[Side effects during dobutamine stress echocardiography: analysis of 582 studies]. / Objawy niepozadane echokardiograficznej próby dobutaminowej--analiza 582 badan.

The purpose of the study was to assess the safety, adverse effects and complications of the dobutamine stress echocardiography (ED). 582 patients without previous infarction were prospectively studied with ED. There were 196 female and 368 male, age varied from 27 to 74 years, mean 52. Dobutamine was given in stepwise increasing doses from 5 to 40 mcg/kg/min. Mean maximal dose achieved was 33 mcg/kg/min. Atropine was added in 253 (43%) cases. Significant coronary artery disease was present in 323 patients (53%). There were no death, no myocardial infarction or episodes of sustained ventricular tachycardia as a result of ED. The test was terminated when following conditions were revealed: target heart rate (28.9%), maximal established dose achieved (25.3%), left ventricular asynergy (19.6%), angina pectoris (10.8%), increase of systolic blood pressure above 220 mm Hg (2.6%), hypotension (7.6%), nonsustained ventricular tachycardia (1.7%). The most common non-cardiac side effects were skin tingling (19.8%), atypical chest pain(16.3%), palpitations (13.9%) and headache (7.9%). The most side effects were usually well tolerated, without the need for test cessation. The ED was terminated only in 4 (0.6%) patients because of non-cardiac side effects including nausea (0.3%) and headache (0.3%). We conclude that ED may be safely performed in routine clinical practice. Side effects were rare and usually minor. Most severe ischemic pain was relieved by test interruption and sublingual nitro-glycerine or short acting beta-blocker administration.

[Lovastatin in the treatment of hypercholesterolemia]. / Lowastatyna w leczeniu hipercholesterolemii.

In 9 clinics 177 patients (68 men and 109 women) aged 23-69 years with primary hypercholesterolemia (TC above 6.5 mmol/L) were treated with lovastatin for 12 weeks. The treatment was started with 20 mg daily. The dose was doubled every 4 weeks, if the total serum cholesterol level did not fall below 5.2 mmol/L. For 4 weeks before treatment with lovastatin all patients received placebo. After the first 4 weeks of therapy the mean TC level decreased significantly (from 8.09 mmol/L to 6.54 mmol/L) by 18.5%. In comparison with the results after placebo (the starting value), after the 8 weeks of the therapy the TC level reduction reached 22.4% and after 12 weeks 23.5%. The mean LDL cholesterol decreased by 26.1%, 30.8% and 32.9% after 4.8 and 12 weeks of lovastatin treatment respectively. An increase in HDL cholesterol by 5.9%, 6.0% and 7.6% and decrease in triglyceride level by 10.7%, 14.9% and 14.0% respectively was also observed. In 6 patients on lovastatin treatment symptoms of acute pancreatitis in 1 case, a cataract in 1 case and aggravation of coronary insufficiency in 4 cases were noticed. These symptoms in the light of our knowledge of the mechanism of action of the drug used and of its side effects described in other trials, may be considered of independent on lovastatin. The treatment was discontinued in 5 cases (because of gastrointestinal intolerance in 2 patients, of aggravation of coronary insufficiency in 2 patients and of pain in the right hypochondrium in 1 patient who himself decided to stop the therapy).(ABSTRACT TRUNCATED AT 250 WORDS)

[Effect of lovastatin on platelet function in hypercholesterolemic patients]. / Wplyw lowastatyny na czynnosc plytek krwi u chorych z hipercholesterolemia.

18 patients were studied with primary hypercholesterolemia (type II according to Fredricksen) and fasting cholesterol level during low fat diet above 250 mg/dl. Blood samples were taken: I--before lovastatin administration on diet, II--after 4 weeks administration of 20 mg, III--after 4 weeks of 80 mg and IV--4 weeks after the drug discontinued. The following tests were performed: platelets aggregation induced by ADP and adrenaline, PF3 and PF4, platelet MDA, serum triglycerides, total cholesterol, HDL-cholesterol and LDL-cholesterol. Before treatment patients showed significant platelets hyperaggregation and MDA concentration comparing to the control group. During the drug administration significant lowering of platelets MDA concentration, was observed small but significant HDL cholesterol level increase which correlated with platelet MDA concentration. Availability of PF3 and release of PF4 did not change during study.

[Value of Doppler echocardiography in evaluating pulmonary arterial pressure in patients with mitral valve defect]. / Wartosc badania echokardiograficznego metoda Dopplera w ocenie cisnienia w tetnicy plucnej u chorych z wada mitralna.

