What is the evidence for the effect of physical exercise on bone health in menopausal women? An umbrella systematic review.

This study aimed to analyze the effects of physical exercise (PE) on bone health in menopausal women through an umbrella review and to assess the quality of systematic reviews (SRs) and meta-analyses (MAs) included. The review was registered in PROSPERO (CRD42020208130) and the Rayyan application was used. The methodological quality of the included studies was evaluated by A MeaSurement Tool to Assess Systematic Reviews (AMSTAR), and Grading of Recommendations Assessment, Development and Evaluation (GRADE) was applied to assess the level of evidence of the results. The results showed that low-intensity jumping exercises with longer sessions proved to be efficient in the hip segment. Swimming requires further investigation, as it showed high heterogeneity. Aerobic and resistance exercises showed inconsistent results, requiring further studies with these modalities of PE. Concurrent training showed improvements in the lumbar spine, femoral neck, Ward's triangle and trochanter. Finally, combined resistance exercises are effective in preserving bone mineral density (BMD) of the femoral neck and lumbar spine in postmenopausal women. In conclusion, jumping exercises were efficient in the hip, while aerobic and resistance exercises are still inconsistent. Concurrent training showed improvements in BMD of the lumbar spine, femoral neck, Ward's triangle and trochanter. Finally, combined resistance protocols are effective in preserving BMD of the femoral neck and lumbar spine in postmenopausal women.

The O K-2V spectrum of CO: the influence of the second core-hole.

Using synchrotron radiation in the tender X-ray regime, a photoelectron spectrum showing the formation of single site double-core-hole pre-edge states, involving the K shell of the O atom in CO, has been recorded by means of high-resolution electron spectroscopy. The experimentally observed structures have been simulated, interpreted and assigned, employing state-of-the-art ab initio quantum chemical calculations, on the basis of a theoretical model, accounting for their so-called direct or conjugate character. Features appearing above the double ionization threshold have been reproduced by taking into account the strong mixing between multi-excited and continuum states. The shift of the σ* resonance below the double ionization threshold, in combination with the non-negligible contributions of multi-excited configurations in the final states reached, gives rise to a series of avoided crossings between the different potential energy curves.

Responses of obese and non-obese boys cycling in the heat.

This study compared rectal temperature (Tre), heat sensation and sweating between obese and non-obese boys during cycling in the heat. Participants (aged 12-15 years) were 17 obese and 16 non-obese (BMI=29.4±4.3 and 16.8±1.7 kg · m⁻², respectively) boys. They cycled for 30-min (50-55% VO(2peak)) in a climatic chamber (35°C, 45% RH) and Tre, heat sensation and sweat volume were monitored. From the start to the end of cycling, Tre was similar between the obese (37.4±0.3-37.8±0.3°C) and non-obese (37.3±0.2-37.9±0.2°C) groups. Heat sensation was higher in the obese group from the start (3.6±2.7 vs. 1.3±1.4 cm; P=0.008) to the end (7.6±2 vs. 5.2±2.2 cm; P=0.003) of cycling. Sweat volume corrected by body surface area was similar between the obese (200±123 mL · m⁻²) and non-obese (212±80 mL · m⁻²) groups. Initial and final HR were similar in both groups, and RPE was higher in the obese group at 25th (P=0.040) and 30th (P=0.019) min. In conclusion, the obese pubescent participants presented similar Tre and sweating volume, but higher heat sensation while cycling in the heat.

Does whole body vibration exercise improve oxidative stress markers in women with fibromyalgia?

The objective of this study was to investigate the effect of whole body vibration (WBV) exercise on oxidative stress markers in a group of women with fibromyalgia (FM) compared to a group of healthy women (CT). Twenty-one women diagnosed with FM and 21 age- and weight-matched healthy women were enrolled the study. Plasma oxidative stress markers (primary outcomes) were evaluated at rest and after WBV, and included thiobarbituric acid reactive substances (TBARS), iron reduction capacity (FRAP), superoxide dismutase antioxidant enzymes activity (SOD), and catalase (CAT). At rest, the FM group had higher TBARS (P<0.001) and FRAP (P<0.001), and lower CAT (P=0.005) compared to the CT. In the CT group, the WBV had no effect on TBARS (P=0.559) and FRAP (P=0.926), whereas it increased both SOD (P<0.001) and CAT (P<0.001). In the FM group, the WBV reduced TBARS (p <0.001), FRAP (P<0.001), and CAT (P=0.005), while it increased SOD (P=0.019). There was an interaction effect (moments vs groups) in the TBARS (effect size=1.34), FRAP (effect size=0.93), CAT (effect size=1.45), and SOD (effect size=1.44) (P<0.001). A single trial of WBV exercise improved all oxidant and antioxidant parameters towards a greater adaptation to the stress response in FM women.

Electronic and structural properties of the (1010) and (1120) ZnO surfaces.

