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At least 19 recordsLinked to original sources
PubMed1995

Left ventricular dimensions and autonomic balance during head-up tilt differ between patients with isoproterenol-dependent and isoproterenol-independent neurally mediated syncope.

OBJECTIVES: This study sought to elucidate differences in mechanisms of neurally mediated syncope between patients with syncope induced by head-up tilt alone and those requiring isoproterenol infusion to induce syncope during head-up tilt. BACKGROUND: Some patients with neurally mediated syncope require isoproterenol to induce syncope during head-up tilt (isoproterenol dependent), and others do not (isoproterenol independent). Differences in mechanisms between these two groups have not been well elucidated. METHODS: A 60 degrees head-up tilt test was performed in 13 patients with isoproterenol-independent syncope (Group I, mean [+/- SD] age 28 +/- 12 years), 14 patients with isoproterenol-dependent syncope (Group II, mean age 34 +/- 14 years) and 20 control subjects without syncope (Group III, mean age 32 +/- 12 years). Left ventricular size and contractility were determined by echocardiography, and sympathovagal balance was determined with power spectral analysis of heart rate variability using a maximal entropy method. RESULTS: Group I patients had smaller left ventricular dimensions than Group II and III during baseline tilt. During head-up tilt with isoproterenol infusion (0.01 to 0.04 microgram/kg body weight per min), left ventricular dimensions decreased to the same extent in Groups II and III, but fractional shortening was greater in Group II than in Group III at the end of the tilt. The ratio of low (0.05 to 0.15 Hz) to high frequency (0.15 to 1.0 Hz) component became greater in Group I than in Groups II and III during the last period of baseline tilt. However, the ratio was greater in Group II than in Group III during the last period of the tilt with isoproterenol. CONCLUSIONS: Patients with isoproterenol-independent syncope had an exaggerated decrease in left ventricular size and sympathetic predominance preceding syncope during head-up tilt. In contrast, in patients with isoproterenol-dependent syncope, similar changes in autonomic nervous balance were evident only during isoproterenol infusion in addition to head-up tilt.

Adolescent↗
PubMed1982

Alteration in sensitivity to isoproterenol and acetylcholine in the rat heart after repeated administration of isoproterenol.

Alteration of sensitivity to the inotropic responses to isoproterenol and acetylcholine (ACh) and of saturation constants for the specific binding of [3H]dihydroalprenolol and [3H]quinuclidinyl benzilate to particulate fractions were investigated in rat hearts chronically treated with isoproterenol. The EC50 value for the inotropic response to isoproterenol in the atria of rats injected i.p. with isoproterenol (0.01 or 0.1 mg/kg) twice a day for 10 days, was 9.0-fold higher than in controls. Isoproterenol (0.17 mg/kg i.p.)-induced stimulation of cardiac ornithine decarboxylase activity was significantly (P less than .05) attenuated in atria from animals of the treated groups. Scatchard analysis of specific binding of [3H]dihydroalprenolol revealed that repeated isoproterenol injection produced a significant decrease in the maximum number of binding sites (Bmax), but not in the dissociation constant (KD) for this antagonist. In comparison to the isoproterenol-induced changes in beta adrenergic positive inotropic response, repeated treatment with isoproterenol decreased 2-fold the EC50 value for the negative inotropic response to ACh in isolated atria. Scatchard analysis of specific [3H]quinuclidinyl benzilate binding, however, indicated a significant (P less than .01) decrease in Bmax. Repeated isoproterenol injections also elicited a significant increase in cardiac weight. It is suggested that repeated administration of isoproterenol induces a decrease in density of beta adrenergic receptors which may in part underlie a cardiac hyposensitivity to isoproterenol and an increase in the number of muscarinic ACh receptors and inotropic responsiveness to ACh.

Acetylcholine↗
PubMed1985

Isoproterenol-induced desensitization to the positive inotropic effect of isoproterenol in ventricular strips isolated from carp heart (Cyprinus carpio).

