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PubMed1981

[Thrombolytic therapy in a case of mitral valve thrombosis (author's transl)].

In this paper we present a case in which thrombolytic treatment with Streptokinase was successful in a 53-year-old patient, who developed valve thrombosis one year after aortic and mitral-valve replacement by Björk-Shiley tilding-disk-valve prosthesis. The patient suffered from pulmonary congestion and cardiogenic shock. In spite of Arterenol infusion the blood pressure fell down to 90/50 mm Hg. The systolic pulmonary artery-pressure rose up to 120 mm Hg, the cardiac output was 1.8 l/min. The patient became anuric. A transport to the next department of cardiovascular surgery was impossible. In this extraordinary critical situation for the patient we introduced a thrombolytic therapy with Streptokinase. Within a few hours, the systolic pulmonary artery-pressure fell down by 33%, the cardiac output increased by 100%. One and half days later the patient did not need Arterenol infusion and the blood pressure was 120/80 mm Hg. Referring to this observation, we conclude that Streptokinase therapy can be a successful emergency-treatment of a life-threatening artificial heart-valve thrombosis, if surgical treatment is impossible.

Female↗

PubMed1995

A possible nonspecific site of action of amiodarone on newborn rat heart cell in culture.

Amiodarone and its major metabolite desethylamiodarone are potent antiarrhythmic drugs that have multiple pharmacological effects on the heart. We examined the effect of both drugs on the neonatal rat heart monolayer cell culture. The cells were stimulated with L-arterenol (10(-7) M) and choleratoxin (1.5 micrograms/ml). Both the spontaneous pulsation rate and intracellular cAMP level were followed. Amiodarone (10(-7) M) or desethylamiodarone (10(-7) M), incorporated into phosphatidylcholine vesicles, decreased the stimulated cell pulsation rate 3 min after addition of drugs, and the level of intracellular cAMP 30 min after addition as well. Propranolol (10(-7) M) had no further effect on the pulsation rate after 3 min. In the presence of amiodarone and propranolol the stimulation of L-arterenol was completely abolished and both the pulsation rate and cAMP level proved to be lower than the control values. The stimulation of choleratoxin on pulsation rate was also decreased by addition of amiodarone and the cAMP level was lowered after 30 min as well. Desethylamiodarone exhibited similar behavior to amiodarone although it proved to be less effective. It is unlikely that amiodarone and desethylamiodarone act on beta-adrenergic receptors in a competitive manner. Our data suggests that amiodarone and its metabolite could act in a nonspecific manner perturbing the hydrophobic interaction in the cell membrane and thereby decoupling the receptor or the nucleotide regulator protein and adenylate cyclase.

Amiodarone↗

PubMed1979

Chromosome analysis of primary large bowel tumors: a new method for improving the yield of analyzable metaphases.

Colon tumors were processed immediately after surgical resection. Using L-Arterenol and sodium citrate in combination with standard chromosome culture techniques, 12 of 17 consecutive tumors (75%) had countable figures ranging from 5 cells to 59 cells. Seven of the 12 cases had over 25 countable cells. Chromosome counts did not vary more than +/- 4 for any one case. Seven tumors were karyotyped, 6 with banding techniques. One of these specimens had mosaic patterns. The chromosome counts varied: 2 were hypodiploid; 1 was pseudodiploid and 4 were hyperdyploid. There were some similarities in the karotypes although no identical karyotypes were seen in this series.

Adenocarcinoma↗

PubMed2004

Enantioseparation using sulfated cyclosophoraoses as a novel chiral additive in capillary electrophoresis.

Highly sulfated cyclosophoraoses (HS-Cys) were synthesized by the chemical modification of a family of neutral cyclosophoraoses isolated from Rhizobium leguminosarum bv. trifolii. The HS-Cys were then analytically characterized using Fourier transform-infrared spectroscopy and elemental analysis. These HS-Cys were successfully used as a novel chiral additive, in low-pH aqueous background electrolytes, for capillary electrophoretic separation of five basic chiral drugs such as arterenol, atenolol, isoproterenol, propranolol, and metoprolol.

Atenolol↗

PubMedDate not supplied

Bitolterol mesylate: a beta-adrenergic agent. Chemistry, pharmacokinetics, pharmacodynamics, adverse effects and clinical efficacy in asthma.

