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Biomedical subjects

B Beermann

Publications and source records attributed to B Beermann.

At least 37 records · Page 2Linked to original sources
PubMed1991

Skeletal muscle depressed calcium and phosphofructokinase in chronic heart failure are upregulated by captopril--a double-blind, placebo-controlled study.

The effects of the angiotensin converting enzyme inhibitor captopril, after treatment for 5-6 weeks with 25 mg t.i.d., were studied in 12 patients with stable moderate heart failure. Five patients received placebo treatment, and the two groups were comparable at baseline. Angiotensin II levels decreased in response to captopril therapy. Skeletal muscle potassium, magnesium and chloride levels did not differ from reference values. Calcium was subnormal (P less than 0.0001), but increased to the reference range during captopril treatment. Phosphofructokinase, a rate-limiting glycolytic enzyme, was in the lower reference range and increased (P less than 0.04) in response to captopril therapy. In conclusion, stable moderate heart failure is associated with low levels of skeletal muscle calcium and phosphofructokinase activity, these metabolic changes tending to return to normal levels with captopril treatment.

Aged↗
PubMed1990

Intracoronary adenosine causes angina pectoris like pain--an inquiry into the nature of visceral pain.

STUDY OBJECTIVE: The aim was to study the tentative role of adenosine as a messenger between myocardial ischaemia and angina pectoris. DESIGN: Adenosine was administered in serial doses of 0.1-20 mg either as an intravenous bolus, or intra-arterially over 10 s into the left coronary artery, the aorta and the iliac artery. Coronary sinus flow was determined by thermodilution. ECG was monitored continuously. The patient was not aware of which site or dose was used. After each injection, the start of, maximum, end, magnitude, and location of pain were noted. PATIENTS: Six patients with angina pectoris referred for coronary angiography entered the study. MEASUREMENTS AND RESULTS: After intracoronary adenosine injection in the absence of ischaemic ECG changes, a dose dependent degree of chest pain was experienced not different in quality or location from the patients' habitual angina pectoris. Adenosine into the aorta provoked pain in lower chest and upper abdomen, whereas injection into the iliac artery provoked pain in the ipsilateral leg. On intravenous injection equipotent doses of adenosine caused chest pain of the same degree and quality as after intracoronary injection. Immediately after intracoronary injection the coronary sinus blood flow started to increase, but the onset of chest pain was delayed. Onset of pain was earlier the higher the dose, the maximum dose resulting in onset after 18(SEM 2) s. Coronary sinus blood flow increased dose dependently after left coronary artery injection but following intravenous injection no further increase was seen beyond that induced by the lowest dose. CONCLUSIONS: We suggest that adenosine is an important messenger for the sensation of angina pectoris and the effect is not due to coronary steal leading to myocardial ischaemia.

Adenosine↗
PubMed1990

Nicotine enhances angina pectoris-like chest pain and atrioventricular blockade provoked by intravenous bolus of adenosine in healthy volunteers.

An attempt was made to study possible interaction between neuromodulation by adenosine and nicotine stimulatory effects. Dose-effect curves were made double blind in 7 nonsmoking, nonsnuffing healthy volunteers (25-49 years) before and during exposition to nicotine roughly corresponding to the nicotine of one cigarette, 2 mg ingested from a chewing gum (800 chews during 20 min). Chest pain was estimated by the Borg CR-10 scale. ECG was followed, and respiration was recorded continuously by spirometry. Maximal tolerable dose of adenosine was 12.7 +/- 3.0 mg. Chest pain increased dose dependently to 5.7 +/- 1.7 units. Nicotine increased the pain response by 20 +/- 15%, (p less than 0.02). The total time with atrioventricular (AV) block provoked by adenosine increased with nicotine (7 +/- 12%, p less than 0.03) while increased ventilation provoked by adenosine was unaffected by nicotine. In conclusion, interaction between adenosine and nicotine was demonstrated. Nicotine enhanced both stimulatory (chest pain) and inhibitory actions (AV-block) of adenosine.