Whether the positive inotropic effect of isoproterenol in ventricular strips of carp heart is altered by previous exposure to the agonist was studied. Isoproterenol produced a concentration-dependent positive inotropic effect in these preparations which was competitively antagonized by propranolol. Isoproterenol dose-response curves were shifted significantly downward and to the right after previous treatment with and removal of isoproterenol. The desensitization could be demonstrated after 5 min incubation and near maximal desensitization was observed after 30 min exposure to 1000 nM isoproterenol. The responsiveness was only partially recovered after 180 min incubation in drug-free medium. Isoproterenol produces a rapidly developing desensitization to inotropic effects of the beta-adrenergic agonist. This phenomenon may be mediated by alterations in beta-adrenergic receptors, adenylate cyclase and/or the beta receptor-adenylate cyclase coupling mechanism.

Animals↗
PubMed1998

Role of endogenous opioids in syncope induced by head-up tilt test and its relationship with isoproterenol-dependent and isoproterenol-independent neurally-mediated syncope.

This study was designed to evaluate the role of endogenous opioids in neurally-mediated syncope. Head-up tilt test was performed on 35 patients with syncope of unknown origin. Plasma beta-endorphin was measured (1) at baseline, (2) at the end of tilt test or at time of syncope, (3) 15 min before isoproterenol-test, (4) at the end of the isoproterenol-test or at time of syncope. Subjects with a positive tilt testing showed a larger rise in plasma beta-endorphin concentrations at time of syncope (baseline 13.7+/-8.0 vs. syncope 41.4+/-26.4 pmol l(-1); P<0.01). On the contrary, patients with a positive isoproterenol-test showed no rise in plasma beta-endorphin levels (baseline 7.9+/-3.6 vs. syncope 7.4+/-2.7 pmol l(-1); P=ns). Patients with a passive negative tilt test (baseline 6.7+/-2.8 vs. end of test 7.0+/-3.3 pmol l(-1); P=ns) and negative isoproterenol tilt test (baseline 7.4+/-3.8 vs. end of test 8.1+/-3.4 pmol l(-1); P=ns) showed no changes in beta-endorphin concentrations. To further examine the efficacy of i.v. naloxone to prevent syncope, 10 patients were randomized to naloxone (0.02 mg/kg) or placebo. Second head-up tilt testing was negative in 1/5 patients with naloxone and in 2/5 patients with placebo. We conclude that, (1) endogenous opioids seem to be involved in vasovagal syncope induced by baseline head-up tilt test, (2) changes in plasma beta-endorphin concentrations show significant differences between patients who have isoproterenol-dependent and isoproterenol-independent syncope, this finding might occur in the setting of different pathophysiologic mechanisms, and (3) intravenous naloxone at a dose of 0.02 mg/kg was not superior to placebo in order to prevent positive responses to baseline tilt test.

Adolescent↗
PubMed1984

In vivo cardiovascular responses to isoproterenol, dopamine and tyramine after prolonged infusion of isoproterenol.

Effects of prolonged in vivo infusion of isoproterenol on acute cardiovascular responses to isoproterenol, dopamine and tyramine were studied in pithed rats. Isoproterenol infusion resulted in a significant decrease in control values for maximum left ventricular dP/dt; heart rate and left ventricular systolic blood pressure were not altered. This treatment also depleted both atrial and ventricular stores of norepinephrine and caused cardiac hypertrophy. Isoproterenol infusion resulted in a desensitization of drug-induced cardiovascular responses. The acute in vivo effects of isoproterenol on maximum left ventricular dP/dt, heart rate and left ventricular systolic blood pressure responses to isoproterenol were severely attenuated. The ED50 for maximum left ventricular dP/dt was increased 36-fold and maximal responses were reduced by half; changes in heart rate occurred in a parallel fashion. By contrast, ED50 values for inotropic responses to tyramine and dopamine were increased 14- and 4-fold, respectively, whereas increases in heart rate were blunted. Tyramine and dopamine-mediated increases in heart rate were completely attenuated by desensitization; chronotropic effects were again evident after pretreatment with the selective alpha-1 blocker prazosin. In addition, prazosin blocked the inotropic responses to tyramine and dopamine after desensitization and this antagonism was only slightly enhanced by addition of propranolol (prazosin + propranolol); propranolol alone was ineffective. These results are consistent with the down-regulation of beta adrenoceptors after prolonged exposure to catecholamines and indicate that under such conditions the alpha-mediated cardiovascular responses may be unmasked. Compared to pure beta agonists, agents with a degree of alpha-1 activity might be superior inotropes in heart failure patients who characteristically present with depleted stores of myocardial norepinephrine and minimal beta adrenoceptor reserve.

