Search

Copyright of Acta Angiologica is the property of VM Medica-VM Group (Via Medica) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Chronic obstructive pulmonary disease (COPD) affects almost 10% of the adult population of our country; obstructive sleep apnoea is increasingly being recognized and concerns, according to accepted criteria, 2-9% of females and 4-24% of men. The greatest mortality in chronic obstructive pulmonary disease is not caused by respiratory failure, but cardiovascular complications, including ischaemic heart disease. Obstructive sleep apnoea in half the cases is complicated by hypertension, often refractory to antihypertensive therapy. The paper discusses the pathogenesis of ischaemic heart disease in patients with COPD with particular attention to the inflammation that occurs in these two diseases. The pathogenesis of hypertension in the course of obstructive sleep apnoea is also presented with particular emphasis on hypoxia and sympathetic stimulation. Prevention of coronary heart disease should be a priority of the procedure in chronic obstructive pulmonary disease. The paper also discusses the treatment of ischaemic heart disease, paying attention to the modification of treatment in patients with chronic obstructive pulmonary disease, and discussing the influence of drugs used in COPD on the progression of ischaemic heart disease. Hypertension in the course of obstructive sleep apnoea is often resistant to therapy despite the use of continuous positive airway pressure devices, and often decrease after the use of aldosterone antagonists. Attention is drawn to the anti-inflammatory action of statins and trials of their use in the prevention of exacerbations of chronic obstructive pulmonary disease.

Decreased adiponectin level, the adipose tissues hormone, is related to high body mass and insulin resistance, which are risk factors for atherosclerosis. It was shown, that cigarette smoking and high homocysteine (Hcy) level are associated with low level of adiponectin. In the presented study we search for the associations between 5 polymorphisms in genes involved in Hcy metabolism - methylenetetrahydrofolate reductase (MTHFR) and paraoxonase 1 (PON1), smoking, adiponectin levels and insulin resistance in subjects with coronary artery disease (CAD). The studied group consisted of 152 patients subjected to coronary arteriography. In 116 patients significant atherosclerotic changes in vascular vessels were confirmed (CAD group), remaining patients were considered as the control group. In studied group, the levels of glucose, insulin, adiponectin and blood lipids profile were measured. Adiponectin and insulin levels were determined by radioimmunological assays. The insulin resistance was calculated using mathematical HOMA model. MTHFR 677C>T, 1298A>C, PON1 -108C>T, L55M, Q192R polymorphisms were ascertained by PCR-RFLP methods. In the studied group (N = 152), significantly decreased adiponectin levels and higher degree of insulin resistance were present in subjects with angina pectoris (N = 129) and peripheral atherosclerosis (N = 32), whereas in the cases of CAD, confirmed in coronary arteriography (N = 116), only the higher degree of insulin resistance was noted. Arterial hypertension (p = 0.004), diabetes mellitus (p = 0.03) and smoking (p = 0.04) were the most significant vascular risk factors associated with the low adiponectin levels. In CAD group, negative correlations between the level of adiponectin and the dose of MTHFR 677T (r = - 0.238; p < 0.05) and PON1 55M (r = -0.251; p < 0.05 alleles were found. The MTHFR 677T allele was also correlated with degree of insulin resistance (r = 0.391; p < 0.05). In smokers, these genetic associations were stronger (r = -0.394; = -0.353; r = 0.440; respectively), which demonstrates, that the negative effects of MTHFR 677T and PON1 55M alleles are enhanced by smoking. Moreover, only in smokers the correlations between adiponectin levels and: the degree of insulin resistance (r = -0.465; p < 0.01) and the levels of HDLC (r = 0.479; p < 0.01) were seen. In summary, in CAD patients, particularly in smokers, occurrence of MTHFR and PON1 risk alleles is associated with the decreased adiponectin levels and/or increased degree of insulin resistance.

Hyponatremia is the most frequently encountered electrolyte disturbance in hospitalized patients. It is usually caused by dysregulation of arginine vasopressin (AVP) homeostasis which accompanies disorders associated with water retention such as congestive heart failure and cirrhosis, or follows euvolemic states such as syndrome of inapprioprate secretion of antidiuretic hormone. Available therapy, i.e. restriction of fluid intake, saline and diuretics, is often ineffective with unpredictable results and potentially serious side effects. Recent clinical trials with non-peptide AVP receptor antagonists (vaptans) have indicated that these drugs are effective in the treatment of hyponatremia. Vaptans lead to aquaresis, an electrolyte-sparing excretion of free water, that results in the correction of serum sodium concentration. Until now the Food and Drug Administration in the USA has approved the use of intravenous conivaptan for treatment of euvolemic hyponatremia. In this article, we review results from recent clinical trials on vaptans (lixivaptan, tolvaptan, conivaptan and satavaptan) which showed their efficacy in the treatment of hyponatremia.

