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PubMed1984

Ionic basis for the antagonism between adenosine and isoproterenol on isolated mammalian ventricular myocytes.

We studied the effects of adenosine and isoproterenol on membrane currents of isolated bovine and guinea pig ventricular myocytes with a two-microelectrode voltage clamp technique. Adenosine (50 microM to 0.2 mM) alone had no effect on any of the membrane currents measured, but it antagonized the effects induced by 10 nM isoproterenol. Peak calcium membrane current was augmented by isoproterenol from a control of 4.8 +/- 0.6 to 8.6 +/- 0.8 nA and adenosine reduced it to 5.7 +/- 0.7 nA (mean +/- SEM of six cells). The inactivation time constant was not altered by isoproterenol alone or isoproterenol plus adenosine, and neither was the voltage dependence of peak calcium membrane current. Thus, the changes caused by isoproterenol could be described as an increase in maximal calcium conductance from 0.86 +/- 0.7 to 1.55 +/- 0.04 mS/cm2 and partially antagonized by adenosine to 0.97 +/- 0.04 mS/cm2. Isoproterenol also increased the non-inactivating component of calcium membrane current from 17 +/- 1 to 24 +/- 4%, and adenosine reduced it to 18 +/- 2% (n = 4). The steady state activation and inactivation variables remained unchanged. Consistent with these effects on calcium membrane current, adenosine completely antagonized the isoproterenol-induced increase of the slow action potentials obtained in sodium-free medium. Isoproterenol increased the steady state outward currents at potentials between -90 and -30 mV (i.e., probable iK1). Adenosine alone had no effect on potassium membrane current, but it antagonized the effects of isoproterenol. Slow action potentials in 25 mM potassium were enhanced by isoproterenol, but were only moderately attenuated by adenosine. Accordingly, in 25 mM potassium the isoproterenol-induced changes in membrane currents were not antagonized by adenosine. This lack of inhibition by adenosine of the isoproterenol effects in 25 mM potassium could not be mimicked by 1-minute-long conditioning prepulses to -45 mV. The results indicate that adenosine by itself (absence of isoproterenol) has no effect on maximal calcium conductance, that the isoproterenol-induced increase in cyclic adenosine 3',5'-monophosphate, which leads to an increase in maximal calcium conductance, is antagonized by adenosine, and that such action can account for the ability of adenosine to attenuate the stimulatory effects of isoproterenol.

Action Potentials↗
PubMed2001

Elevated parasympathetic nerve tone in isoproterenol-induced neurally mediated syncope during head-up tilt testing.

To clarify the autonomic nerve mechanisms whereby isoproterenol induces vasovagal reaction, 32 patients with recurrent syncopal episodes of unknown origin underwent head-up tilt testing. Syncope was induced in 11 patients by a control tilt (control/+ group). The remaining 21 patients (control/- group) underwent the procedure during isoproterenol infusion. Syncope was induced in 13 (isoproterenol/+ group), but not in the remaining 8 patients (isoproterenol/- group). High-frequency component (HF) and low-frequency component (LF)/HF, which are indices of heart rate variability, were assessed for 2-min intervals at baseline (T1) during the initial phase (T2) and at the end (T3) of tilting in each test. The ratios of HF and LF/HF at T2/T1 and T3/T2 were calculated. The HF value at T3 in the control/+ group was greater than that in the control/- group (1.47+/-0.91 vs 0.75+/-0.34; p<0.05). The HF value at T3 in the isoproterenol/+ group was significantly greater than those in the isoproterenol/- group (1.19+/-1.04 vs 0.43+/-0.23; p<0.05). The HF value at T2 in the isoproterenol/+ tended to be greater than in the isoproterenol/- group (1.30+/-0.85 vs 0.66+/-0.53; p=0.07). The ratio of HF for T2/T1 in isoproterenol/+ was greater than in the other groups (2.04+/-1.26 in isoproterenol/+ vs 0.58+/-0.39 in control/-, 0.47+/-0.18 in control/+ and 0.71+/-0.45 in isoproterenol/-; p=0.0001), whereas that of HF for T3/T2 in the control/+ group was greater than in the other groups (1.48+/-0.62 in control/+ vs 0.97+/-0.33 in control/-; p<0.05, 0.79+/-0.35 in isoproterenol/- and 0.88+/-0.37 in isoproterenol/+; p<0.01). No difference was observed in either LF/HF or the ratio of LF/HF among the groups. The early and persistent increase in parasympathetic nerve tone provoked by isoproterenol plays an important role in enhancing the vasovagal reaction during head-up tilt testing.