Animals↗
PubMed1994

Differential therapeutic responses of patients with isoproterenol-dependent and isoproterenol-independent vasodepressor syncope.

Orthostatic stress during tilt table testing (TTT) is used to examine patients who may have vasodepressor syncope. This response is thought to be mediated by activation of left ventricular mechanoreceptors. Isoproterenol, by increasing the rate of discharge of these mechanoreceptors, has been proposed to increase the sensitivity of TTT without decreasing its specificity. This mechanism is not, however, totally consistent with recent observations of vasodepressor responses after cardiac transplantation in patients with denervated hearts. These reports and data showing that not all sympathomimetic agents increase the sensitivity of TTT suggest that more than one mechanism may be responsible for a positive TTT result. Therefore we hypothesized that patients with positive TTT results tests not requiring isoproterenol (iso-independent) would have a different clinical and therapeutic response than patients who required isoproterenol (iso-dependent). One hundred sixty-one consecutive patients who underwent TTT for the evaluation of unexplained syncope were included in the study. TTT was performed without and during isoproterenol infusion. A positive TTT result was defined as syncope or presyncope with a sudden decrease in systolic blood pressure and reproduction of the patient's clinical symptoms. Patients with a positive TTT result underwent a second test after 1 to 2 weeks of therapy with an oral beta-blocking agent; if the result remained positive, TTT was performed again with other agents until a satisfactory therapeutic response was obtained. Sixty-six (41%) of 161 patients had a positive result; 18 (27%) were iso-independent, and 48 (73%) were iso-dependent. There were no significant differences in age, gender, or presence of underlying heart disease between these two groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenergic beta-Antagonists↗
PubMed1982

Early decrease in secretin-, glucagon-, and isoproterenol-stimulated cardiac adenylate cyclase activity in rats treated with isoproterenol.

Male Wistar albino rats received three times daily for one to five days 0.25 to 5.0 mg/kg D,L-isoproterenol intraperitoneally. D.L-Isoproterenol injections provoked a time dependent- and dose-related cardiac hypertrophy. With moderate hypertrophy, a selective decrease in secretin-stimulated adenylate cyclase activity occurred. When heart hypertrophy was more pronounced, greater losses in secretin-, as well as in D,L-isoproterenol-, glucagon-, guanine nucleotide-, and fluoride-stimulated enzyme activity developed. Hormone stimulations of adenylate cyclase were more severely, curtailed (60 to 65%) than guanine nucleotide or fluoride stimulations (40 to 45%). The accompanying loss in beta-receptors (35%) was proportionately lower than the loss of D,L-isoproterenol sensitivity of adenylate cyclase. This complex pattern of adenylate cyclase desensitization in heart membranes from animals chronically treated with D,L-isoproterenol is reminiscent of that observed in heart membranes from spontaneously hypertensive rats.

Adenylyl Cyclases↗
PubMed1977

Dose-response effects of albuterol aerosol compared with isoproterenol and placebo aerosols: response to albuterol, isoproterenol, and placebo aerosols.

Albuterol aerosol was an effective bronchodilator as reflected by indices of pulmonary function obtained from spirometry and flow volume curves; Compared with isoproterenol, there were minimal side effects even at the highest doses, and bronchodilation lasted significantly longer. In addition albuterol was successfully used by a patient with idiopathic hypertrophic subaortic stenosis who was unable to tolerate isoproterenol, as well as by some patients with idiosyncratic responses to isoproterenol; A few patients appeared to derive little benefit from either albuterol or isoproterenol.

Adolescent↗
PubMed2004

Evaluation of isoproterenol in patients undergoing resuscitation for out-of-hospital asystolic cardiac arrest (the Israel Resuscitation with Isoproterenol Study Prospective Randomized Clinical Trial).

The Israel Resuscitation with Isoproterenol Study included 79 consecutive patients with witnessed out-of-hospital asystolic cardiac arrest who were resuscitated with epinephrine and atropine and randomized to receive additional isoproterenol or no isoproterenol. The rate of return of spontaneous circulation and survival to hospital admission did not differ in patients receiving standard therapy and those receiving additional isoproterenol.

Adrenergic beta-Agonists↗
PubMed1977

A double-blind parallel study of acetylcysteine-isoproterenol and saline-isoproterenol in patients with chronic obstructive lung disease.