Development of the systolic left ventricular insufficiency in patients with coronary artery disease (CAD) markedly decreases the survival rates, so the factors affecting the clinical status of these patients should be reevaluated. The left ventricular contractile function has been assessed by measurements of the left ventricular ejection fraction (LVEF) values. The studied group of 160 males comprised 102 CAD patients diagnosed by coronarography, and 58 persons without CAD and left ventricular systolic insufficiency. The CAD patients were divided into 2 subgroups according to the LVEF values: 53 patients qualified to have normal left ventricular contractile function (with LVEF > 40%), and 49-patients, with LVEF < or = 40%, were considered as subgroup with the left ventricular contractile insufficiency. In the case-control set up the effects of smoking, concentrations of homocysteine (Hcy) and folic acid (FA) and of the known risk factors of the vascular diseases in the development of the left ventricular contractile insufficiency were assessed. Moreover, analysis was performed of the association between LV insufficiency and the statin therapy and the number of infarcts. LV insufficiency in CAD patients associated with increased diastolic pressure (p = 0.006) and with increased uric acid concentrations in plasma (p = 0.02). The smoking, decrease in HDL-C and increased index TC/HDLC were the risk factors of CAD, independent of the LV insufficiency. In comparison to the CAD patients with the preserved systolic function, in the group of CAD patients with LV systolic insufficiency, more persons had recurrent infarcts (34.7% vs. 5.7%), and less persons had no infarct (8.2% vs. 20.8%, p < 0.05). In CAD patients with LV systolic insufficiency smoking associated with the higher values of HC/FA index (p = 0.01), younger age of the patients (p = 0.01), the number of persons not treated with statins (0.01) and the number of persons not having had heart infarct before (p < 0.05). These findings confirm both the effects of infarcts on the development of LV insufficiency, and the presumed association between the pathogenicity of smoking in LV insufficiency and the unbalanced metabolism of Hcy. The straight of the effect of smoking on the development of LV insufficiency in susceptible persons is shown also by the findings of the younger age of the smoking CAD patients as compared to the nonsmoking patients with LV insufficiency.

Cardiovascular disease is a major cause of morbidity in patients with end-stage renal failure. Arterial stiffness measured by pulse wave velocity (PWV) is an independent risk factor for morbidity in end stage renal failure patients. The aim of our study was to evaluate the arterial stiffness in patients with chronic renal failure. In 20 chronic renal failure patients treated by hemodialysis (HD) we assessed the PWV of the carotic artery as well as artery diameter and distensibility, systolic pressure (SBP), diastolic pressure (DBP), pulse pressure (PP), and basal biochemical parameters and compared them with the values determined in 20 healthy controls of comparable age. PWV and PP are significantly (p < 0.001, p < 0.05) higher and distensibility of the carotic artery was significantly lower (p < 0.001) compared to a control group SBP and DBP were < 140/90 mmHg in HD patients (high normotensive range) but were significantly (p < 0.05) higher than in a control group. In HD patients PP was correlated with arterial distensibility r = -0.600 (p < 0.005), and systolic artery rice r = -0.408 (p < 0.05). SBP was correlated with PP r = 0.689 (p < 0.0007) and with arterial distensibility r = -0.476 (p < 0.03), arterial diameter to systolic artery rice r = -0.463 (p < 0.03), systolic artery rice to arterial distensibility r = 0.885 (p < 0.00001), intima media to arterial distensibility r = 0.815 (p < 0.00001), intima media to arterial compliance r = 0.893 (p < 0.00001). Our results suggest that not only established hypertension but also high normotensive pressure could cause arterial stiffness absened in chronic renal failure patients.

