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Biomedical subjects

M Wysocki

Publications and source records attributed to M Wysocki.

At least 109 records · Page 6Linked to original sources
PubMed1989

Renal and hemodynamic effects of isradipine in essential hypertension.

Twenty-three men with essential hypertension participated in a double-blind placebo-controlled study with a crossover design to evaluate the long-term (nine weeks) effects of isradipine on central and renal hemodynamics. Isradipine as monotherapy was titrated from 2.5 to 5 and then to 7.5 mg twice daily. At the end of the crossover periods, cardiac output (dye-dilution) and intraarterial blood pressure were assessed. Compared with placebo, isradipine reduced ambulatory blood pressure from 174/104 to 154/91 (p less than 0.001), whereas the heart rate was unchanged. The reduction of blood pressure was entirely due to a reduction (36 percent; p less than 0.001) of the peripheral resistance. The baroreceptor sensitivity did not change (RR intervals during infusion of phenylephrine) but, with isradipine, the setpoint was shifted to lower blood pressure levels. Renal plasma flow (para-amino hippurate clearance) increased (465 versus 391 ml/minute; p less than 0.05), but glomerular filtration rate ([51Cr]ethylenediaminetetraacetic acid clearance) did not change. Hence, the filtration fraction decreased. With isradipine, there was a post-dose increase in natriuresis (0.45 to 0.34 mmol/minute; p = 0.06). Side effects were mild.

Antihypertensive Agents↗
PubMed1989

Blood pressure control and haemodynamic adaptation with the dihydropyridine calcium antagonist isradipine: a controlled study in middle-aged hypertensive men.

Twenty-three middle-aged men (59 +/- 2 years) with sustained, essential hypertension (WHO Stage II) and with diastolic blood pressure exceeding 100 mmHg during a run-in placebo month were included in a trial designed to assess the clinical and haemodynamic effects of isradipine, a novel dihydropyridine calcium antagonist. The study was double-blind with a placebo-controlled crossover design. Isradipine as monotherapy was titrated in three, 3-week periods in doses of 2.5, 5 and 7.5 mg twice daily, or as apparently identical placebo capsules. A 3-week placebo wash-out period separated the two phases of the study. Clinical characteristics were followed during each treatment phase and an invasive haemodynamic examination was performed on the last day of the final active or placebo dose. In the haemodynamic investigation, cardiac output was measured using a dye-dilution technique and blood pressure via a catheter in the brachial artery. Plasma renin activity (PRA) was assessed by radio-immunoassay of generated angiotensin I and arterial noradrenaline concentrations using high-performance liquid chromatography (HPLC). Baroreceptor sensitivity was calculated from R-R intervals of the ECG and beat-to-beat systolic blood pressure during increasing bolus injections of phenylephrine. During optimal therapy with isradipine (7.5 mg twice daily), highly significant decreases in supine systolic (from 174 +/- 4 to 154 +/- 3 mmHg) and diastolic blood pressures (from 104 +/- 2 to 91 +/- 1 mmHg) were observed. Heart rate was unchanged (79 +/- 3 versus 81 +/- 2 beats/min) during chronic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗
PubMed1989

Long-term renal effects of isradipine, a calcium entry blocker, in essential hypertension.

The long-term effects (9 weeks) on renal hemodynamics of the new calcium entry blocker isradipine (PN 200-110) were assessed in 20 middle-aged male patients with essential hypertension. The study was double-blind placebo-controlled with a crossover design. Isradipine or placebo tablets were titrated from 2.5, 5, and 7.5 mg b.i.d. every 3rd week to achieve a diastolic blood pressure of less than or equal to 90 mm Hg. The renal parameters were assessed 2-4 h after dosing. Despite a decrease in diastolic blood pressure (91 vs. 104 mm Hg, p less than 0.001) the renal plasma flow increased (465 vs. 394 ml/min, p less than 0.05). The glomerular filtration rate was unchanged and the filtration fraction was reduced (0.21 vs. 0.23, p less than 0.05). The plasma renin activity increased (0.71 vs. 0.51, p less than 0.05). The patients probably did not retain sodium because the body weight was unchanged. Rather, long-term treatment with isradipine was associated with a repetitive postdose increase in natriuresis (0.45 vs. 0.34 mmol/min, p = 0.06).