A double-blind parallel study in patients with asthma compared the safety and efficacy of saline-isoproterenol (SI) and acetylcysteine-isoproterenol (AI), when administered at home as an aerosol, over a one-week period, using a conventional nebulizer compressor. Measurements of pulmonary function revealed statistically significant differences between the two therapies for FEV1 and FVC in favour of AI. In the group treated with AI, the average sputum viscosity after six days of treatment was significantly less than pre-treatment values, or when compared to the results with SI treatment. No serious side-effects were reported during treatment with either therapy. These results indicate that acetylcysteine combined with a bronchodilator, such as isoproterenol, may be safe and of significant value in the treatment of patients with asthma who are also sputum producers.

Acetylcysteine↗
PubMed1977

Comparison of aerosolized atropine, isoproterenol, atropine plus isoproterenol, disodium cromoglycate and placebo in the prevention of exercise-induced asthma.

In 15 asthmatic children post-exercise bronchospasm was partially inhibited by placebo and by aerosolized atropine sulphate (1 mg) compared with no treatment, not significantly inhibited by atropine alone compared with placebo, partially blocked by disodium cromoglycate (20 mg) and by isoproterenol (0.625 mg) and completely blocked by the combination of isoproterenol and atropine. Pre-treatment with isoproterenol or atropine resulted in post-exercise values for specific conductance which were significantly greater than those following disodium cromoglycate by virtue of the bronchodilator effect of these drugs independent of or in addition to any specific inhibition of exercise-induced asthma. These results suggest that the bronchoconstrictor response to exercise is partially influenced by suggestion but is influenced to a significantly greater degree by mediator release and beta-adrenergic mechanisms and that bronchodilator drugs have therapeutic advantages over an inhibitor of mediator release in the prevention of exercise-induced asthma.

Adolescent↗
PubMed1982

Lack of cardiotoxic effect of isoproterenol in streptozotocin diabetic rats. A morphometric study of isoproterenol induced fibrosis.

The well known cardiotoxic effect of isoproterenol (ISO) was investigated in normal and streptozotocin diabetic rats. Seven days after the subcutaneous injection of ISO (15 mg/kg) the hearts were perfusion fixed and 12 sections from each heart were stained (Masson's trichrome). ISO induced myocardial fibrosis was quantified at the light microscopic level according to established morphometric principles. Pulse rate and ST elevation were recorded by EEC (3 standard leads) before and after the ISO injection. Non-diabetic control animals showed marked fibrosis after ISO, but surprisingly the diabetic animals showed no fibrosis after ISO treatment. These findings were in accordance with an ISO induced ST elevation seen only among control animals although both groups showed the same degree of tachycardia. Insulin treatment prevented the protection against ISO and when streptozotocin was injected 24 h after the ISO a normal quantitative and qualitative appearance of the scar tissue was seen. It thus seems that streptozotocin diabetic rats are protected against the toxic effect of ISO, leaving the haemodynamic response unaffected. Which factor in the diabetic metabolism is responsible for the present phenomenon is not known, but a defect in the signal transmission from the beta-receptor to the adenylcyclase is suggested as a possible explanation.

Animals↗
PubMed1985

Acute insulin treatment normalizes the resistance to the cardiotoxic effect of isoproterenol in streptozotocin diabetic rats. A morphometric study of isoproterenol induced myocardial fibrosis.

The acute effect of insulin treatment on the earlier reported protective effect of streptozotocin diabetes against the cardiotoxic effect of high doses of isoproterenol (ISO) was investigated in rats. Thirty to 135 min after the injection of crystalline insulin, ISO was given subcutaneously and when ISO induced fibrosis in the myocardium was morphometrically analyzed 7 days later, a highly significant correlation (r = 0.83, 2 p = 0.006) to the slope of the fall in blood glucose after insulin treatment appeared. The myocardial content of catecholamines was estimated in these 8 day diabetic rats. The norepinephrine content was significantly increased while epinephrine remained unchanged. An enhanced sympathetic nervous system activity with a consequent down regulation of the myocardial beta-adrenergic receptors could, therefore, explain this catecholamine resistance. The rapid reversion after insulin treatment excludes the possibility that streptozotocin in itself causes the ISO resistance and points towards a direct insulin effect on myocardial catecholamine sensitivity in diabetic rats. The phenomenon described might elucidate pathogenetic mechanisms behind toxic myocardial cell degeneration and may possibly have relevance for acute cardiovascular complications in diabetic patients.

Animals↗