Bitolterol, (3-4 diester colterol) is a new beta 2-adrenergic agonist. Since it in itself is biologically inactive, bitolterol is considered a pro-drug. When administered it is activated within the lung by esterase hydrolysis to the active compound colterol catecholamine N-t-butyl-arterenol). In preclinical and clinical studies to date, bitolterol has proved to be an effective bronchodilator for adult and pediatric patients with chronic stable asthma and for some with chronic obstructive pulmonary disease. Bitolterol has been compared with other beta 2 agents, including isoproterenol, metaproterenol and albuterol. There is no evidence for cardiotoxicity when bitolterol is used in combination with theophylline in human studies. It is effective for control of exercise-induced asthma.

Animals↗

PubMed1996

Characterization and hemodynamic implications of renal vascular angiotensin II receptors in SHR.

The intrarenal renin-angiotensin system (RAS) contributes to the increased renal vascular resistance and reactivity observed in spontaneously hypertensive rats (SHR) and to the pathogenesis of high blood pressure (BP). Thus, we decided to characterize angiotensin II (ANG II) receptors in the renal arteries and glomeruli of 16-week-old SHR and their age-matched, normotensive Wistar-Kyoto (WKY) controls. SHR had significantly higher BP (153 +/- 4 v 96 +/- 10 mmHg) and heart weight (440 +/- 5 v 327 +/- 4 g/100 g body weight) than WKY rats. There was no difference in plasma renin activity between strains. Radioligand binding assays using non-peptide antagonists for AT1 (losartan) and AT2 (PD 123319) showed that renal preglomerular microvessels and glomeruli expressed a single receptor population (AT1) for ANG II. AT1 density tended to be lower in glomeruli of SHR compared to WKY (377 +/- 45 v 555 +/- 74 fmol/mg protein), but was significantly higher in preglomerular vessels (93 +/- 7 v 57 +/- 1 fmol/mg protein). No difference in receptor affinity was found in either preparation. Isolated kidney perfusion revealed that at low flow (3-10 ml/min), perfusion pressure was similar in both strains; however, at higher flow levels, SHR showed higher reactivity and less compliance than their controls. In addition, SHR presented a higher renal vascular reactivity to ANG II (but not to arterenol) than WKY rats. Thus, upregulation of ANG II receptors in the renal vasculature may mediate the hyperreactivity to ANG II observed in SHR kidney.

Angiotensin II↗

PubMed1991

The effect of adrenergic agonists and antagonists on cysteine-proteinase inhibitor (cystatin) in rat saliva.

The effect of a number of adrenergic agonists and antagonists on the induction of rat salivary cystatin was investigated. A highly sensitive and specific radioimmunoassay was used to determine cystatin in rat whole saliva. Treatment for 10 consecutive days with a non-specific beta-adrenergic agonist isoproterenol, or the beta 1-adrenergic agonists dobutamine or methoxyphenamine, resulted in the induction of the salivary cystatin. Induction was also found in rats treated for 10 days with arterenol. Only trace quantities of cystatin could be detected in saliva of rats treated with the beta 2-adrenergic agonists terbutaline or salbutamol. When isoproterenol was injected concomitantly with the mixed beta-antagonist propranolol or the beta 1-adrenergic antagonists metaprolol, proctocol or atenolol the production of cystatin was totally suppressed. However, the beta 2-antagonist, ICI 118551, produced only a partial reduction in salivary cystatin induction elicited by isoproterenol. The findings suggest that the induction of salivary cystatin is regulated, in part, by beta 1-adrenergic receptor stimulation.

Adrenergic beta-Agonists↗

PubMed1994

In vitro regulation of lipogenesis in turkey liver explants.

A mechanical tissue chopper was used to obtain liver explants (35-75 mg) from 2-3-week old turkeys to determine both tissue sensitivity and metabolic effects of adrenergic agonists (isoproterenol, propranolol, norepinephrine and phenoxybenzamine). A previously noted catecholamine induced decrease in in vitro lipogenesis in chicken liver explants was also noted in turkey liver explants. Thus, one set of control points for in vitro regulation is under control of the cAMP system. Preincubation of slices (1 hr) with propranolol blocked the inhibition of lipogenesis caused by alpha and beta-adrenergic agonists (arterenol or isoproterenol) during a subsequent 1-hr incubation. Preincubation of slices with either of these agonists decreased lipogenesis even following an extensive washout. Inhibition could be overcome with propranolol, a beta adrenergic antagonist.

Animals↗

PubMed2003

Beta-adrenergic receptor agonists and antagonists counteract LPS-induced neuronal death in retinal cultures by different mechanisms.