Blood Pressure↗
PubMed1989

Adrenaline infusion in man increases muscle sympathetic nerve activity and noradrenaline overflow to plasma.

This study was conducted to determine if muscle sympathetic nerve activity (MSA) and/or the neuronal release of noradrenaline per impulse are modulated by adrenaline in the physiological plasma concentration range. We gave step-wise infusions of adrenaline (0.05-0.6 nmol/kg per min) to 10 healthy young men and measured: intra-arterial blood pressure; heart rate; central venous pressure (CVP); efferent MSA (microneurography in the peroneal nerve); arterial (brachial artery) and femoral venous plasma concentrations of noradrenaline, and the spillover of noradrenaline to arterial and venous plasma (radiotracer infusion). The infusion of adrenaline caused a fall in diastolic blood pressure and tachycardia, and was associated with increases in MSA and noradrenaline spillover. These observations suggest that part of the adrenaline-induced increase in transmitter release is due to enhanced nerve impulse activity, but such a conclusion rests on the absence of diffusion limitations from the site of noradrenaline infusion into the blood stream. After termination of adrenaline infusion the tachycardia and elevated plasma noradrenaline levels persisted, but these changes were probably due mainly to a profound increase in nerve activity. Concurrently, there was a reduction in CVP which may have triggered the increase in efferent sympathetic nerve activity. Infusions of adrenaline did not influence the clearance of noradrenaline from arterial plasma, but the fractional extraction over the leg was moderately reduced, indicating that more arterial noradrenaline is recovered in venous plasma during adrenaline infusion. The present data suggest that the reasons for the adrenaline-induced increase in noradrenaline release are complex, but they are consistent with the hypothesis that stress levels of adrenaline enhance sympathetic nerve activity, and that circulating adrenaline may modulate both haemodynamic and neural responses to stress.

Adult↗
PubMed1988

Are chronic wheezing and asthma-like attacks related to FEV1 decline? The Cracow Study.

Analysis is presented of the relationship between decline in ventilatory function and possible symptoms of bronchial hyperreactivity. Data comes from three consecutive surveys within a 13-year follow-up study of a population sample of 1747 persons (718 males and 1029 females) who completed spirometric testing and interviews. Chest symptoms recorded in the two initial surveys were used as baselines for the prognostic study on FEV1 change. To evaluate changes in lung function the FEV1 decline index, expressed as percentage of FEV1 loss during the study period, was calculated. Chronic wheezing and asthma-like attacks were very strongly related to FEV1 baseline level. Multiple linear regression analysis for each separate symptom including age and smoking habits as confounders and showed that the FEV1 decline index was higher and more significant when wheezing and asthma-like attacks or chronic cough were present. When the combination of symptoms were introduced into the regression model, the effect of wheezing became insignificant. Only attacks of shortness of breath in both sexes and chronic cough in women were significantly associated with more rapid FEV1 decline. However, the effect of persistent wheezing in men had a rather substantial impact on FEV1 change. Comparing the effect of the number of cigarettes smoked with the effect of symptoms, one can see that FEV1 decline due to attacks of shortness of breath is comparable to that seen with heavy smoking. There was no strong evidence that the symptoms under study precede the more rapid FEV1 decline.

Adult↗
PubMed1988

Occupational exposures and changes in pulmonary function over 13 years among residents of Cracow.

In a 13 year follow up study conducted among residents of Cracow the relation of annual rate of decline in FEV1 to occupational exposures was analysed. The study group consisted of 696 men and 983 women aged 19-60 at the start of the study in 1968. They were interviewed three times, in 1968, 1973, and 1981, and decline in FEV1 was estimated for each subject from spirometric measurements in 1968 and 1981. The interviews provided data on exposure at the workplace to dusts, variable temperature, and chemicals or irritating gases, which established duration and time of the exposure. The FEV1 mean level, height, and smoking habits were considered as confounders in the analysis. The study indicated that the most pronounced influence on decline in FEV1 was prolonged and continuing exposure to variable temperature. The effects of dusts, independent of exposure to variable temperature, were much smaller but analysis in occupational subgroups suggest that dust may be important in some, such as workers in the building materials and pottery industry. Relatively immediate effects of exposure to chemicals were detected independently of effects of other exposures. The estimated effects of occupational exposures were of a similar magnitude as those of tobacco smoking though related to much smaller groups. Both effects were additive in accelerating decline in lung function. These results, obtained in the general population and less biased by selection than studies performed in industrial settings, show the importance of occupational factors in the natural history of limitation of airflow.