In 40 patients aged 25-52 years (mean 36 years) with mitral valve disease but without overt circulatory failure haemodynamic studies and echocardiographic examinations were carried out recording the blood flow in the pulmonary artery and the blood flow through the tricuspid valve by pulsating and continuous-wave methods. From the obtained curves the time was calculated from the beginning of the flow to its maximum (TPV), the pre-ejection time (RPEP) and the right-ventricular ejection time (RVET), and the indices TPV/RVET and RPEP/RVET. Moreover, in 14 patients with coexistent insufficiency of the tricuspid valve the systolic pressure in the pulmonary artery was calculated by determining the systolic gradient across the tricuspid valve. On the basis of the results of haemodynamic examination the patients were divided into two groups: with normal (24 patients) and with raised (16 patients) pressure in the pulmonary artery. In the group of mitral valve disease and pulmonary hypertension a significantly shorter TPV, lower values of the TPV/RVET index and greater values of the RPEP/RVET index were found as compared with the patients with mitral disease and normal value of the systolic arterial pressure in the pulmonary artery. The systolic arterial pressure in the pulmonary artery determined on the basis of Doppler echocardiography with measurement of the regurgitation wave in tricuspid valve insufficiency showed a high agreement (r = 0.94) with the pressure recorded during cardiac catheterization.

[Comparative investigation of cardiac output using impedance rheography and invasive methods]. / Badania porównawcze rzutu minutowego serca metoda reografii impedancyjnej i metodami inwazyjnymi.

Authors performed comparative measurements of cardiac output using the impedance rheography and Fick's method in healthy men (6) reaching the value of correlation coefficient 0.88 and in patients with acquired cardiac defects (n = 21; r = 0.68). Authors also compared cardiac output values measured at rest and during exercise by means of thermodilution and rheographic methods in patients with heart failure (n = 9). Correlation coefficient was respectively 0.92 and 0.81.

gamma-Aminobutyric acid and cholinergic transmission in the guinea-pig ileum.

1. The effects of GABA on release of acetylcholine and on contractility of the smooth muscle were studied in the myenteric plexus-longitudinal muscle preparation of the guinea pig. Acetylcholine was determined as radiolabelled transmitter from strips preloaded with 3H-choline. 2. GABA (1 - 300 microM) caused an increase in resting tension of smooth muscle as well as an increase in release of acetylcholine that was considerably reduced by tetrodotoxin. The facilitation by GABA of acetylcholine release exhibited a marked tachyphylaxis. The increase in muscle tension was clearly related to the increase in acetylcholine release. Muscimol (0.1 - 10 microM) also enhanced the release of acetylcholine. The effects of GABA on acetylcholine release and on longitudinal muscle contraction were competitively antagonized by bicuculline and picrotoxin. 3. GABA (1 - 300 microM) inhibited both release of acetylcholine and contractions evoked by electrical stimulation. Muscimol (1, 10 microM) did not modify the evoked release. The inhibitory effects of GABA were not antagonized by bicuculline or picrotoxin. 4. It is suggested that GABA facilitates and inhibits acetylcholine release, and in turn intestinal motility via two receptors with different pharmacological properties.

The influence of strychnine and glycine on the metabolism of acetylcholine in the rat striatum and hippocampus.

Intracerebroventricular injection of glycine elevated the level and synthesis rate of acetylcholine and the activity of choline acetyltransferase in the striatum. Administration of strychnine alone did not change these parameters, but pretreatment with strychnine abolished the stimulatory effect of glycine on the cholinergic system of the rat striatum. Separate or combined administration of strychnine and glycine did not affect the striatal acetylcholinesterase activity. The drugs did not produce any changes in the cholinergic system indices in the hippocampus.

The effects of intracerebroventricularly applied kainic acid on acetylcholine content and release in rat brain cortex and striatum.

Kainic acid applied intracerebroventricularly at a dose of 0.1 micrograms/rat decreased the ACh level inthe cortex and increased it in the striatum 3 h after the injection. ACh release 3 h from the moment of injection was depressed in both examined structure. 1, 5 and 20 days after injection, ACh level and release were depressed in the striatum.

The effect of intraventricular phenylethylamine and octopamine on the central effects of tremorine and pilocarpine and the acetylcholine level in the rat brain.