The structural and electronic properties of ZnO (1010) and (1120) surfaces were investigated by means of density functional theory applied to periodic calculations at B3LYP level. The stability and relaxation effects for both surfaces were analyzed. The electronic and energy band properties were discussed on the basis of band structure as well as density of states. There is a significant relaxation in the (1010) as compared to the (1120) terminated surfaces. The calculated direct gap is 3.09, 2.85, and 3.09 eV for bulk, (1010), and (1120) surfaces, respectively. The band structures for both surfaces are very similar.

Reversal of lidocaine effects on sodium currents by isoproterenol in rabbit hearts and heart cells.

We demonstrated recently that isoproterenol enhanced the cardiac voltage-dependent sodium currents (INa) in rabbit ventricular myocytes through dual G-protein regulatory pathways. In this study, we tested the hypothesis that isoproterenol reverses the sodium channel blocking effects of class I antiarrhythmic drugs through modulation of INa. The experiments were performed in rabbit ventricular myocytes using whole-cell patch-clamp techniques. Reversal of lidocaine suppression of INa by isoproterenol (1 microM) was significant at various concentrations of lidocaine (20, 65, and 100 microM, P < 0.05). The effects of isoproterenol were voltage dependent, showing reversal of INa suppression by lidocaine at normal and hyperpolarized potentials (negative to -80 mV) but not at depolarized potentials. Isoproterenol enhanced sodium channel availability but did not alter the steady state activation or inactivation of INa nor did it improve sodium channel recovery in the presence of lidocaine. The physiological significance of the single cell INa findings were corroborated by measurements of conduction velocities using an epicardial mapping system in isolated rabbit hearts. Lidocaine (10 microM) significantly suppressed epicardial impulse conduction in both longitudinal (theta L, 0.430 +/- 0.024 vs. 0.585 +/- 0.001 m/s at baseline, n = 7, P < 0.001) and transverse (theta T, 0.206 +/- 0.012 vs. 0.257 +/- 0.014 m/s at baseline, n = 8, P < 0.001) directions. Isoproterenol (0.05 microM) significantly reversed the lidocaine effects with theta L of 0.503 +/- 0.027 m/s and theta T of 0.234 +/- 0.015 m/s (P = 0.014 and 0.004 compared with the respective lidocaine measurements). These results suggest that enhancement of INa is an important mechanism by which isoproterenol reverses the effects of class I antiarrhythmic drugs.

Autonomic control of ventricular tachycardia: direct effects of beta-adrenergic blockade in 24 hour old canine myocardial infarction.

The purpose of this study was to determine whether alpha- or beta-adrenergic influences directly modulate the rate of spontaneous ventricular tachycardia occurring 24 hours after left anterior descending coronary artery occlusion. Chloralose-anesthetized, open chest dogs (n = 41) with ventricular tachycardia were studied. The left anterior descending artery was cannulated distally. Neither intracoronary saline solution nor phenylephrine (0.3 to 12 micrograms) changed the rate of ventricular tachycardia; however, isoproterenol (0.01 to 10 micrograms) produced dose-dependent increases in the rate. In six dogs, metoprolol, 5 mg given intravenously, slowed ventricular tachycardia from 174 +/- 10 (mean +/- SE) to 140 +/- 17 beats/min (p less than 0.05). This was accompanied by decreases in mean arterial pressure from 106 +/- 7 to 95 +/- 8 mm Hg, cardiac output from 2.6 +/- 0.3 to 1.6 +/- 0.3 liters/min and prolongation of atrioventricular conduction from 134 +/- 10 to 189 +/- 29 ms (all p less than 0.05) during atrial pacing at a cycle length of 300 ms. In 10 dogs, metoprolol (0.5 mg) given intracoronary, a dose that shifted the isoproterenol dose-response curve to the right, slowed ventricular tachycardia from 174 +/- 7.2 to 140 +/- 9.7 beats/min (p less than 0.05) without hemodynamic changes. Additional metoprolol (4.5 mg) given intravenously produced hemodynamic alterations, but ventricular tachycardia did not slow further. Therefore, beta- but not alpha-adrenergic influences control the rate of ventricular tachycardia occurring 24 hours after left anterior descending coronary artery occlusion. Furthermore, beta-adrenergic blockade slows ventricular tachycardia solely by a direct electrophysiologic effect on the tachycardia foci and not indirectly as a result of hemodynamic effects.

Autonomic control of ventricular tachycardia. III. Effects of adenosine and N6-R-1-phenyl-2-propyladenosine.