Adult↗
PubMed1987

Acute systemic and renal haemodynamic effects and long-term antihypertensive action of cadralazine in patients pretreated with beta-blockers and diuretics.

The antihypertensive effects of the hydralazine-related compound cadralazine (2-(3-[6-(2-hydroxypropyl)ethylamino]pyridazinyl)ethyl carbazate, ISF 2469), were investigated in 16 patients with primary hypertension concurrently treated with beta-blockers and diuretics. The protocol included a double-blind placebo controlled haemodynamic evaluation after the first tablet and two 4-week double-blind placebo controlled cross-over periods followed by an open evaluation during 2 months. Cadralazine induced a moderate, prolonged fall in blood pressure that was associated with vasodilatation and slight increases in cardiac output (dye-dilution) and heart rate. Renal plasma flow (PAH) and glomerular filtration rate (51Cr-EDTA) were not significantly influenced, but the filtration fraction was reduced. Plasma concentrations of noradrenaline and adrenaline rose, whereas plasma renin activity was unchanged. The haemodynamic parameters were not correlated with the plasma concentrations of cadralazine. During chronic cadralazine treatment the supine blood pressure was significantly lower than during the double-blind placebo phase (160/93 vs 174/102 mmHg). The compound was generally well tolerated but the body weight increased slightly (1.1 kg), probably because of fluid retention. Several patients who had previously experienced side effects with hydralazine, including one with hydralazine-syndrome, tolerated cadralazine well. This suggests that cadralazine does not cross-react with hydralazine.

Acute Disease↗
PubMed1987

[Non-cardiogenic pulmonary edema associated with severe diabetic ketoacidosis].

Non cardiogenic pulmonary oedema occurs rarely in patients with diabetic ketoacidosis, except in conjunction with an infection. A case is reported of non cardiogenic pulmonary oedema in a patient with severe diabetic ketoacidosis, which resolved within 72 h with oxygen supply only. There were no objective facts which could explain its pathogenesis, despite the important pulmonary asymmetry due to a unilateral diaphragmatic paralysis.

Adult↗
PubMed1987

Haemodynamic and haemorheological effects of hypervolaemic haemodilution in men with primary hypertension.

The haemorheological disturbances observed in primary hypertension arise mainly from haemoconcentration, which leads to an elevation of blood and plasma viscosity and increased aggregation of red blood cells (RBCs). We evaluated the rheological properties of blood and central haemodynamic indices in 13 men with untreated primary hypertension (WHO stage I and II), during a baseline period and after intravenous infusion of 1000 ml of 0.9% NaCl (within 12-15 min). The rheological properties studied were: whole blood viscosity (WBV), plasma viscosity (PV), haematocrit (HCT) and plasma fibrinogen concentration (PF). The central haemodynamic indices were: mean intra-arterial blood pressure (MAP), central venous pressure (CVP), cardiac index (CI), stroke volume index (SVI), total peripheral resistance index (TPRI) and the vascular hindrance index (VHI). Plasma renin activity (PRA) and plasma noradrenaline concentration (P-NA) were also measured. Volume expansion with saline caused haemodilution as expressed by a fall in HCT (P less than 0.001), WBV (P less than 0.001) and PV (P less than 0.01). At the same time, CVP, MAP and VHI increased (P less than 0.05) while PRA decreased (P less than 0.05) and P-NA remained unchanged. Mean values of the cardiac index (CI) and stroke volume index (SVI) did not change significantly. We did not observe any significant relationship between haemodynamic and haemorheological parameters, during baseline or between their respective changes after the infusion. The results indicate that although hypervolaemic haemodilution produced by saline infusion in hypertensive patients may improve blood flow properties (HCT, WBV, PV), blood pressure (BP) is not reduced; rather the converse is true. The reduction in HCT and hence the improved blood rheology, did not affect calculated vascular resistance. Thus, correction of WBV does not acutely normalize BP in primary hypertension.

