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Biomedical subjects

M Nowicki

Publications and source records attributed to M Nowicki.

At least 73 records · Page 4Linked to original sources
PubMed1995

Graduate programs in health administration: faculty academic reputation and faculty research reputation by program location and program reputation.

This study used program location and program reputation to describe two important faculty characteristics: academic reputation and research reputation. The study involved 44 graduate programs in health administration representing four program locations: schools of public health, business, medicine/allied health, and graduate/independent. Fourteen programs were identified as ranked programs and the remaining 30 programs were identified as unranked programs. While the study identifies many differences, few are significant, thus adding credence to the argument for diversity in program location and diminishing credence in the argument for program reputation.

Analysis of Variance↗
PubMed1995

Erythropoietin and hypertension.

Erythropoietin (Epo) is a glycoprotein hormone responsible for the control of the proliferation and differentiation of cells of erythroid lineage. Recombinant erythropoietin (rHuEpo) is widely used as a pharmacological agent for the treatment of the anaemia of renal failure. Efficacy of rHuEpo and its superiority over blood transfusions have been proven in large multicentre trials. The most important side-effect of the therapy is the increase of BP which is observed in approximately 30-35% of dialysis patients receiving rHuEpo. It appears that the haemodynamic resetting that occurs with partial correction of anaemia may be inappropriate resulting in an altered vascular resistance in relation to the cardiac output. This is in turn due to the combination of increased blood viscosity and loss of hypoxic vasodilatation. Both these factors, however, cannot account completely for the rise in vascular resistance, and therefore the possibility of a direct and/or hormonally-mediated vasopressor effect of rHuEpo has recently been raised. Moreover, scarce information exists on the possible involvement of endogenous erythropoietin in the pathogenesis of arterial hypertension and haematological disturbances observed in primary and some secondary forms of hypertension.

Blood Viscosity↗
PubMed1995

[Imidazol receptor agonists--new possibilities for treating hypertension].

Adrenergic alpha 2-receptors mediate important regulatory functions in both the brain and the periphery. Activation of these receptors lowers blood pressure through a decrease in sympathetic and vasomotor nerve activity. Agonists of the alpha 2-adrenoceptors are often used in the treatment of arterial hypertension. As recently discovered, their chemical structure includes so called "imidazoline ring" and compounds with such chemical structure bind to nonadrenergic sites known as imidazoline receptors. These receptors are localized in midportions of the brain but they are also present in other organs such as lungs, heart, adrenal medulla, liver and kidneys. Their selective activation lowers blood pressure without inducing sedation typical for alpha 2-agonists. Several substances binding with high selectivity to imidazoline receptors have recently been synthesized. Some of them as rilmenidine and moxonidine have successfully been introduced to the treatment of arterial hypertension in humans.

Adrenergic alpha-Agonists↗
PubMed1995

[Nephrologic analysis of 94 women with diagnosed "primary" gestosis].

Among 94 women with diagnosed "primary" gestosis during pregnancy, 67 patients demonstrated (3-6 months after delivery) chronic glomerulonephritis (25 women) or chronic pyelonephritis (28 women) or hypertension caused by others than nephrologic reasons. "Primary" gestosis was diagnosed correctly only in 29% cases. The most often reason of "secondary" gestosis was undiagnosed chronic nephropathy before and during pregnancy. Obtained results confirm other data informing that "primary" gestosis is a rare phenomenon.

Adult↗
PubMed1994

OACE inhibition does not interfere with acute extrarenal or renal potassium disposal in chronic renal failure.