Background: Cardiovascular diseases are the main cause of death in the adult Polish population. Beside lipid disorders and cigarette smoking, hypertension represents the most important risk factor leading to cardiovascular complications. Representative studies conducted in Poland in 1994-2002 showed that in 2002 the number of respondents in the survey who stated they knew their own blood pressure values dropped by 3.5 million, compared with 1994. This decrease was predominantly seen in small towns and in the countryside. Preventive programmes should therefore be addressed mainly to the most vulnerable communities. Modern methods of social marketing may play a substantial role in the creation of a healthy lifestyle., Aim: The aim of the Polish Four Cities Programme (PP4M), conducted in 2000-2001, was to develop the most effective methods of detection of and improvement in treatment for hypertension among the residents of small towns and rural areas. One of the programme tasks was to compare the effectiveness of a standard medical screening intervention with a similar approach combined with the use of social marketing methods.Methods. The programme was conducted by an interdisciplinary team in three small Polish towns -- Kartuzy, Oborniki Wlkp. and Braniewo, as well as in one of the districts of a large city Łódź -- Olechów. Medical intervention combined with social marketing (community intervention) took place in Oborniki Wlkp. whereas the residents of Kartuzy and Łódź were subjected only to the traditional medical intervention. Braniewo served as a control location -- neither medical nor community intervention was implemented. Community intervention with elements of social marketing consisted of a three-month, intensive education and information campaign, initiated four weeks prior to the start of medical intervention. Epidemiological situation was assessed in all the four cities before and after the completion of the preventive interventions (screening), using representative surveys, with the objective to assess the changes in the awareness of one's own blood pressure values, detection of hypertension and knowledge concerning cardiovascular risk factors.Results. In two survey locations -- Kartuzy and Łódź - awareness of one's own blood pressure values after the medical intervention did not significantly change (61% and 67.6% at baseline versus 62.1% and 71.6% after the intervention, respectively). In contrast, social marketing activities conducted in Oborniki significantly increased this parameter from 61.5% to 79.8% (p<0.01). While medical intervention did not change the proportion of non-diagnosed hypertension in a small town (a non-significant decrease from 49% to 45% in Kartuzy), its effect in a large city was clearly visible (a decrease from 46% to 28% in Łódź). In Oborniki Wlkp. (medical intervention combined with social marketing) the effects were the most noticeable -- a reduction from 50% to 27% was achieved. The efficacy of hypertension treatment at baseline was low (4.7% in Kartuzy, 6.6% in Oborniki, and 6.5% in Łódź), but it then improved significantly (a twofold increase in Kartuzy and Oborniki, and more than twofold increase in Łódź). When the target value of blood pressure was set at 160/95 mmHg, the highest efficacy of hypotensive therapy was observed directly after the completion of medical and community intervention in Oborniki (an almost twofold increase in treatment efficacy)., Conclusions: 1. Medical intervention combined with a community intervention and marketing campaign leads to a statistically significant improvement in self-awareness of blood pressure values among residents of small towns. 2. Medical intervention combined with community intervention brings the detection rate of hypertension in small towns up to the level observed in large cities. 3. Medical intervention, especially when combined with community intervention, improves the efficacy of the treatment of hypertension, regardless of the size of agglomeration.