Treatment with lipopolysaccharide (LPS) for 72 h was shown to dose-dependently increase nitric oxide production from 6-day-old retinal cultures. Cell death, as determined by lactate dehydrogenase (LDH) release and an increase in neuronal labelling for TUNEL, was elevated concurrently. During treatment there was an increase of both inducible nitric oxide synthase and glial fibrillary acidic protein labelling in glial cells and a reduction in the number of gamma-aminobutyric acid-positive neurones. The NOS inhibitors, N-nitro-L-arginine methyl ester, dexamethasone and indomethacin potently inhibited both nitric oxide stimulation and cell death caused by LPS. In this study, the beta(2)- (ICI-18551), beta(1)- (betaxolol) and mixed beta(1)/beta(2)- (timolol, metipranolol) adrenergic receptor antagonists were all shown to attenuate LPS-induced LDH release from these cultures, but to have no effect on LPS-stimulated nitric oxide production. This effect was mimicked by the calcium channel blocker, nifedipine. Interestingly, the beta-adrenergic receptor agonists, salbutamol, arterenol and isoproterenol were also able to attenuate cell death caused by LPS. Moreover, these compounds also inhibited LPS-stimulated nitric oxide release. These studies suggest that LPS stimulates nitric oxide release from cultured retinal glial cells and that this process leads to neurone death. beta-adrenergic receptor agonists prevent the effects of LPS by inhibiting the stimulation of nitric oxide production. The data also suggest that beta-adrenergic receptor antagonists can attenuate LPS-induced death of neurones, but that these compounds act in a manner that is neurone-dependent, is mimicked by blockade of calcium channels and is independent of the stimulation of nitric oxide release.

Adrenergic beta-Agonists↗

PubMed2000

Comparison of the performance of butanol and pentanol as modifiers in the micellar chromatographic determination of some phenethylamines.

A procedure was developed for the determination of several phenethylamines (amphetamine, arterenol, ephedrine, phenylephrine, phenylpropanolamine, mephentermine, methoxyphenamine, pseudoephedrine and tyramine), using micellar mobile phases of sodium dodecyl sulfate (SDS), a C18 column and UV detection. The drugs were eluted at short retention times with conventional acetonitrile-water or methanol-water mobile phases. In contrast, in the micellar system, they were strongly retained due to association with the surfactant adsorbed on the stationary phase, and needed the addition of butanol or pentanol to be eluted from the column. These modifiers allowed a simple way of controlling the retention. The chromatographic efficiencies obtained with the hybrid mobile phases of SDS-butanol and SDS-pentanol were also very high, mostly in the N=3000-7000 range, significantly greater than those achieved with a conventional acetonitrile-methanol-water mobile phase. Butanol and pentanol yielded similar selectivities, but the latter modifier permitted significantly shorter retention times than butanol, and was preferred to expedite the analysis of the pharmaceuticals. Most binary combinations of the nine phenethylamines can be resolved with these mobile phases. A mobile phase of 0.15 M SDS-5% pentanol was used to assay five of the phenethylamines (amphetamine, ephedrine, phenylephrine, phenylpropanolamine and pseudoephedrine) in 22 pharmaceutical preparations, which contained diverse accompanying compounds. The results agreed with the declared compositions and with those obtained with a mobile phase of methanol-acetonitrile-0.05 M phosphate buffer (pH 3) 10:5:85, with no interferences and relative errors usually below 2%. However, with the aqueous-organic mobile phase, the retention time for phenylephrine was too low and could not be usually evaluated.

Butanols↗

PubMed2002

In vitro rat bladder function after neonatal estrogenization.

PURPOSE: Experiments were done to evaluate the functional effects of neonatal diethylstilbestrol (DES) treatment on bladder function in male and female Noble rats. MATERIALS AND METHODS: At 5 months after neonatal DES bladders were removed and weighed. Ventral and dorsal bladder strips were prepared to evaluate the effects of neonatal DES on contractile responses to electrical field stimulation, carbachol, adenosine triphosphate, phenylephrine and KCl. Relaxant responses to the catecholamines arterenol (norepinephrine), epinephrine and isoproterenol were also monitored. RESULTS: Neonatal DES resulted in significant increases in bladder mass in males and females. Contractile and relaxant responses were largely unchanged by neonatal DES treatment and the only change observed was a decreased response of ventral strips from male neonatal DES rats to 4 and 8 Hz. stimulation. Ventral strips from male control and neonatal DES rats responded to field stimulation and carbachol with significantly greater responses than dorsal strips and were more sensitive to the relaxant actions of norepinephrine and epinephrine. CONCLUSIONS: The data confirm that neonatal DES causes infravesical obstruction. However, in contrast to published reports of the effects of surgically induced mild outlet obstruction, neonatal DES treatment has little effect on in vitro bladder strip contractile or relaxant function. Thus, the neonatal DES treated rat does not seem to be a useful model in which to study the in vitro effects of partial outlet obstruction on the bladder.

