hemorrhage (DAH) was in group 2 according to Fisher's classification (Fisher Group-2) and (3) 25 patients undergoing early operation whose SAH was in group 3 (Fisher Group-3). In delayed operation group, the combination therapy improves the outcome to some extent resulting in increase of "Excellent" and "Good" patient from the rate of 25% to 35% (Table 1). Vasospasm appears at a low rate of 26% as well as in mild degree in Fisher Group-2 regardless of the treatment, which contributes to the satisfactory result observed in this group (Table 2). The outcome of the treated group in Fisher Group-3 is proved to be fairly good with "Excellent" and "Good" patient rate of 70% (Table 3), which seems largely to be attributed to the prophylactic effect of hypervolemia on vasospasm (Table 4). From these results, the combination therapy is considered to be performed with relatively small load on cardiovascular system compared with conventional hypervolemia-hypertension therapy.
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PMID:[Combination therapy (hypervolemia, Fluosol-DA 20%, hypertension) in the treatment of symptomatic vasospasm]. 241 80

Vasopressin secretion is stimulated by hyperosmolality, hypovolemia, or hypotension and is inhibited by hypoosmolality, hypervolemia, or hypertension. These osmotic and hemodynamic influences are mediated by neuronal afferents that originate in separate osmoreceptors or baroreceptors but ultimately converge to act on the same neurosecretory neurons. Functionally, the two control systems are integrated in such a way that osmoregulation is altered but not disrupted by hemodynamic influences. In patients with uncomplicated essential hypertension, basal as well as osmotically stimulated vasopressin is completely normal. The vasopressin response to an acute reduction in blood pressure is also normal if the values are expressed relative to the change in pressure. However, if the plasma vasopressin response is plotted as a function of absolute blood pressure, the line describing the relationship lies well to the right of normal. Thus, although it is completely intact, the baroregulatory mechanism appears to be reset to a higher level in essential hypertension. These results suggest that increased secretion of vasopressin does not contribute to the genesis or maintenance of uncomplicated, untreated essential hypertension but may antagonize the therapeutic effect of some antihypertensive drugs. If so, antagonists of V1 receptors may be useful as second-line adjunctive therapy for this condition.
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PMID:Osmoregulation and baroregulation of plasma vasopressin in essential hypertension. 243 80

We have reviewed records of 12 children underwent CAPD between January 84 and May 88, ranging in age from 7 month to 16 years (mean age 8.9 +/- 4.9 years). CAPD treatment lasted from 3 to 24 months (average 10.3 months). Exchanges of dialysis fluid were performed by parents (8 cases) or children (3); mean volume was 41.7 +/- 8.7 ml/kg/exchange (range 32-58 ml/kg). During 132 patient months of treatment laboratory data showed a good metabolic control expect a tendency to hypoalbuminemia. There were 3 catheter changes. Complications were: peritonitis (15 episodes or one infection every 8.8 patient/treatment/months), hypertension (5 cases), hypervolemia (2), cuff extrusion (4), local exit site (5) and tunnel (2) infections and hernias (2). CAPD has been continued in 3 children; 6 other received renal transplantation, one was switched to hemodialysis and 2 died. This study has demonstrated that CAPD was an effective treatment for renal failure in children waiting renal transplant. Cuff extrusion and hypoalbuminemia were common complications in our children.
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PMID:[Continuous ambulatory peritoneal dialysis: efficient treatment for children with terminal uremia]. 263 90

Hypertension is a common problem encountered after renal transplantation. Many different mechanisms may be responsible for hypertension in this setting, and therapy will depend upon the mechanism(s) affecting the individual patient. Factors that may cause or aggravate post-transplantation hypertension include renal dysfunction secondary to rejection or other diseases of the transplanted kidney, renin production from the diseased native kidneys if these kidneys have not been surgically removed, extracellular fluid volume expansion, toxic effects of medications used after transplantation, especially cyclosporine and intravenous prednisolone, or primary hypertension in the donor or recipient. Renal artery stenosis may predispose to acute renal failure in the presence of treatment with angiotensin-converting enzyme inhibitors. Severe renal artery stenosis may also lead to refractory salt and water retention and fluid overload with congestive heart failure and hypertension, mediated primarily due to extracellular fluid volume excess. Therapy with percutaneous transluminal renal angioplasty or, as a last resort, surgery, can be successful in controlling these problems.
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PMID:Refractory hypertension after renal transplantation. 266 26

The patients suffering from hypertonic nephritis were examined for renal hemodynamics, the activity of the renin-angiotensin-aldosterone system (RAAS), excretion of PGE2 and PGF2 alpha, and for a number of the parameters of water-electrolyte homeostasis. In A series, the patients suffering from latent and hypertonic nephritis (n = 11 in each group) were compared. In B series, two groups of the patients (n = 13 in each group) suffering from hypertonic nephritis associated with moderate or grave arterial hypertension were compared. The patients under comparison belonging to A and B series did not differ as regards the sex, age, nephritis standing, serum creatinine or proteinuria. As compared with the patients suffering from latent nephritis (A series), the patients with hypertonic nephritis showed a lower effective renal plasma flow, a greater resistance of the renal vessels, lesser PGE2 secretion, and a higher serum sodium concentration. As compared with the patients suffering from moderate hypertension (B series), the patients with associated hypertonic nephritis and grave hypertension demonstrated a higher resistance of the renal vessels, a higher activity of plasma renin, a larger concentration of plasma aldosterone and its excretion with urine, as well as a greater volume of the circulating blood. It is assumed that the development of arterial hypertension associated with hypertonic nephritis may be caused by renal hemodynamics deterioration, by relative activation of the renin-angiotensin system, inhibition of the depressor prostaglandin system and sodium retention. The progression of hypertension may be related to further deterioration of renal hemodynamics attended by RAAS activation and hypervolemia.
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PMID:[Mechanisms of the development of arterial hypertension in hypertonic nephritis]. 279 11