Structural and mechanical properties of the arterial wall are altered in patients with renal failure. Age and hypertension are known to affect the vessel wall structure. Aging process of arterial wall appears to be accelerated in patients with end-stage renal failure. The mechanisms responsible for reduced arterial compliance and distensibility in dialyse patients and renal transplant recipients without hypertension remain to be evaluated. 20 normotensive dialyse patients (D), 20 normotensive renal transplant recipients (T) and 20 healthy volunteers (N) matched for age, sex and blood pressure as controls were enrolled in to the study. Patients with cardiovascular risk factors and diabetes were excluded. The arterial blood pressure of all patients placed below 140/90 mmHg. The dialyse patients and renal transplant recipients were eligible for the study if the serum creatinine level was below 2 mg/dl. In all subjects, fasting concentrations of serum creatinine, total cholesterol, HDL-cholesterol, LDL-cholesterol, hemoglobin and glucose were determined at enrollment to the study. Long-term immunosuppression consisted of cyclosporine and prednisolone. Blood pressure was measured using an automatic sphygmomanometer (Criticon Dinamap model 1846 SX). Pulse wave velocity (PWV) was evaluated using non-invasive automatic Complior device. The vessel wall properties of the left common carotid artery were studied using multigate pulsed Doppler's system (Pie Medical Equipment BV Maastricht, The Netherlands). The frequency of transducer used was 7.5 MHz. With this non-invasive method, the end-diastolic diameter (d) and the systolic increase of vessel diameter (distension delta d) were measured using ECG trigger. From these data relative systolic increase of vessel diameter (delta d/d) and arterial wall distensibility coefficient (DC) were calculated. Simultaneously with the ultrasound measurements at the left common carotid artery carotid pulse waveforms are recorded using applanation tonometry (Micro Tip Pulse Transducer, SPT 301 and Transducer Control Unit TCB-500, Millar Instruments, Houston, TX, USA). Systolic blood pressure (SBP) and central pulse pressure (CPP) were significantly higher in (T) than in (D) and (N) group respectively 139 +/- 18 mmHg and 58 +/- 16 mmHg vs 127 +/- 13 mmHg and 49 +/- 11 mmHg and 132 mmHg and 50 +/- 11 mmHg. The end-diastolic diameter (d) did not change significantly between all groups. The systolic increase of vessel diameter (distension delta d) was significantly lower in patients group (D) and (T) respectively 461 +/- 33 microm and 501 +/- 34 microm than in controls. Similar relative systolic increase of vessel diameter (delta d/d) was in these groups significantly lower than in healthy volunteers, respectively (D) 6.26 +/- 0.5%, (T) 6.91 +/- 0.4% vs (N) 9.14 +/- 0.4%. The distensibility coefficient were also significantly lower in (D) and (T) than in (N) groups respectively (D) 18.31 +/- 1.4 10(-3)/kPa and (T) 17.97 +/- 1.4 10(-3)/kPa and (N) 24.3 +/- 0.5 10(-3)/kPa. PWV in both groups of patients was statistically significant higher than in control group correspondingly (D) 11.2 +/- 1.02 m/s and (T) 12.8 +/- 1.12 m/s, (N) 9.5 +/- 0.88 m/s. There was significant correlation between the change of arterial DC, PWV and CPP in (T) group (n = 20; r = -0.42; p < 0.01 and n = 20; r = 0.47; p < 0.05). The arterial wall elastic properties in dialyse and renal recipients patients are decreased. End-stage renal disease accelerates arterial stiffening despite arteriosclerosis and hypertension. Renal transplantation do not reverse lost of elastic properties of arteries in end-stage renal insufficiency.

Recently many researchers have described the presence of insulin resistance and hyperinsulinemia in a substantial number of patients with essential hypertension. Reduced insulin binding to the receptors may play important role in development of insulin resistance in these patients. The study was aimed to assess the value of insulin binding to erythrocyte receptors in the patients with essential hypertension and compare to values in healthy persons. Additional purpose was the evaluation of insulin degradation by erythrocytes in patients with essential hypertension. 23 patients with essential hypertension (BMI 22.7 +/- 3.2) and 21 healthy persons (with BMI value 23.3 +/- 2.9) were studied. In all examined individuals the blood glucose and blood insulin concentrations were determined, insulin binding to erythrocyte receptors and insulin degradation by erythrocytes were measured by the method of Gambhir and al. Insulin concentration was significantly higher in patients with essential hypertension than in healthy subjects. We demonstrated a statistically significant positive correlation between body weight and insulin concentration in blood serum only in healthy people. Insulin binding to the receptors of red blood cells was significantly stronger (p < 0.001) in healthy persons than in patients with essential hypertension (0.972 +/- 0.395 pg 10(11) RBC and 0.446 +/- 0.14 pg 10(11) RBC respectively). In patients with hypertension insulin binding to receptors of red blood cells does not depend on body weight and insulin concentration in blood serum. Values of insulin degradation by erythrocyte in patients with essential hypertension and healthy persons were not significantly different. It seems that decreased insulin binding to insulin receptors is an important mechanism of insulin resistance patients with essential hypertension.

Calcium antagonists are widely used in therapy of hypertension and angina pectoris. Their advantage is good efficacy, relatively few and not dangerous side effects and first of all lack of bad metabolic effects (hypokalemia, hyperuricemia, hyperinsulinemia and hyperlipoproteinemia). In contrast to beta-blockers and diuretics, which decline mortality from myocardial infarctions and strokes there are not similar information concerning calcium antagonists. Two meta-analysis from 1995 unexpectedly suggest, that some preparations of calcium antagonists increase mortality from myocardial infarctions and strokes. In our paper we discuss possible pathogenetic (harmful) mechanisms, pay attention to each class of calcium antagonists and time of action of the particular drugs. Short acting nifedipine formulation should be withdrawn from chronic hypertension and angina pectoris therapy. Ongoing multicenter trials in several European countries and in USA will decide the usefulness of other calcium antagonists preparations.