Adolescent↗
PubMed1984

Spontaneous and provoked resistance to isoproterenol in isolated human bronchi.

Cumulative concentration-response curves to isoproterenol were constructed in 74 preparations of human airways (group A) contracted with acetylcholine (80% of maximal contraction). In 52 bronchi (group A1), the maximal relaxation to isoproterenol represented at least 70% of the acetylcholine contraction (average 98% +/- 3) and the mean concentration (+/- SD) causing 50% of the relaxation (EC50) was 6.0 X 10(-8)M +/- 0.8. Resistance to isoproterenol (significant decrease of the maximal relaxation and right shift of the concentration-response curve) was provoked in 25 preparations by incubating them with isoproterenol (concentration 100 times higher than the individual EC50) for 30 min. The response to isoproterenol remained stable over the same time interval in eight control preparations. Incubation with isoproterenol did not modify the relaxing response to theophylline (n = 8). Indomethacin had no effect on the resistance provoked by isoproterenol incubation (n = 11). Incomplete relaxation to isoproterenol (maximal relaxation averaging 47% +/- 2 of the acetylcholine contraction) was observed in 22 preparations (group A2; mean EC50 = 1 X 10(-6)M +/- 0.2, significantly different [p less than 0.001] from group A1). Such preparations could be completely relaxed by theophylline (n = 7). For the whole group A, a significant negative correlation was found between isoproterenol EC50 and the magnitude of the maximal relaxation to isoproterenol (expressed as percent of acetylcholine contraction). There was no significant correlation between acetylcholine EC50 and isoproterenol maximum relaxation. Spontaneous resistance to isoproterenol was neither related to the technique of isoproterenol administration (cumulative versus noncumulative; n = 11) nor the magnitude of acetylcholine contraction (70% and 95% of maximal contraction; 14 bronchi, group B).

Airway Resistance↗
PubMed1990

Electrophysiologic effects of isoproterenol in patients with atrioventricular reentrant tachycardia treated with flecainide.

UNLABELLED: The electrophysiologic effects of isoproterenol in patients treated with flecainide for atrioventricular (AV) reentrant tachycardia were studied to evaluate the mechanism of tachycardia inducibility after isoproterenol and the value of isoproterenol challenge as a predictor of spontaneous arrhythmia recurrence. Seventeen patients underwent electrophysiologic study before and after oral flecainide administration and after the addition of isoproterenol to flecainide. No patient had inducible sustained supraventricular tachycardia after flecainide alone. Two patients had inducible sustained and six had inducible nonsustained tachycardia after isoproterenol was added to flecainide. The patients were then followed up on the same flecainide dose they received at the time of the electrophysiologic study. FINDINGS: 1) Flecainide treatment prolonged HV and VA intervals, and the addition of isoproterenol did not affect these variables. 2) Isoproterenol shortened anterograde and retrograde block cycle length and the refractory period of the accessory pathway and the AV node. It also decreased the tachycardia cycle length, an effect that was due solely to shortening of AV node conduction time. 3) Flecainide treatment prevented tachycardia induction by affecting retrograde conduction over the accessory pathway. Isoproterenol allowed for tachycardia induction and for more sustained episodes of tachycardia by reversing the effect of flecainide on retrograde accessory pathway conduction. 4) Tachycardia recurred during follow-up in all three patients in whom tachycardia of greater than or equal to 10 s duration was induced after isoproterenol but in no patient who had no or shorter episodes of induced tachycardia (and who did not have a change in medical regimen). CONCLUSIONS: 1) Isoproterenol reverses flecainide-induced prolongation of block cycle length and refractory periods of the accessory pathway and AV node. 2) Isoproterenol reverses flecainide-induced prevention of tachycardia induction through reversal of the effects of flecainide on the retrograde accessory pathway. 3) The addition of isoproterenol during flecainide restudy is valuable in predicting long-term drug efficacy.

Cardiac Pacing, Artificial↗
PubMed1998

The combination of epinephrine and isoproterenol as a simulated epidural test dose in isoflurane-anesthetized adults.