The influence of angiotensin converting enzyme (ACE) inhibition on acute extrarenal and renal potassium elimination in stable chronic renal failure has been examined in 10 male patients median age 44 y; mean CLCR 42 ml.min-1.1.73 m-2. In a double blind, placebo-controlled cross-over study, K+ 0.3 or 0.4 mmol.kg-1 body weight was infused IV on two occasions while the patients also received an infusion either of placebo or 0.5 mg of the ACE inhibitor perindoprilat in random order. Plasma K+ levels and urinary K+ excretion were measured at regular intervals. During the study patients adhered to an isocaloric diet providing a standardised daily intake of potassium and sodium (50 mmol K+ and 40 mmol Na+). The median rise in plasma K+ was not significantly different after placebo (delta K 0.66 mmol.l-1) compared with to the infusion of perindoprilat (delta K 0.66 mmol.l-1). The median baseline urinary K+ excretion rate was 6.5 mmol.3 h-1 before the placebo infusion and 5.9 mmol.3 h-1 before infusion of perindoprilat. During the potassium load, the urinary excretion rate rose to 16.1 mmol.3 h-1 (after placebo) and 15.1 mmol.3 h-1 after perindoprilat in the first 3 h, and it returned almost to the baseline value within the next 3 h (5.6 mmol.3 h-1 after placebo and 5.7 mmol.3 h-1 after perindoprilat); the differences were not statistically significant. With perindoprilat a decrease in mean arterial blood pressure and ACE activity, an increase in renin plasma activity and a decrease in aldosterone concentrations were observed compared to the placebo infusion. There was no significant differences plasma in adrenaline or insulin levels after either infusion. Thus, ACE inhibition did not interfere either with the extrarenal or the renal disposal of an acute potassium load in patients with chronic renal failure.

Adult↗
PubMed1994

Renal clearance of endogenous erythropoietin in patients with proteinuria.

Recent data indicated the importance of urinary losses of erythropoietin (Epo) in the pathogenesis of anaemia in patients with nephrotic syndrome. In the present study we aimed to investigate plasma and urinary Epo levels and their renal handling in relation to beta 2-microglobulin (beta 2m), sodium metabolism and the renin-angiotensin-aldosterone system (RAAS), respectively, in patients with sub-nephrotic range proteinuria (SNP), microalbuminuric diabetics and hypertensives, and in healthy subjects studied on a standardized diet containing 120 mmol sodium and 70 g protein per day. We found that patients with SNP were characterized by lower plasma levels of Epo than healthy subjects but no differences were found in urinary excretion of Epo, endogenous Epo clearance and its fractional excretion (FEEpo). There were no differences between groups in FE beta 2m and FENa and plasma aldosterone levels but plasma renin activity was higher in patients with SNP than in the controls. No relationships were found between Epo levels and activity of the RAAS and sodium metabolism, respectively. Our data suggest that lower levels of plasma Epo in patients with SNP and normal renal excretory function are not due to urinary losses of Epo but rather to the decreased production/degradation ratio.

Adult↗
PubMed1994

Effect of isobaric hyperoxemia on erythropoietin secretion in hypertensive patients.

We assessed the influence of hyperoxemia on erythropoietin secretion in patients with various etiological forms of arterial hypertension (essential, n = 15; renoparenchymal, n = 16; renovascular, n = 15) and in 15 healthy subjects. On the first day of the study, blood was withdrawn at 1-hour intervals for the estimation of erythropoietin during a total of 6 hours and at 2-hour intervals for the assessment of PO2. Three days later the same parameters were assessed again at identical time intervals, but the subjects were breathing pure oxygen during the first 2 hours. Breathing with pure oxygen resulted in a significant increase of blood PO2 (184.85 +/- 4.47 versus 85.92 +/- 2.28 in essential, 185.21 +/- 5.52 versus 84.55 +/- 3.04 in renoparenchymal, and 181.7 +/- 3.14 versus 87.49 +/- 2.25 in renovascular hypertension groups and 189.84 +/- 5.2 versus 85.89 +/- 1.73 mm Hg in healthy subjects; P < .001 in all groups). Baseline plasma erythropoietin was not different among the groups (29.33 +/- 4.14 in essential, 24.56 +/- 3.09 in renoparenchymal, and 27.77 +/- 3.29 in renovascular hypertension groups and 24.23 +/- 2.70 mU/mL in the control group). The pattern of erythropoietin decline was different in the groups of hypertensive patients. In patients with essential hypertension, unlike in healthy subjects and patients with other etiological forms of arterial hypertension, only a very short-term suppression of erythropoietin levels was observed during hyperoxemia. No significant changes in blood pressure during breathing with pure oxygen were found in any of the studied groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Excess cardiovascular mortality in the uremic patient--what does it teach for other risk factors in the non-renal patient?