Adenosine↗
PubMed1989

Adenosine receptor mediated stimulation of ventilation in man.

We wanted to examine how adenosine stimulates ventilation in man. Bolus doses of adenosine were given i.v. in an antebrachial vein in multiples of 2.65 mg. The minute ventilation was increased by adenosine 5.3 to 15.9 mg (median values) from control 12.6 +/- 1.9 l min-1 to 42.5 +/- 4.7 l min-1 in a dose-dependent manner. The adenosine receptor antagonist theophylline, 58.3 +/- 3.3 (mean +/- SEM) mumol l-1 plasma, inhibited the response by approximately 25%. Dipyridamole 10 mg, an adenosine uptake blocker, enhanced the effect of adenosine by approximately 60%. The ventilation was not affected by metoprolol, atropine, naloxone or cromolyn sodium but was attenuated by hyperventilation. The respiratory stimulation started before chest pain and cardiovascular effects such as AV-block were encountered. It is concluded that this respiratory stimulation shows characteristics of adenosine receptor mediated responses but the location of such adenosine receptors is uncertain. The findings are compatible with a stimulatory or facilitating effect of adenosine on afferent pathways.

Adenosine↗
PubMed1988

Pharmacokinetics of lisinopril.

The angiotensin-converting enzyme inhibitor, lisinopril, has an oral bioavailability of 25 percent +/- 4 percent, which is unaffected by food. The accumulation half-life averages 12.6 hours despite a terminal serum half-life of approximately 40 hours. Steady state is attained after two daily doses (every 24 hours) in healthy volunteers. The drug is not metabolized but is eliminated via the kidneys. Lisinopril probably undergoes glomerular filtration, tubular secretion, and tubular reabsorption. There is no pharmacokinetic interaction between lisinopril and furosemide.

Administration, Oral↗
PubMed1988

Increased nonrenal clearance and increased diuretic efficiency of furosemide in cystic fibrosis.

The pharmacokinetics of furosemide and its diuretic effect were studied in six patients with cystic fibrosis (CF) and in six age-matched healthy volunteers. Furosemide was given intravenously at a dose of approximately 0.5 mg/kg. Renal excretion of furosemide was decreased in CF because nonrenal clearance was more than twice as high as in controls (p = 0.03). Nonrenal clearance correlated with the volume of distribution (r2 = 0.52, p = 0.01), which makes a difference in the distribution and binding determinants for clearance. Another reason for increased nonrenal clearance could be induction of drug metabolism in CF, but the excretion of furosemide conjugate did not differ significantly between the groups. Although 26% less furosemide was excreted in CF than in controls (p = 0.03), the diuretic response (calculated as excretion of water and electrolytes) did not differ. Thus the diuretic efficiency was higher in CF for Na+ (p = 0.02), Cl- (p = 0.01), K+ (p = 0.07), and volume (p = 0.005). This difference is probably secondary to the different rates of delivery of furosemide into urine.

Adolescent↗
PubMed1988

Provocation of chest pain in patients with coronary insufficiency using the vasodilator adenosine.

Chest pain provoked by intravenous injection of adenosine was compared with natural angina pectoris in five patients with ischaemic heart disease. In seven healthy subjects a possible myocardial site for provocation of the chest pain was evaluated by analysis of time delays from injection to symptoms. The healthy volunteers were given the maximum tolerable dose of adenosine intravenously, together with 99Technetium-diethylentriaminpentaacetate (99Tcm-DTPA). Chest pain started after 4.1 +/- 2.4 s and reached its maximum 8.4 +/- 4.1 s after maximum left ventricular radioactivity. The patients with a history of typical angina pectoris were given similar doses of intravenous adenosine and the provoked chest pain did not differ in quality from the patients' habitual angina pectoris. The patients did not develop electrocardiographic signs suggesting myocardial ischaemia. Heart rate and blood pressure did not indicate increased myocardial work. In conclusion, the results concur with the hypothesis that adenosine elicits angina pectoris by stimulation of intracardiac adenosine receptors.

