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Biomedical subjects

J Petrtýl

Publications and source records attributed to J Petrtýl.

At least 19 recordsLinked to original sources
PubMed1991

[The effect of diltiazem on hemodynamic parameters in patients with liver cirrhosis].

Previous investigations of authors abroad provided evidence of a reduction of portal pressure by blockers of slow calcium channels group II by verapamil. We decided to investigate the effect of a quite new preparation dilthiazem on the portal haemodynamics in patients with compensated cirrhosis of the liver and oesophageal varices. Doppler examinations of the width, rate of blood flow and flow through the trunk of the portal vein did not prove a statistically significant effect of dilthiazem on the investigated parameters. After the preparation a significant decline of the median pressure in the pulmonary artery was recorded at the 5% level of significance. The significantly elevated pressure values in the wedged position in the hepatic vein (WHVP) as well as of the portohepatic gradient (P-H) rose further after administration of the preparation (WHVP by 12.3%, p P-H by 15%). Even maximum doses of dilthiazem did not influence the portal flow in patients and did not lead to a reduction of the portohepatic gradient. From the results it is apparent that dilthiazem is not suitable for the treatment of portal hypertension.

Diltiazem↗
PubMed1991

[The effect of glucagon on portal hemodynamics in patients with liver cirrhosis].

The authors assessed in 12 patients with compensated cirrhosis of the liver, portal hypertension and oesophageal varices, using a Doppler flowmeter Toshiba SAL 50A/SDL 01 under basal conditions, changes in the width, rate of blood flow and blood flow though the trunk of the portal vein before and after intravenous administration of 1 mg glucagon. The width of the trunk of the portal vein did not change significantly during assessment. A statistically significantly increased flow through the portal vein was recorded starting during the 5th minute, and it correlated with the increased velocity of the blood flow. The increased flow persisted to the 20th minute after glucagon administration. The drop of pressure in a wedged position assessed in the hepatic veins after administration of the drug was not significant, the pressure in the free hepatic vein increased insignificantly. On the whole the portohepatic gradient declined by 10.5%, the drop was not significant. Glucagon in pharmacological doses has an early onset of action even in cirrhotic subjects whereby the increased flow through the portal vein does not lead to a rise of the portohepatic gradient. Glucagon administration thus does not increase the risk of haemorrhage from oesophageal varices during acute fibroscopy of the oesophagus and stomach in patients with portal hypertension.

Blood Flow Velocity↗
PubMed1991

[Endoscopic sclerotization of esophageal varices and nitrates in the treatment of portal hypertension with bleeding esophageal varices].

The authors investigated changes of some haemodynamic parameters after sclerotization of oesophageal varices and after administration of isosorbide dinitrate in the preparation Iso Mack retard. Twenty patients with cirrhosis of the liver with oesophageal varices grade 3-4 were treated by endoscopic sclerotization only, while to a second comparable group of cirrhotic patients from the first stage of sclerotization oral Iso Mack retard was administered in daily doses of 80-120 mg, depending on tolerance. The haemodynamic parameters were investigated before the onset of treatment and again after completed sclerotherapy or at least three-month treatment with ISDN. After sclerotization of oesophageal varices the pressure in the portal circulation rises significantly as well as the flow through the portal vein due above all to an accelerated blood flow. On the other hand, ISDN prevents a rise of portal hypertension and leads even to a slight decline which is, however, not associated with a decline of the portal flow. A relative disadvantage is the adverse effect on systemic haemodynamics after large nitrate doses. The decline of the portal pressure caused by the vasodilatating effect of ISDN in the splanchnic and portal area is manifested in a very positive way by reduction of relapses of haemorrhage from oesophageal varices. ISDN may play a positive role in the treatment of portal hypertension with oesophageal varices, during acute haemorrhage as well as in the prevention of relapses of haemorrhage. A particularly favourable procedure is the combination with sclerotherapy of oesophageal varices. None of the procedures leads to reduction of the portal flow and preserves hepatic function.

Blood Pressure↗
PubMed1991

[Distal renal tubular acidosis in patients with Wilson's disease].