With hypervolemia, hemoconcentration, high vascular resistance and hypertension the SIH offers opposite changes as the physiological pregnancy. The absence of a decrease in hematocrit and MAP is as yet not used as early screening possibility. Doppler flow measurements allow a detection of a fetal brain sparing effect which seems to be a typical answer to placental insufficiency. According to the till published results the hypervolemic hemodilution is of advantage for the mother and the fetus. With Doppler flow measurements we have a new method to verify therapeutic conceptions for the SIH.
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PMID:[Pregnancy-induced hypertension: maternal and fetal hemodynamics]. 280 10

Increased levels of a humoral inhibitor of active sodium transport have been associated with the response to acute and chronic hypervolemia and various forms of experimental as well as human essential hypertension. In this report, we describe the purification of inhibitors of Na+, K+-adenosine triphosphatase (ATPase) from the plasma of volume-expanded individuals. Of the two amphipathic materials obtained, only one of the factors when present in high concentrations showed the slow time-dependent component of inactivation similar to that of the cardiac glycosides. Inhibition was reduced in the presence of plasma proteins and was freely reversible. Both factors inhibited potassium-dependent p-nitrophenylphosphatase activity and specific [3H]ouabain binding in a manner similar to the cardiac glycosides. In contrast to ouabain and vanadate, however, high concentrations of potassium or norepinephrine, respectively, did not affect the magnitude or kinetic characteristics of inhibition. Structural analysis by mass spectroscopy showed a mass of 444 for factor 1, whereas factor 2 was conclusively identified as lysophosphatidylcholine-gamma-palmitoyl. These factors probably inhibit Na+, K+-ATPase by a nonspecific mechanism involving reversible perturbation of lipid-enzyme interactions required for normal catalytic activity. The significance of these factors as modulators of sodium transport may be limited to pathological states associated with abnormalities in plasma protein binding or lipid metabolism. They do not appear to be directly related to the humorally mediated disturbance of cellular sodium transport in hypertension.
Hypertension 1987 Nov
PMID:Purification and characterization of digitalislike factors from human plasma. 282 70

The influence of a 6-week treatment of female Wistar rats with one-kidney, one clip (1-K, 1 C) renal hypertension, with the calcium antagonist nifedipine on plasma volume, red cell Na+ handling and plasma atrial natriuretic peptide immunoreactivity (ANP-IR) was studied. Measurements were performed at 2 and 6 weeks after surgery. In 1-K, 1 C rats plasma volume was increased and red cell Na+ pump activity was reduced only after 2 weeks. Blood pressure, heart weights and plasma ANP were massively increased after both 2 and 6 weeks. 1-K, 1 C-rats treated with nifedipine had normal plasma volume, plasma ANP, and red cell Na+ pump activity in comparison with sham-operated rats. Increases in blood pressure and heart weights were attenuated. It is concluded that 1-K, 1 C hypertension in the rat is associated with cardiomegaly, rise in plasma ANP, initial hypervolemia and depression of the membrane Na+ pump. Nifedipine prevents the occurrence of hypervolemia and secondary phenomena such as rises in plasma ANP and cardiomegaly. This may play an important contributory role in the prevention of pathological sequelae.
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PMID:Modulation by chronic nifedipine of plasma atrial natriuretic peptide, cell Na+ transport and plasma volume in rats with renal hypertension. 284 89

During a 12-year period, when more than 106,000 women were delivered, 28 women with peripartum heart failure of obscure etiology that initially was diagnosed as peripartum cardiomyopathy were studied. None had obvious underlying cardiac disease or iatrogenic fluid overload, and in all an assiduous search for underlying cardiovascular disease was launched. In 21 of these 28 women, heart failure was attributed to chronic underlying disease (chronic hypertension in 14, forme fruste mitral stenosis in four, and morbid obesity in one) or viral myocarditis. Importantly, these women also had multiple compounding cardiovascular factors--preeclampsia, cesarean section, anemia, and infection--which, when superimposed on those of pregnancy, acted in concert to cause heart failure. In seven women, the cause for cardiomegaly and global hypokinesis was not found, and peripartum cardiomyopathy was diagnosed. Compared with women with explicable causes of peripartum heart failure, these women did poorly: six had persistent cardiomegaly and heart failure, and four of these died within four months to eight years. From these observations, the authors conclude that idiopathic peripartum cardiomyopathy is uncommon, and that in most women with peripartum heart failure of obscure etiology, underlying chronic disease will be identified. Heart failure in these women ensues when the cardiovascular demands of normal pregnancy are amplified further by common pregnancy complications superimposed upon these underlying conditions that cause compensated ventricular hypertrophy.
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PMID:Peripartum heart failure: idiopathic cardiomyopathy or compounding cardiovascular events? 293 58


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