Adenosine↗
PubMed1988

Dose-effect relationship of adenosine provoked angina pectoris-like pain--a study of the psychophysical power function.

In an analysis of the psychophysical power function of chest pain induced by adenosine, this agent was repeatedly given in increasing doses into a peripheral vein to six healthy volunteers (five men) aged 23-44 years. On the first day the maximum tolerable dose was determined. On the second day seven doses of adenosine (20, 30, 40, 50, 60, 80 and 100% of the maximum dose) were given single blind in randomized order followed by another seven doses in reversed order. The heart rate was calculated from electrocardiographic recordings. Chest pain was continuously rated according to the CR-10 scale. Before the adenosine test, the perception of sourness was tested similarly with six concentrations of citric acid (1-100 mM). The psychophysical power functions were similar for the perception of sourness provoked by citric acid and chest pain provoked by adenosine, with exponents of 0.69 +/- 0.21 and 0.60 +/- 0.32, respectively. The two modalities showed the same high goodness of fit to the power function (rxy being 0.965 +/- 0.030 and 0.967 +/- 0.033, respectively). For adenosine the group mean relation was R = 1.66(S-2.36)0.6, rxy = 0.999. No signs of tolerance were observed for the chest pain provoked by adenosine. In conclusion, chest pain provoked by adenosine follows a psychophysical power function as with other sensory modalities.

Adenosine↗
PubMed1987

Non-linear elimination and protein binding of probenecid.

Six healthy volunteers were given probenecid 0.5, 1 and 2 g p.o. and 0.5 g i.v. The protein binding of probenecid at different concentrations in human plasma was estimated by equilibrium dialysis. The free fraction was found to increase nonlinearly with increasing total probenecid concentration, up to a maximum free fraction of 26%. The plasma concentration-time data after the oral doses were described by a one-compartment open model with first-order absorption and Michaelis-Menten elimination. The mean absorption rate constant 0.0072 min-1 was dose-independent, and the maximal rate of elimination (mean 1429 micrograms/min) did not differ between doses whether calculated from the total or free concentrations. The Michaelis-Menten constant constant decreased significantly from 67.1 to 55.5 micrograms/ml as the dose increased from 1 g to 2 g, while the unbound Michaelis-Menten constant remained unchanged. The elimination of probenecid after the 0.5 g dose was in the linear region of the Michaelis-Menten elimination when calculated from the total and the free concentrations. The volume of distribution increased only slightly from 9.5 to 11.41 as the dose increased from 0.5 to 2 g, but the unbound volume of distribution decreased significantly from 164 to 99 1. Absorption was complete and was independent of the dose administered.

Absorption↗
PubMed1987

Renal function and tubular transport effects of sulindac and naproxen in chronic heart failure.

Renal function and excretion of water, salt, and the prostacyclin hydration product (6-keto-PGF1 alpha) were evaluated in 10 furosemide-treated patients with well-controlled congestive heart failure. Four doses of sulindac (200 mg b.i.d.) and naproxen (500 mg b.i.d.) were given every 12 hours in a double-blind crossover design. Naproxen significantly decreased the urinary excretion of water (19%), sodium (26%), chloride (26%), and 6-keto PGF1 alpha (76%) and decreased osmolal clearance (18%). No significant changes in these functions were observed in the patients receiving sulindac. Plasma renin activity, plasma aldosterone, freewater clearance, or clearance of furosemide did not change significantly with either treatment. Although the basal glomerular filtration rate (GFR) and renal plasma flow (RPF) were reduced, these patients with cardiac disease, with normal serum sodium concentration, did not have any further reduction of GFR or RPF despite naproxen-induced inhibition of renal prostacyclin synthesis. It is concluded that renal prostaglandins contribute to the natriuretic effect of oral furosemide in patients with compensated congestive heart failure. In this clinical setting, GFR and RPF are not critically dependent on intact renal PGI2 synthesis. The lack of effect on renal prostaglandin synthesis and the renal response to oral furosemide supports the concept of a renal sparing effect of sulindac.

Aged↗