Two groups of hypertensive patients: 137 responsive (on one or two drugs) and 162 resistant on antihypertensive treatment in the similar age were compared. Resistant patients (on three or more drugs) characterize by significantly higher body weight and BMI, longer history of hypertension, more frequent hypertension prevalance in family members and lower education. Level of triglycerides in resistant on antihypertensive treatment patients was significantly higher than in responsive patients. Insulin level in blood in 31 patients with essential hypertension was significantly higher than in 36 healthy persons and 20 patients with renovascular hypertension and resistant on antihypertensive therapy. In 14 patients with essential hypertension resistant to treatment insulin level one hour after oral glucose load was significantly (p < 0.01) higher than in 16 patients with essential hypertension responsive to antihypertensive treatment.

Activity of pyrimidine 5'nucleotidase was measured in hemolysate of erythrocytes of healthy persons and patients with essential hypertension. Cytidine 5'monophosphate (CMP) and uridine 5'monophosphate (UMP) were used as the substrates for evaluation of activity of so called I-isoenzyme and uridine 3'monophosphate (U3'MP) was used as a substrate for the II isoenzyme of Py5'Nd. It was found that the activity of Py5'Nd I was lower in hypertensives (26.8 mU/gHb (CMP)) and 69.3 mU/gHb (UMP) in comparison with normotensives (62.3 and 117.4 mU/gHb respectively) (p < 0.05). The activity of Py5'Nd II did not differ between studied groups. Possible metabolic consequences of decreased activity of Py5'Nd are discussed.

The study aimed at evaluating an excretion of beta 2-microglobulin with the urine of hypertensive patients. Thirty patients with mild-to-moderate hypertension (diastolic blood pressure 14.26 +/- 0.86 kPa) and 13 patients with severe hypertension (diastolic blood pressure 17.8 +/- 1.7 kPa) were included into the studies. Significantly increased beta 2-microglobulin excretion with the urine was noted in both groups with the highest values in patients with severe blood hypertension. Moreover, significant correlation between tubular reabsorption of beta 2-microglobulin and diastolic blood pressure was noted in both groups. Increased excretion of beta 2-microglobulin in the arterial hypertension may be due to an increased glomerular filtration of this protein and/or decreased reabsorption in proximal tubule.

Lack of normalization of arterial pressure in spite of treatment of hypertension is most frequently caused by irregular and incomplete taking of hypotensive drugs or by erroneous medical instructions (drug interactions). "True" resistance to 3 simultaneously administered hypotensive drugs in optimal doses may be caused by secondary hypertension. In a part of cases of refractory essential hypertension an increased insulin concentration is found. In the paper the importance is discussed of "resistance" to insulin in the development of hypertension.

Serum uric acid and oxypurines (hypoxanthine and xanthine) renal excretion of uric acid and oxypurines as well as plasma adenosine deaminase activity and AMP deaminase activity were studied in 18 patients with essential hypertension and in 17 healthy subjects. The aim of the study was to evaluate uric acid production rate in essential hypertension. Serum uric acid was significantly higher (7.04 +/- 2.03 mg% = 370.5 +/- 106 mumol/l; p < 0.01) in essential hypertension in comparison with control group (5.2 +/- 1.0 mg% = 275.0 +/- 51.9 mumol/l) and plasma oxypurines were increased insignificantly. Impairment of fractional excretion of uric acid (p < 0.05) was found in patients with essential hypertension. Plasma adenosine deaminase activity and plasma AMP deaminase activity did not differ in the studied groups. Increased production of uric acid does not contribute the incidence of hyperuricemia in essential hypertension. The results suggest that tubular defect of oxypurines excretion similar to that of uric acid exists in patients with essential hypertension.

A case of female patient with non-compensated diabetes mellitus is presented. Pathological bone fractures caused by the diabetic osteoporosis were produced in the relatively short period of time. An emphasis is on the role of pathogenetic factors leading to the diabetic osteoporosis, prevention and treatment of this disease are discussed.

In the paper below are presented the undesirable effects of aluminium in patients with chronic renal failure. Until now aluminum treatment has been used to reduce the level of phosphates in blood serum or in haemodialysis a this group of patients. The toxic activity is a result of cumulation of the element in organism, mainly owing to limited elimination through kidneys, but also as a consequence of disturbed absorption in digestive tract or intravenous infusion of blood serum and albumins. It can be expressed by several clinical syndromes, especially dialysis, encephalopathy, osteomalacia, microcystic++ anaemia, more rarely calcinosis and increased general morbidity and mortality rate. The diagnosis of suspected toxic activity of aluminium in patients with uraemia is based mainly on estimation of concentration of this ion in blood serum and aluminium deposits in skeletal system and skin. The effective treatment consist in intravenous infusions of deferoxamine in a dose 2 g 3 times a week for a long time.