Renal affection is part of the clinical picture of developed Wilson's disease. The most frequent sign of affection of the distal nephron is distal tubular acidosis (DRTA), more frequently its latent form with a normal systemic pH, but inability to reduce the urinary pH below 5.5 after an acid load. More detailed assessment of the type of this disorder was not made so far. To elucidate in greater detail the pathogenesis of DRTA in Wilson's disease the authors examined renal acidification in 13 patients with bioptically verified Wilson's disease, using three acidification tests: 1) the test involving oral administration of calcium chloride (CaCl2), 2) the test involving infusion of sodium sulphate (Na2SO4) and 3) the test using an infusion of NaHCO3. In none of the examined patients with Wilson's disease manifest (complete) DRTA was found with systemic acidosis, however, in five patients latent (incomplete) DRTA was revealed, i.e. after administration of CaCl2 the pH of urine did not decline below 5.5. Patients with Wilson's disease and DRTA differed from patients with Wilson's disease and normal renal acidification by the age at the time of assessment of the diagnosis (30.4 +/- 3.6 vs. 20.75 +/- 2.14 years, p less than 0.02) and the duration of the disease (i.e. the time from assessment of the diagnosis to the acidification examination: 4.6 +/- 4.86 vs. 15.38 +/- 2.40 years, p less than 0.01). In three of four patients with Wilson's disease and DRTA who were given Na2SO4, after its administration the pH of urine did not decline below 5.2.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed1991

[Hypertension in patients with polycystic kidneys--the effect of volume expansion].

Arterial hypertension is found in as many as 75% patients with autosomal dominant polycystic kidneys with normal renal function, its pathogenesis is however not quite clear so far. The authors examined 16 patients with polycystic kidneys with normal or only slightly reduced renal function (plasma creatinine lower than 140 umol/l), 8 of these patients were normotonic (N) and 8 hypertonic (H). In all examined subjects right-sided cardiac catheterization was performed with assessment of the minute cardiac volume by thermodilution. To all patients in the course of one hour 1500 ml saline per 70 kg body weight were administered and the haemodynamic examinations were repeated after termination of the infusion. In all subjects before and after expansion the plasma renin activity was assessed (PRA), as well as plasma aldosterone (PA), plasma catecholamines (PC) and the atrial natriuretic factor (ANF), the renal blood flow and glomerular filtration by means of clearance and extraction of PAH and inulin clearance. The authors did not find differences in plasma concentrations, cardiac output and splanchnic and renal ANF extraction in groups N and H, nor in PRA, PA and PC. Volume expansion led in both groups to a comparable rise of ANF and suppression of PRA and PA. Group H did not differ from group N in any of the investigated haemodynamic and renal parameters except for systemic vascular resistance. In hypertensive patients before expansion a close correlation was found between pressure in the pulmonary artery in a wedged position and diuresis (r = 0.935, p less than 0.01) and natriuresis (r = 0.895, p less than 0.01). The volume expansion was in both groups associated with a comparable rise of diuresis, the haemodynamic response of patients N and H was however quite different. While in patients of group N a decline of the systemic vascular resistance occurred as well as an increase of the minute volume without a change of the renal flow and glomerular filtration, in hypertonic patients the systemic vascular resistance and minute volume did not change but there was a significant rise of the renal flow and glomerular filtration. The relationship of diuresis and natriuresis of hypertensive patients with polycystic kidneys to volume parameters and the rise of the renal perfusion pressure during volume expansion indicates the importance of pressure natriuresis for ensuring the sodium and volume homeostasis in these patients.

Humans↗
PubMed1990

[Distal renal tubular acidosis in primary biliary cirrhosis].

5 patients with primary biliary cirrhosis (PBC), 9 patients with compensated hepatic cirrhosis of different etiology and 12 control persons were tested for renal acidification after peroral CaCl2 administration and urine Na2SO4 and pCO2 infusion as well as the gradient between partial urine pressure and blood pressure after NaHCO3 application. Distal renal tubular acidosis (DRTA) was diagnosed in one patient with PBC, latent DRTA in other 2 patients with PBC. Not even one patient's acidification disorder was eliminated through an increased sodium application to the acidification site after Na2SO4 application. After NaHCO3 application, the gradient between the CO2 partial pressure in the urine and blood in both patients with PBC was, however, latent, DRTA normal. After pH gradient elimination in patients with PBC and DRTA, the hydrogen iont secretion is thus comparable with the control persons. Based on this study, the authors believe that the gradient type of DRTA is characteristic of primary biliary cirrhosis.

Acidosis, Renal Tubular↗
PubMed1990

[Pharmacokinetics and pharmacodynamics of furosemide in liver cirrhosis].