A high rate of cardiovascular death in renal patients, particularly patients with endstage renal failure, has not been well appreciated in the past. It is obvious that cardiovascular lesions are more severe than can be explained by the classical risk factors of elevated blood pressure and dyslipidemia. In renal failure, a number of pathomechanisms are operative which may be paradigms of more general relevance, e.g. activation of the renin and sympathetic system, inhibition of the vasoconstrictor NO system, left ventricular hypertrophy in excess of what is expected for high blood pressure. A paradox inverse relation between lipid concentrations and cardiovascular death, i.e. a protective effect of hyperlipidemia, in dialysed patients, presumably results from the confounding effect of malnutrition, high lipid levels being a substitute marker of adequate nutrition.

Animals↗
PubMed1994

Proteinuria and hypertension.

Albuminuria is more prevalent in patients with primary hypertension than in normotensive subjects of the general population. The presence of albuminuria predicts the presence of more severe target organ damage and is related to the risk of cardiovascular events. Preliminary results show albuminuria even in some normotensive individuals with a genetic risk of hypertension and in association with insulin resistance. While albuminuria is generally more frequent in the elderly, it is also found in young patients with mild to moderate primary hypertension. It is uncertain whether in these circumstances albuminuria indicates some "renal component" in the etiology of primary hypertension. Massive albuminuria may occur in subjects with "benign" nephrosclerosis. Whether albuminuria is a predictor of hypertensive renal damage requires further study. Albuminuria is reduced by antihypertensive treatment, but diverse effects on albuminuria are seen with different antihypertensive agents.

Adult↗
PubMed1994

Treatment with high doses of loop diuretics in chronic renal failure.

In the late 60s, A. Heidland and his collaborators were amongst the first to characterize the renal action of frusemide in preterminal renal failure by giving quantitative information on dose requirements, fractional Na and K excretion, effects on renal haemodynamics, and by recognizing reversible inner ear dysfunction as the major dose-limiting side-effects. These early studies have been largely reconfirmed. They have been extended by more clearly characterizing (a) altered pharmacokinetics of frusemide, e.g. the importance of altered transepithelial transport in the proximal tubule and intratubular protein binding, and (b) the mechanisms underlying altered pharmacodynamics, particularly high baseline fractional Na rejection and increased absolute distal Na reabsorption. Apart from increasing the dose of frusemide, continuous administration by infusion and combination of frusemide with thiazide diuretics have emerged as rational therapeutic strategies in chronic renal failure.

Animals↗
PubMed1993

Influence of the renin-angiotensin system stimulation on erythropoietin production in patients with various forms of arterial hypertension.

Recent studies suggest the existence of a relationship between the renin-angiotensin system and erythropoietin (EPO) secretion. It has been studied whether patients with various forms of arterial hypertension (essential, renal, renovascular, in the course of arteritis) differ with respect to EPO secretion and whether EPO serum levels are related to renin response induced by dietary sodium restriction to 10-20 mmol Na/24 h for 3 days and upright body position for 3 h. Patients with different forms of hypertension and normal renal excretory function and healthy subjects did not differ in hematocrit value, markers of iron metabolism, and EPO secretion except for patients with arteritis who had higher ferritin values. In these patients a positive correlation between EPO levels and hematocrit values suggests the existence of an altered regulation of EPO secretion. In essential hypertension a negative correlation found between changes in EPO and PRA levels in response to sodium restriction and upright body position may also reflect an altered regulation of both EPO and renin production.

Adult↗
PubMed1993

Nephroprotective effect of ACE inhibitors.

In most cases of renal disease, progression of renal failure occurs via nonspecific mechanisms that can be dissociated from the primary cause of renal damage. Progression of disease is accompanied by glomerulosclerosis and tubulointerstitial fibrosis. Loss of autoregulation and afferent renal vasodilation renders the glomerular microcirculation particularly susceptible to systemic hypertension. Glomerular growth is an ancillary factor permitting the development of glomerulosclerosis. Experimental and clinical studies indicate that angiotensin converting enzyme (ACE) inhibitors may prevent progressive renal deterioration. Furthermore, it appears that this effect can be dissociated, at least in part, from the haemodynamic effects of ACE inhibitors. Some evidence indicates that the renal-protective effects of ACE inhibitors results from their effects on glomerular growth and glomerular permselectivity. The role of reduced generation of angiotensin II or accumulation of kinins in the renal effects of ACE inhibitors is under investigation. Prospective clinical trials have demonstrated that ACE inhibitors reduce proteinuria and interfere with progression of renal disease to a greater degree than can be explained by their blood pressure lowering effects alone.

Angiotensin-Converting Enzyme Inhibitors↗