UNLABELLED: During isoflurane anesthesia, an epinephrine-containing test dose produces unreliable heart rate (HR) responses with a high incidence of hypertension, whereas an isoproterenol-containing test dose results in a high incidence of hypotension. We designed this study to determine whether different combination doses of epinephrine and isoproterenol produce reliable HR changes without overt fluctuations of systolic blood pressure (SBP). Seventy-five healthy patients were anesthetized with 1% end-tidal isoflurane after endotracheal intubation and randomized to one of five groups (n = 15 each) according to the combination dose given i.v.: epinephrine 15 microg, epinephrine 15 microg + isoproterenol 1.5 microg, epinephrine 7.5 microg + isoproterenol 3 microg, isoproterenol 3 microg, and saline. HR and SBP were measured at 20-s intervals for 4 min after injection. Based on the conventional HR criterion (positive if > or = 20 bpm increase), the epinephrine 15 microg + isoproterenol 1.5 microg, the epinephrine 7.5 microg + isoproterenol 3 microg, and the isoproterenol 3 microg groups yielded 100% sensitivities, specificities, and positive and negative predictive values, whereas all groups yielded 100% efficacy according to the modified HR criterion (positive if > or = 10 bpm increase). Four (27%) and three patients (20%) in the epinephrine 15 microg and the epinephrine 15 microg + isoproterenol 1.5 microg groups, respectively, developed systolic hypertension (SBP > or = 180 mm Hg), whereas four (27%) patients in the isoproterenol 3 microg group developed systolic hypotension (SBP < or = 80% of the preinjection value). We conclude that epinephrine 7.5 microg + isoproterenol 3 microg provides the most reliable HR changes with the least SBP fluctuations. IMPLICATIONS: To test whether an epidural catheter may be in a blood vessel, various vasoactive drugs are administered during general anesthesia. The authors found that the combination of epinephrine 7.5 microg and isoproterenol 3 microg produced the most reliable heart rate changes with minimal blood pressure fluctuations.

Adrenergic Agonists↗
PubMed1998

Role of adenosine receptors in the paradoxic bradycardia response of rats to inferior vena cava occlusion during an infusion of isoproterenol.

BACKGROUND: In susceptible humans, vasodepressor reactions are induced by restriction of venous return (upright tilting) and administration of isoproterenol. Because paradoxic bradycardia is a major manifestation of vasodepressor reactions, and allowing for extrapolation between paradoxic bradycardia in rats and vasodepressor reactions, we examined whether adenosine receptors mediate the paradoxic bradycardia reaction. METHODS AND RESULTS: Paradoxic bradycardia was induced in rats by inferior vena cava occlusion during an isoproterenol infusion. We studied whether dipyridamole, an adenosine transport inhibitor, and aminophylline (nonselective) or DPCPX (selective) A1 antagonists augmented or inhibited paradoxic bradycardia, respectively, during inferior vena cava occlusion. The maximum changes in R-R during 60 seconds of inferior vena cava occlusion were that (1) in control, the rate accelerated (DeltaR-R, -9.7+/-0.8 ms, P<0.001); (2) during isoproterenol (0.8 microg . min-1), paradoxic bradycardia occurred (DeltaR-R, +92.0+/-32.0 ms, P<0.001); (3) during isoproterenol but after dipyridamole, paradoxic bradycardia occurred at a much lower dose of isoproterenol (0.2 microg . min-1), and the magnitude was increased at all doses (at 0.8 microg . min-1 isoproterenol, DeltaR-R, +195.6+/-27.6 ms, P<0.001 versus isoproterenol alone, DeltaR-R, +92.0+/-32 ms); (4) during isoproterenol and dipyridamole, atropine did not block paradoxic bradycardia, but cervical vagotomy inhibited paradoxic bradycardia (DeltaR-R, +5.6+/-1.8 ms, P<0.001 compared with isoproterenol and dipyridamole alone); and (5) during isoproterenol alone, aminophylline or DPCPX blocked paradoxic bradycardia (DeltaR-R, -5.4+/-1.0 ms, and DeltaR-R, -2.6+/-0.5 ms, respectively, each P<0.001 compared with isoproterenol alone). CONCLUSIONS: The adenosine A1 receptor mediates the paradoxic bradycardia reflex during inferior vena cava occlusion in the face of isoproterenol via vagal afferents.

Adenosine↗
PubMed1988

Isoproterenol-induced inhibition of immunoglobulin E-mediated release of histamine and arachidonic acid metabolites from the human lung mast cell.