Adenosine Triphosphate↗

PubMed1999

Changes in fat cell size and in vitro lipolytic activity of abdominal and gluteal adipocytes after a one-year cross-sex hormone administration in transsexuals.

We prospectively studied the effects of cross-sex hormone administration on fat cell size and in vitro lipolytic activity in subcutaneous abdominal and gluteal fat biopsies obtained from 19 male-to-female (M-F) transsexuals and 17 female-to-male (F-M) transsexuals. The amount of subcutaneous fat at the abdominal and gluteal levels was quantified with the use of magnetic resonance imaging (MRI). Before cross-sex hormone administration, M-F transsexuals had less subcutaneous fat with smaller fat cells compared with F-M transsexuals, with a higher baseline in vitro lipolytic activity expressed as glycerol release per milligram of triglyceride (TG) in the abdominal region (P < .05). Before cross-sex hormone treatment, no differences in lipolytic activity stimulated with arterenol (ART), isoproterenol (ISO), or ISO + insulin (INS) were observed between groups or regions. After a 1-year treatment with estrogens and antiandrogens in M-F transsexuals, subcutaneous fat areas on MRI and fat cell size were increased (P < .001) and reductions were observed in the basal lipolytic activity of gluteal and abdominal fat biopsies (P < .05). Following administration of testosterone to F-M transsexuals, subcutaneous fat and fat cell size at the gluteal and abdominal depots were decreased (P < .01) and basal lipolysis was increased significantly at the abdominal level (P < .05) but not at the gluteal level. In both M-F and F-M transsexuals, no effect of sex hormone administration was observed on stimulated lipolytic activities. In conclusion, regional sex differences in the amount of subcutaneous fat, adipocyte size, and in vitro basal lipolytic activity were demonstrated that could be largely reversed by cross-sex hormone treatment in adult subjects, providing evidence for their dependence on the sex steroid milieu.

Abdomen↗

PubMed2004

Dynamics of beta2-adrenergic receptor-ligand complexes on living cells.

The agonist-induced dynamic regulation of the beta(2)-adrenergic receptor (beta(2)-AR) on living cells was examined by means of fluorescence correlation spectroscopy (FCS) using a fluorescence-labeled arterenol derivative (Alexa-NA) in hippocampal neurons and in alveolar epithelial type II cell line A549. Alexa-NA specifically bound to the beta(2)-AR of neurons with a K(D) value of 1.29 +/- 0.31 nM and of A549 cells with a K(D) of 5.98 +/- 1.62 nM. The receptor density equaled 4.5 +/- 0.9 microm(-2) in neurons (rho(N)) and 19.9 +/- 2.0 microm(-2) in A549 cells (rho(A549)). Kinetic experiments revealed comparable on-rate constants in both cell types (k(on) = 0.49 +/- 0.03 s(-1) nM(-1) in neurons and k(on) = 0.12 +/- 0.02 s(-1) nM(-1) in A549 cells). In addition to the free ligand diffusing with a D(free) of (2.11 +/- 0.04) x 10(-6) cm(2)/s, in both cell types receptor-ligand complexes with two distinct diffusion coefficients, D(bound1) (fast lateral mobility) and D(bound2) (hindered mobility), were observed [D(bound1) = (5.23 +/- 0.64) x 10(-8) cm(2)/s and D(bound2) = (6.05 +/- 0.23) x 10(-10) cm(2)/s for neurons, and D(bound1) = (2.88 +/- 1.72) x 10(-8) cm(2)/s and D(bound2) = (1.01 +/- 0.46) x 10(-9) cm(2)/s for A549 cells]. Fast lateral mobility of the receptor-ligand complex was detected immediately after addition of the ligand, whereas hindered mobility (D(bound2)) was observed after a delay of 5 min in neurons (up to 38% of total binding) and of 15-20 min in A549 cells (up to 40% of total binding). Thus, the receptor-ligand complexes with low mobility were formed during receptor regulation. Consistently, stimulation of receptor internalization using the adenylate cyclase activator forskolin shifted the ratio of receptor-ligand complexes toward D(bound2). Intracellular FCS measurements and immunocytochemical studies confirmed the appearance of endocytosed receptor-ligand complexes in the cytoplasm subjacent to the plasma membrane after stimulation with the agonist terbutaline (1 microM). This regulatory receptor internalization was blocked after preincubation with propranolol and with a cholesterol-complexing saponin alpha-hederin.