Adult↗
PubMed1987

Significant relationship between renin suppression and atrial natriuretic peptide (alpha-hANP) during volume loading in hypertensive men.

We have studied eight men with moderate hypertension to determine the atrial natriuretic peptide (alpha-hANP) response to acute volume expansion. Rapid infusion of 1,000 ml 0.9% saline (10-20 min) caused an increase in central venous pressure (4.7 +/- 1.6 cmH2O) while blood pressure and pulse pressure (arterial baroreceptor load) did not change. Stroke volume and heart rate were not affected by the volume load but plasma renin activity (PRA) was significantly suppressed (from 0.83 +/- 0.14 to 0.68 +/- 0.34 microgram AI I/ml-h; p less than 0.01). A significant hemodilution was also observed. Renal sodium excretion was significantly increased. Arterial alpha-hANP increased significantly from 21.1 +/- 6.1 to 30.5 +/- 4.0 pmol/l (p less than 0.02) during volume expansion. There was a significant correlation between corrected plasma volume increase (urine volume subtracted from the infused volume) and alpha-hANP plasma elevation (r = 0.78; p less than 0.05). There was also a significant negative correlation between changes alpha-hANP and PRA (r = -0.78, p less than 0.05). We conclude that only moderate volume loading in human hypertensives is a mechanism for increase in plasma alpha-hANP levels. The significant negative correlation between changes in alpha-hANP and PRA suggests that alpha-hANP may be the humoral factor at least partly responsible for suppression of renin in hypertensive man. Since increased fluid volume also affects sympathetic renal efferents as well as vasopressin secretion, our observed relationship between volume load and renin may well be related also to such mechanisms.

Adult↗
PubMed1987

Carcinoembryonic antigen (CEA), alphafetoprotein (AFP) alpha and beta subunits of human chorionic gonadotropin (hCG) in cerebrospinal fluid of children with acute lymphoblastic leukaemia.

The cerebrospinal fluid (CSF) and plasma levels of CEA, AFP, alpha and beta hCG were determined by radioimmunoassay in 19 children with acute lymphoblastic leukaemia (ALL). CSF in 15 patients at the onset of ALL was examined in the first week after diagnosis and subsequently every two months. In 4 other children in second complete remission of ALL, CSF was examined every two months as well. Elevated values of CEACSF were present in 1/15 patients at the onset of ALL, of AFPCSF 0/15, alpha hCGCSF in 2/15, beta hCGCSF in 2/15 cases. The elevated levels of these markers in CSF became normal in successive lumbar punctures and none of these children developed central nervous system (CNS) relapse in further follow-up. Isolated CNS relapses were diagnosed 13 times in 7 children. Elevated CEACSF levels were found in 6/13 cases (maximum, 25.0 ng/ml) and in one patient CEACSF levels correlated well with pleocytosis. Elevated AFPCSF values were present in 0/13 cases, alpha hCGCSF in 0/13 and beta hCGCSF in 3/13 patients and became normal by the next CSF examination. The determination of CEA, AFP, alpha and beta hCG in plasma did not play a role in monitoring CNS relapse in ALL patients.

Adolescent↗
PubMed1987

Carcinoembryonic antigen, alphafetoprotein and alpha and beta subunits of human chorionic gonadotropin in plasma of children with acute leukaemia.

The plasma carcinoembryonic antigen, alpha-fetoprotein and the alpha and beta subunits of human chorionic gonadotropin levels were measured by radioimmunoassay in 44 children with acute leukaemia. These markers were determined repeatedly every 3 months at different stages of the disease (at onset, in complete remission, during bone marrow and extramedullary relapse). Elevated CEA levels were present in 64% of children at the onset of acute leukaemia and during bone marrow relapse. Elevated CEA levels decreased during induction treatment and they became normal with attainment of complete remission. In 7/12 patients who developed bone marrow relapse elevated CEA levels and in 4 of them raised levels appeared 3-4 months before there had been any other evidence of relapse. In 6/13 patients with extramedullary relapse, elevated CEA levels were found. AFP, alpha and beta hCG values in different stages of the disease were elevated sporadically; they did not reflect the activity of leukaemia.

Adolescent↗