12 patients with cirrhosis of the liver (6 with ascites) and 6 control persons were given 80 mg furosemide intravenously and were followed up for pharmacokinetic, renal and haemodynamic effects. The patients with ascitic cirrhosis (AC) and the control persons were found to have the same plasma furosemide concentrations; however, the AC patients excreted significantly less furosemide into the urine in an 8-hour period than the control persons, which was due especially to lower urine furosemide excretion during the first hour after application in comparison with the control group (75 +/- 6.8 vs. 100.8 +/- 8.8 mumol/h, p less than 0.05). During the first post-furosemide hour, the AC patients had a significantly lower diuresis (13.3 +/- 2.4 vs. 23.9 +/- 1.1 ml/min, p less than 0.01) as well as natriuresis (1367.4 +/- 771.4 vs. 3242 +/- 137.5 mumol/min, p less than 0.01) than the control group and a significantly lower excretion fraction of sodium than the patients with live cirrhosis without ascites (6.5 +/- 0.8 vs. 10.7 +/- 1.5%, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Furosemide↗
PubMed1990

[The effect of dopamine on hemodynamic and hormonal parameters in liver cirrhosis].

To 11 patients with liver cirrhosis (5 with ascites) and 6 controls a one-hour dopamine infusion, 1.5 micrograms/kg/min., was administered. In all before administration of the infusion catheterization of the hepatic veins and lesser circulation was performed with concurrent assessment of the cardiac minute volume by thermodilution, and haemodynamic measurements were repeated also after the dopamine infusion. Before the dopamine administration and after termination of the infusion the plasma renin activity was assessed (PRA), plasma aldosterone, the atrial natriuretic factor (ANF), prolactin and in some patients also plasma catecholamines. Dopamine administration was not associated with an increase of the cardiac output, heart rate or peripheral resistance; the infusion had only purely dopaminergic effects. Plasma prolactin declined after dopamine administration significantly in controls (from 29.17 +/- 7.01 to 11.83 +/- 3.22, p less than 0.05, in patients with liver cirrhosis without ascites) from 18.16 +/- 2.44 to 8.64 +/- 2.01, p less than 0.01) in patients with ascites liver cirrhosis (from 23.5 +/- 9.3 to 15.2 +/- 7.47, p less than 0.05). In the controls after the dopamine infusion PRA suppression occurred (from 2.37 +/- 0.81 to 0.9 +/- 0.27, p less than 0.05), while in patients with compensated liver cirrhosis (from 0.97 +/- 0.41 to 0.85 +/- 0.34, n.s.) and in patients with decompensated liver cirrhosis the PRA did not change significantly either (from 4.56 +/- 1.67 to 5.065 +/- 2.29, n. s.). After the dopamine infusion in none of the investigated patient groups changes of plasma aldosterone and ANF were recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗
PubMed1990

[Atrial natriuretic factor in liver cirrhosis. Relation to hemodynamic parameters].

In 12 patients with cirrhosis of the liver (six with ascites) and six controls the authors made catheterizations of the hepatic veins and portal circulation, assessing concurrently the in cardiac output by thermodilution. The patients with ascitic cirrhosis had, as compared with controls, a significantly higher portohepatic gradient, central venous pressure, mean pressure in the pulmonary artery and also pulmonary capillary wedged pressure and a significantly lower mean arterial pressure and systemic vascular resistance. These patients had also, as compared with controls, a significantly higher concentration of ANF (atrial natriuretic factor) in the pulmonary artery (15.89 +/- 2.26 vs. 8.04 +/- 0.97, p less than 0.01) and in the hepatic vein (7.44 +/- 0.44 vs. 3.91 +/- 0.63, p less than 0.01); the difference between ANF concentrations in the peripheral blood stream was not significant (9.52 +/- 2.46 vs. 5.71 +/- 1.24 n. s.). Patients with ascitic cirrhosis of the liver had a significantly higher calculated cardiac production of ANF than controls (24.36 +/- 3.44 vs. 8.12 +/- 2.9, p less than 0.01); the difference in the splanchnic extraction of ANF between patients with ascitic cirrhosis of the liver (0.46 +/- 0.1) and controls (0.51 +/- 0.06) was not significant. The ANF concentration in the pulmonary artery in patients with cirrhosis of the liver correlated significantly with the central venous pressure (r = 0.677, p = 0.02) and the pressure in the pulmonary artery in a wedged position (r = 0.639, p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1989

[The significance of clinical findings in evaluating the degree of portal hypertension in patients with liver cirrhosis].