The inhibitory effect of isoproterenol was examined on the release of histamine, leukotriene C4 (LTC4), and prostaglandin D2 (PGD2) from human lung mast cells. Isoproterenol was more potent in inhibiting anti-immunoglobulin (Ig) E-induced LTC4 and PGD2 release than histamine release from the dispersed lung cell preparations (2-5% mast cells). The negative log molar EC50 values of isoproterenol for inhibiting histamine, LTC4 and PGD2 release were 8.2 +/- 0.2, 8.9 +/- 0.2 and 8.7 +/- 0.3, respectively (mean +/- S.E.M., n = 8). Isoproterenol seldom inhibited histamine release by more than 60%, but usually abolished the release of LTC4 and PGD2. The potency of propranolol (KB = 6 X 10(-10) M) was the same for competitively antagonizing isoproterenol mediated inhibition of histamine, LTC4 or PGD2 release. Using the irreversible beta adrenergic receptor antagonist, bromoacetylalprenololmenthane, the estimated dissociation constant of isoproterenol was 2 X 10(-7) M irrespective of whether inhibition of anti-IgE-induced histamine or LTC4 release was examined. When the divalent cation ionophore A23187 was used to induce histamine release, isoproterenol had either no effect or potentiated the release. In contrast, isoproterenol was capable of virtually abolishing A23187-induced LTC4 release. Qualitatively similar effects of isoproterenol were observed on purified mast cell preparations (greater than 80% mast cells); however, the potency of isoproterenol in inhibiting mediator release from these preparations was reduced. The results demonstrate that there is a substantial receptor reserve for isoproterenol-mediated inhibition of histamine, LTC4 and PGD2 release from the human lung mast cell. The intrinsic efficacy of isoproterenol in inhibiting anti-IgE-induced release of arachidonic acid metabolites is approximately 3 times greater than that for inhibiting histamine release.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprenolol↗
PubMed1990

Effects of isoproterenol on accessory pathway conduction in intermittent or concealed Wolff-Parkinson-White syndrome.

The effects of isoproterenol on accessory pathway conduction were evaluated in 24 patients with intermittent and 60 patients with concealed pre-excitation, using atrial and ventricular incremental and extrastimulus testing techniques. The atrial paced cycle length that induced block in the accessory pathway could be compared in 11 of the 24 patients with intermittent preexcitation before and after isoproterenol; it decreased from 622 +/- 212 ms to 408 +/- 128 ms (mean +/- standard deviation) after isoproterenol (p less than 0.01). The anterograde effective refractory period of the accessory pathway could be compared in 5 patients before and after isoproterenol; it decreased from 460 +/- 131 to 310 +/- 48 ms after isoproterenol (p less than 0.01). None of the 60 patients with concealed preexcitation showed ventricular preexcitation with isoproterenol infusion. Eighty-one of the 84 patients had clinically documented supraventricular tachycardia, suggesting the accessory pathway was capable of retrograde conduction. Retrograde study was performed in all 84 patients; 83 had retrograde conduction and the other had no retrograde conduction before and after isoproterenol. The ventricular paced cycle length that induced block in the accessory pathway could be compared in 38 patients before and after isoproterenol; it decreased from 342 +/- 71 to 296 +/- 39 ms after isoproterenol (p less than 0.001). The retrograde effective refractory period of the accessory pathway could be compared in 56 patients; it decreased from 293 +/- 76 to 238 +/- 36 ms after isoproterenol (p less than 0.001). In conclusion, isoproterenol facilitates anterograde and retrograde accessory pathway conduction, but the facilitation of anterograde conduction occurs only in those capable of spontaneous conduction.

Adolescent↗
PubMed1999

Value of sublingual isosorbide dinitrate before isoproterenol tilt test for diagnosis of neurally mediated syncope.

Head-up tilt-table test is valuable in diagnosing type of syncope. Sensitivity varies in reports and is mostly poor. Isoproterenol or nitroglycerin is regularly used to increase head-up tilt-table test sensitivity. The aim of this study was to assess the value of sublingual isosorbide dinitrate administration before isoproterenol tilt test as a simple, practical test for diagnosis of neurally mediated syncope. Ninety-six patients (45 men and 51 women, mean age 42.5 years) with recurrent (median 4 times) loss of consciousness that remained unexplained after clinical and noninvasive assessment and 72 healthy volunteers (36 men and 36 women, mean age 40.1 years) were randomly divided into groups: isosorbide-isoproterenol test and isoproterenol test. During isosorbide-isoproterenol test, a positive response (syncope in association with sudden hypotension or bradycardia) occurred in 35 patients (72.9%) with unexplained syncope, an exaggerated response (minor symptoms in association with slowly increasing hypotension alone) occurred in 7 (14.6%), a negative response in 2 (4.2%), and drug intolerance in 4 (8.3%). During isoproterenol testing, these percentages were 52.1%, 16.7%, 25.0%, and 6.2%, respectively. Only 3 control volunteers (8.3%) had a positive response to isosorbide-isoproterenol test and 2 (5.6%) to isoproterenol test. The duration of the test and the time for syncope induction in the isosorbide-isoproterenol test were shorter than those in the isoproterenol test (24.84 +/- 5.15 vs 35.70 +/- 6.28 minutes [p <0.01]; 4.53 +/- 2.86 vs 6.27 +/- 4.11 minutes [p <0.05]). This study concluded that isosorbide-isoproterenol test could be valuable in diagnosing unexplained syncope for its high sensitivity, powerful specificity, and short duration.