The study aimed at presenting own experience in prevention of new urinary calculi in 18 patients with metabolically active calcium urolithiasis treated with hydrochlorothiazide in daily doses of 100 mg (group I) for 2 years, and in 6 patients with the same disease treated with magnesium oxide in daily doses 300 mg twice a day (group II) for average period of 10 months. In 9 patients a new calculus was formed during the treatment with hydrochlorothiazide, in 7 patients no recurrence was noted, and in 2 remaining patients the results were controversial (coral calculus). Therefore, patients were subdivided into group Ia (failure of hydrochlorothiazide therapy), and group Ib (no recurrence noted). Hydrochlorothiazide did not lead to the stable decrease in the saturation of the urine with calcium oxalate in group Ia whereas in group Ib (without recurrence of urolithiasis) the content of calcium oxalate in the urine was significantly lower than that in group Ia after a 2-year treatment with hydrochlorothiazide (p < 0.01) Recurrence of the disease was seen only in one patient of group II, i.e. treated with magnesium oxide. The treatment of the recurrent calcium urolithiasis is justified and efficient in those patients in whom therapy decreases the content of calcium oxalate in the urine.

The effect of aminophylline administered intravenously in dose 250 mg on plasma oxypurines (hypoxanthine and xanthine) concentration as well as on plasma adenosine deaminase activity and plasma AMP deaminase activity was studied in 17 patients with bronchial asthma or chronic cor pulmonale. Initial plasma oxypurines concentration was 47.5 +/- 10.4 mumol/l and one hour after aminophylline administration decreased significantly (p less than 0.001) to the value 40.3 +/- 8.8 mumol/l. Plasma adenosine deaminase activity increased significantly from 4.74 +/- 2.3 IU to 6.9 +/- 2.77 IU (p less than 0.01), while plasma AMP deaminase activity did not change. The above results suggest indirectly that intravenous administration of aminophylline decreases serum adenosine concentration in studied patients.

The study involved 30 patients treated with nifedipine in daily dose of 30 mg for 7 days. Calcium, magnesium, phosphate, oxalate, and uric acid levels in the urine were measured. It was found that nifedipine significantly decreased oxaluria urinary excretion of calcium, magnesium, phosphate, and uric acid remained unchanged following nifedipine therapy. Results may suggest that nifedipine may exert an influence on renal stone formation.

An effect of cimetidine on parathyroid glands functioning in healthy subjects was evaluated. Serum calcium, phosphate, and magnesium concentrations together with renal excretion++ of these ions in healthy subjects as well as cAMP excretion++ in selected individuals were determined before and following intravenous administration of cimetidine (Altratmet Lek Ljublijana) in total dose of 500 mg (50 mg injected rapidly as a bolus following with 450 mg in an intravenous infusion during 60 minutes). No significant changes in serum calcium, phosphates, and magnesium concentrations were noted. Renal clearance of calcium and magnesium remained unchanged whereas renal phosphate excretion++ increased from 10.69 +/- 4.9 mL/min to 15.1 +/- 5.41 mL/min (p less than 0.02). Excretion++ of 3.5 cAMP increased from 2.65 +/- 2.19 nM/min to 5.16 +/- 2.0 nM/min (p less than 05). The obtained results do not exclude stimulating effect of intravenous cimetidine on parathyroid glands. Cimetidine given intravenously in the bleeding gastric or duodenal ulcers in the course of the primary hyperparathyroidism+ may decrease serum phosphate levels due to increased exretion of this ion with the urine.

Daily excretion of calcium, magnesium, oxalates, and citrates together with daily urine output were determined in 37 patients with calcium urolithiasis and in 25 healthy individuals. Basing on the obtained values, a degree of urine saturation with calcium oxalate with Marshall and Robertson technique and a value of risk factor with Tiselius technique were calculated. It was found that daily diuresis and excretion of calcium with the urine are significantly higher in patients with urolithiasis where as daily excretion of citrates with the urine is significantly lower than in healthy individuals. Risk index proved two-fold higher in the examined patients than in the healthy individuals (p greater than 0.001) while the degree of urine saturation with calcium oxalate did not differ significantly in both groups. The authors, discussing causes of seemingly different changes in both tested parameters, stressed diagnostic value of risk index which includes excretion of crystallization inhibitors (magnesium, citrates) and contrary to the degree of urine saturation is independent of daily urine output.