In 21 patients with bioptically confirmed cirrhosis of the liver catheterization of the lesser circulation and hepatic veins was performed. The portohepatic gradient was considered a measure of the portal pressure. The authors did not find a statistically significant relationship between the portohepatic gradient and the presence of oesophageal varices, haemorrhage into the gastrointestinal tract, biochemical parameters (albumin, gamma-globulin and bilirubin level) and the prothrombin time. The portohepatic gradient was not significantly related with the central venous pressure, the median pressure in the pulmonary artery and the pressure in the wedged pulmonary capillaries. It was, however, significantly higher in patients with ascites (p less than 0.05); patients in group B and C of Child-Turcott's classification had a portal gradient which was significantly higher than in patients of group A (p less than 0.01). The value of the cardiac index and the systemic vascular resistance was not related to values of the portohepatic gradient; a hyperkinetic circulation which a cardiac index above 4.5 l/min/m2 was recorded only in three patients. Based on the above results, the authors assume that a hyperkinetic circulation in patients of groups A and B according to Child-Turcott's classification is not a frequent finding and is not related to the value of the portal pressure. In the author's opinion the most suitable clinical indicator of the degree of portal hypertension is Child-Turcott's classification.

Adult↗
PubMed1989

[The effect of terlipressin (Remestyp Spofa) on hemodynamic parameters in patients with portal hypertension associated with liver cirrhosis].

Remestyp Spofa is used in wide clinical practice, among others also in the comprehensive treatment of acute haemorrhage from oesophageal varices. To patients with portal hypertension, oesophageal varices associated with cirrhosis of the liver by means of an infusion pump Remestyp was administered, 13.4 micrograms/1 kg body weight for one hour. By means of a Doppler flowmeter the rate of the blood flow and the blood flow through the trunk of the portal vein was assessed before, at 10-minute intervals during infusion, and during the 90th, 120th and 150th minute. After administration of the drug no significant effect on the investigated parameters was recorded. Therefore in the same group of patients by means of a catheter before and after infusion the following parameters were assessed: central venous pressure, pressure in the pulmonary artery, cardiac minute output, pressure in the free and wedged hepatic vein. Simultaneously changes of the systemic blood pressure were investigated. After Remestyp a significant rise of the systemic blood pressure was recorded, a rise of the central venous pressure and the pressure in the pulmonary artery. The minute volume declined slightly. The pressure in the free and wedged hepatic vein rose. The authors assume therefore that the direct effect of Remestyp on the portal circulation is not haemodynamically significant. The favourable haemostyptic action of Remestyp in patients with haemorrhage from oesophageal varices is rather due to an increased tonus of the oesophageal sphincters. With regard to the very satisfactory experience with the administration of nitrates in this indication their combined administration with vasopressin or its derivatives is considered.(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamics↗
PubMed1989

[Reaction of the cardiovascular and humoral system to acute hypervolemia in patients with liver cirrhosis].

The results of the study showed that the cardiovascular system of patients with hepatic cirrhosis and ascites tolerate acute hypervolemia better than patients with hepatic cirrhosis without ascites. It can be explained by a rapid transfer of surplus liquid into the abdominal cavity. Further, it was found that the low cardiac output at rest in patients with hepatic cirrhosis evidently indicated a latent cardiac insufficiency becoming manifest only after the volume exertion. In our control group, jaundice produced bradycardia and hypotension without cardiodepressive effects. Patients with cirrhosis and with or without ascites responded to furosemide probably associated with the elution of vasoconstrictive substances in the same way as the control group. Following acute volume expansion, no differences were found between the compensated and decompensated cirrhotic patients and the healthy control group, not even in the natriuretic hormone of the secretion. However, the relevant organs of each control group had a varied response to the elevated plasma level of natriuretic factor.

Adult↗
PubMed1989

[Repeated ergometric loading].

The action of cardioactive substances is tested by repeated ergometric loads. The aim of the present work was to assess whether after previous loads in the organism certain adaptational changes persist, cardiovascular, respiratory or metabolic, which might influence the course of a subsequent load. The authors exposed therefore two groups of patients to identical loads after 2- or 24-hour intervals and investigated the behaviour of some spiroergometric indicators. From the results ensued that a load repeated after 2-hour intervals takes place under different conditions. In this participates probably the increase of the a-v difference for oxygen and to a smaller extent also adaptation of the respiratory system. Loads repeated after 24-hour intervals were comparable.

Adaptation, Physiological↗