Administration, Sublingual↗
PubMed1995

Vagal modulation of RR intervals during head-up tilt and the infusion of isoproterenol.

The objective of this study was to characterize the autonomic effects of 2 interventions, head-up tilt and isoproterenol infusion, which alter autonomic balance by different mechanisms but produce the same RR intervals. We compared the effect of head-up tilt with the effect of isoproterenol on autonomic balance as measured by power spectral analysis of RR variability. Fifteen normal subjects had baseline measurements and then underwent head-up tilt. After return to baseline supine values, isoproterenol was infused at a rate of 1 microgram/min (low-dose isoproterenol), which was then increased to 2.1 +/- 0.5 microgram/min (high-dose isoproterenol). All subjects underwent a second tilt during high-dose isoproterenol, and 9 subjects completed this second tilt study. During the experiment, normal RR intervals were recorded and 5-minute segments were used to calculate power spectra. High-frequency (HF) power (0.15 to 0.40 Hz) was used as a measure of vagal activity. The effects of head-up tilt were compared with the effects of low-dose isoproterenol. Despite nearly identical mean RR intervals (784 ms with tilt vs 792 ms with low-dose isoproterenol, p = NS), there was significantly (p < 0.05) less HF power during head-up tilt in the drug-free state (172 ms2) than during low-dose isoproterenol in the supine position (307 ms2). A second head-up tilt was performed during the infusion of high-dose isoproterenol. During high-dose isoproterenol, tilt caused a decrease in RR intervals (from 573 to 491 ms; p < 0.01) and a decrease in HF power (from 68 to 28 ms2; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Simulation of an epidural test dose with intravenous isoproterenol in isoflurane-anesthetized adults.

UNLABELLED: Although a simulated intravenous (I.V.) test dose containing 3 microg isoproterenol results in a reliable heart rate (HR) increase in anesthetized patients, hypotension may limit its clinical utility. The present study was designed to determine the incidence of hypotension and the reliability of smaller doses of isoproterenol. Forty-five healthy adult patients were anesthetized with 1% end-tidal isoflurane and nitrous oxide after endotracheal intubation and were randomized to one of three groups according to the dose of isoproterenol. Isoproterenol 1-, 2-, and 3-microg groups (n = 15 each) received 3 mL of 1.5% lidocaine with 1, 2, and 3 microg isoproterenol I.V., respectively, to simulate an intravascularly administered test dose. HR and systolic blood pressure were measured at 20-s intervals for 4 min after injection. Mean maximal HR increases were 15 +/- 6, 23 +/- 10, and 32 +/- 7 bpm (mean +/- SD) in the isoproterenol 1-, 2-, and 3-microg groups, respectively. However, the incidence and degree of systolic hypotension were similar among groups. Isoproterenol 3 microg produced 100% sensitivity in both the conventional (> or = 20 bpm increase) and the modified (> or = 10 bpm increase) HR criteria, but 2 microg resulted in 100% sensitivity on the modified criterion alone. Isoproterenol 1 microg did not elicit reliable HR changes. Significant correlation was demonstrated between the isoproterenol dose (microg/kg) and the maximal HR increase. Ninety-five percent confidence intervals to increase HR by 10 and 20 bpm were 0.015-0.02 microg/kg and 0.03-0.04 microg/kg, respectively. The application of isoproterenol as a test dose component seems promising, pending detailed studies of neural toxicity. The appropriate dose needs to be tailored according to the patient's weight. IMPLICATIONS: To determine whether an epidural catheter may be in a blood vessel, various vasoactive drugs are often administered. The author found that isoproterenol might be a useful drug in place of epinephrine.

Adult↗