Phenylethylamine (PEA, 50 and 100 microgram ivc) and octopamine (OCT, 50 and 250 microgram ivc) potentiated the tremorine (10 mg/kg ip) induced hypothermia in the rat. This effect was partially antagonized by atropine (10 mg/kg ip). PEA and OCT significantly prolonged the duration of pilocarpine (100 mg/kg iv) induced catalepsy in rats. PEA (100 microgram ivc) and OCT (250 microgram ivc) depressed the acetylcholine (ACh) level in the cerebral cortex and striatum but did not affect it in the hippocampus. In addition, these amines enhanced the synthesis of ACh in the cerebral cortex, and PEA also in the rat striatum.

Acetylcholine metabolism in rat cerebral cortex after joint and separate administration of gamma-aminobutyric acid and bicuculline.

Bicuculline (BK) administered into the lateral ventricle (i.v.c.) of Wistar rats in a dose of 10 microgram reduced the level and the intensity of acetylcholine (ACh) synthesis in rat brain cortex. On the other hand, Bk administered in the same way in doses of 1, 5 and 10 microgram decreased the activity of acetylcholine esterase. Gamma-aminobutyric acid (GABA) administered i.v.c. in a dose of 600 microgram increased the level and synthesis of ACh and the activity of choline acetyltransferase in rat cortex. The effects of GABA were abolished, however, by pretreatment with Bk.

Gamma-aminobutyric acid and bicuculline effects on acetylcholine metabolism in the striatum in rats.

Gamma-aminobutyric acid (GABA) injected into the lateral ventricles of rat bran in a dose of 600 microgram raised the level and increased the synthesis of acetylcholine (ACh) raising also the activity of choline acetyltransferase (ChAc) but had no effect on the activity of cholinesterase (AChE) in rat striatum. Bucuculline (Bk) in doses of 10 mirogram i.c.v reduced ACh synthesis and in 50 and 10 microgram doses reduced the activity of ChAc. No Bk effect on AChE activity was demonstrated. The observed effects of GABA were abolished by pretreatment with Bk in doses of 1, 5 or 10 microgram.

Investigations on the effects of certain hormones on acetylcholine metabolism in the central nervous system.

The investigations were carried out on white rats determining the level and synthesis of acetylcholine (ACh) in the cerebral cortex, striatum, and in some experiments also in the brain stem. Thyroxine administered subcutaneously increased ACh synthesis in the cerbral cortex and reduced it in the striatum without changing the level of ACh in these structures. After thyroxine administration in vitro these changes were not observed. Intraperitoneal insulin caused no changes in the level and synthesis of ACh while in vitro ACh synthesis was increased in the cortex as well as striatum after insulin. Glucagon, hydrocortisone, adiuretin and oxytocin had no effect on ACh level and synthesis in the tested structures.

The influence of taurine on acetylcholine content and synthesis in rat brain.

Taurine applied to rats intracerebroventricularly in doses 0.1--3.0 mg increased ACh level and decreased ACh synthesis in the cerebral cortex. In the striatum ACh level was increased after doses of 0.1--3.0 mg and ACh synthesis was decreased after 0.01--3.0 mg. In the hippocampus taurine appeared to decrease both ACh level (0.5--3.0 mg) and synthesis (0.1--3.0 mg). Maximum effects of taurine were observed 30--60 min following the injection. A possible role of taurine as a neurotransmitter or neuromodulator is discussed.

Gamma aminobutyric acid effect on acetylcholine level and metabolism in rat cerebral cortex.

Gamma aminobutyric acid injected into the lateral brain ventricle of white rats in doses of 0.6, 0.8 and 1.6 mg raised the level of acetylcholine and in doses of 0.2, 0.4, 0.6, 0.8 and 1.6 mg increased acetylcholine synthesis. The effects were greatest 15 minutes after injection. Gamma aminobutyric acid injected intraventricularly in doses of 0.6 mg increased the activity of choline acetyltransferase but had no effect on the activity of choline esterase.

The effect of gamma-aminobutyric acid on the content and metabolism of acetylcholine in the rat striatum.

Gamma-aminobutyric acid, 0.6, 0.8 and 1.6 mg/rat, ivc, increased the level of acetylcholine (ACh) in the striatum, and in doses 0.2-1.6 mg/rat ivc, accelerated synthesis of ACh. The former effect commenced 5 min. after the injection, reached its peak 15 min. and declined after 30 min. The ACh synthesis increased 15 and 30 min. after the injection and declined after 60 and 120 min. Gamma-aminobutyric acid increased the activity of choline acetyltransferase but did not affect activity of choline esterase.