Adrenergic beta-Agonists↗

PubMed1998

Carnitine inhibits hydrolysis of inositol phospholipids induced by activation of metabotropic receptors.

We previously found that carnitine prevents glutamate neurotoxicity and that this effect is mediated by activation of metabotropic glutamate receptors. We show now that carnitine inhibits the hydrolysis of inositol phospholipids induced by different agonists of metabotropic glutamate receptors (tACPD; (+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid; DHPG, (R,S)-3,5-dyhydroxyphenylglycine or S4C3HPG, (S)-4-carboxy-3-hydroxyphenylglycine). The EC50 was ca. 170 microM and the inhibition was complete at 1 mM carnitine. Carnitine also inhibits completely hydrolysis of inositol phospholipids induced by arterenol (agonist of adrenoceptors) and only partially (ca. 50%) that induced by carbachol (agonist of muscarinic receptors). Carnitine did not inhibit phospholipase C activity but inhibits partially (43%) the hydrolysis of inositol phospholipids induced by direct activation of G proteins with AIF4-. The results reported indicate that carnitine inhibits the hydrolysis of inositol phospholipids induced by activation of metabotropic receptors likely by interfering the function of some types of G proteins.

Animals↗

PubMed1954

The purification of hypertensin I.

The purification of hypertensin I has been described. The final product which is four times as powerful a pressor agent as l-arterenol, is obtained with an over-all recovery of 40 per cent. The product consists of a single component in countercurrent distribution, having a nitrogen content of 15.97 per cent and a specific activity of 7050 Goldblatt units per mg. of N or 1125 units per mg. of solid. Acid hydrolysis and paper chromatography indicate in a preliminary fashion that there are about nine amino acids present in the intact polypeptide.

Amino Acids↗

PubMed1979

The influences of the route of administration on the metabolism and excretion of bitolterol, a new bronchodilator, in the rat.

1. [3H]Bitolterol, an ester prodrug to colterol (N-t-butyl-arterenol), when administered orally, was excreted mostly in the urine; approx. equal amounts of 3H were found in urine and faeces after intraperitoneal or intravenous injection. 2. Half the dose was excreted in the bile following parenteral administration, while only a small amount of radioactivity was found in bile after oral dosage. The biliary-excreted material consisted mainly of glucuronides, for all routes of administration. 3. The glucuronides of colterol and 3-O-methyl-colterol were excreted in urine after oral administration of bitolterol. In addition to the glucuronides, free colterol and 3-O-methyl-colterol were excreted in urine following parenteral administration. 4. A part of bitolterol was hydrolysed to colterol in rat stomach, and bitolterol was more rapidly hydrolysed to colteral with homogenates of intestinal mucosa than with stomach homogenates in vitro.

Administration, Oral↗

PubMedDate not supplied

[Local anesthesia with vasoconstrictors. Clinical and electrocardiographic study].

Adding vaso constrictors to the local anaesthetics used in dentistry has meant an important advance due to the advantage it offers. Many discussions have arisen among medical science professionals as to its possible contra indications. The authors reported on the result of 158 cases of teeth extractions in which simultaneous registers revealed different variants produced in the cardio vascular system. The conclusion they came to is that the local anaesthetics with levo arterenol used in odontology in usual doses is not of risk even in patients who suffer from cardio vascular affections.

Adolescent↗

PubMed1978

Demonstration of early capillary lesions in the brain by means of artificial reperfusion.

Nine patients are reported in whom functional brain death was determined as exactly as possible by neurological (in part also electroencephalographic and/or angiographic) examination in combination with analysis of the clinical history. During the first hour, at 2-4 hr, and later than 4 hr after the occurrence of functional brain death, the mean systemic pressure was raised to 30% above normal by infusion of Arterenol. The infusions lasted 15-30 min; in spite of the raised blood pressure, the patients died of cardiovascular attention to vascular damage; none was found whenever the reperfusion was completed within the first hour after determination of circulatory arrest. In all three cases in which reperfusion was performed, after more than 4 hr the neuropathological findings were similar. In one case the EEG showed a burst-type pattern during reperfusion within the first hour after determination of brain death.

Blood Pressure↗