The purpose of this study was to determine whether adenosine or the adenosine deaminase-resistant analogue, N6-R-1-phenyl-2-propyladenosine (RPIA), could slow the rate of spontaneous ventricular tachycardia occurring 24 hours after left anterior descending coronary artery occlusion. Chloralose-anesthetized, open chest dogs (n = 25) with ventricular tachycardia were studied. The left anterior descending artery was cannulated distally. Intracoronary infusions of adenosine, 10(-7) to 10(-5) M, did not alter the rate of ventricular tachycardia. Ventricular tachycardia slowed by 4.6% with adenosine, 10(-4) M. RPIA, 10(-6) to 10(-4) M, produced a concentration-dependent decrease in the rate of ventricular tachycardia when injected into the left anterior descending coronary artery. This effect of RPIA was reversed by the adenosine antagonist aminophylline, 10(-5) M. After bilateral stellate ganglionectomy, RPIA, 10(-5) M, did not, but metoprolol, 0.5 mg, did slow ventricular tachycardia after intracoronary injection. However, RPIA, 10(-5) M, produced a 43% decrease in the increment in ventricular tachycardia occurring during sympathetic neural stimulation. Therefore, when injected into the left anterior descending artery, adenosine, 10(-4) M, and RPIA, 10(-6) to 10(-4) M, decrease the rate of ventricular tachycardia in 24 hour old myocardial infarction. Furthermore, this decrease in the rate of ventricular tachycardia is the result of prejunctional sympathetic antagonism.

Chronic hypertension and left ventricular hypertrophy facilitate induction of sustained ventricular tachycardia in dogs 3 hours after left circumflex coronary artery occlusion.

The purpose of this study was to investigate the electrophysiology of acute ischemia in hypertrophic as compared with nonhypertrophic myocardium. Left circumflex coronary artery occlusion was produced in anesthetized open chest dogs. Of 40 dogs studied, 22 were normotensive and 18 had chronic hypertension produced by a single kidney renal clamp procedure. Recordings of electrograms and extrastimulus testing were performed in endocardial and epicardial sites in both normal and ischemically damaged zones documented by triphenyltetrazolium chloride. In the hypertrophy group, there was greater endocardial to epicardial conduction delay in ischemic zones, mean +/- SEM 57 +/- 4 ms versus 31 +/- 2 ms in the normotensive group (p less than 0.05). Also, sustained monomorphic ventricular tachycardia was inducible in seven of eight dogs with hypertrophy and in none of eight normotensive dogs surviving to 3 h. Entrainment and several observations during induction were consistent with reentrant ventricular tachycardia. To exclude hypertension alone as an etiology of tachycardia, five normotensive dogs without inducible monomorphic tachycardia remained unchanged during hypertension produced with low doses of phenylephrine or descending aortic occlusion. Thus, the electrophysiologic response to ischemia is altered in hypertrophied myocardium, which predisposes to rapid sustained monomorphic ventricular tachycardia.

Significance of inducible tachycardia in patients with syncope of unknown origin: a long-term follow-up.

The frequency of inducible tachycardia was assessed in patients presenting with syncope whose noninvasive evaluation did not reveal a cause for syncope. It was also determined whether treatment of tachyarrhythmias during programmed electrical stimulation would prevent recurrence of syncope. One hundred five patients were studied and 97 were followed up for a mean period of 25.8 months. Sixty-eight patients (65%) did not have inducible tachycardia. Sixty of these 68 patients could be followed up; 12 (20%) had recurrent syncope. Ventricular or supraventricular tachycardia was inducible in 37 patients (35%). The frequency of organic heart disease was not higher in this group or in those with inducible ventricular tachycardia as compared with those with inducible supraventricular tachycardia. Three patients with inducible ventricular tachycardia died suddenly or were resuscitated from cardiac arrest, and an additional seven had recurrent syncope; thus, the total recurrence rate was 27%. Of 23 patients undergoing effective therapy as predicted by electrophysiologic testing, 3 (14%) had a recurrent event. Results were significantly different in patients receiving ineffective therapy as judged by electrophysiologic testing. Of 13 patients in this latter category, 7 patients (54%) had recurrence of syncope or cardiac arrest (p less than 0.05). In three patients, recurrence took place a mean of 5 months after cessation of therapy; on resumption of effective therapy, no syncope recurred for 15.6 months (p less than 0.025). Tachycardia is frequently induced in patients with syncope of unknown origin, whether or not organic heart disease is present. Treatment of inducible tachycardia may prevent recurrence of syncope.

Propranolol blocks ventricular refractory period changes with orthostatic stress in humans.

The purpose of this study was to test the hypothesis that orthostatic stress shortens the right ventricular effective refractory period by reflex activation of beta-adrenergic receptors. Twelve patients undergoing electrophysiologic testing for standard clinical indications were studied. After a full electrophysiologic study, patients underwent graded lower body negative pressure before and after administration of either propranolol (0.2 mg/kg intravenously) in Group I or atropine (0.035 mg/kg intravenously) in Group II. Before the addition of drugs, lower body negative pressure produced decreases in systolic blood pressure and significant increases in sinus rate. The effective refractory period shortened from 214 +/- 8 (mean +/- SEM) to 206 +/- 7 ms at -40 cm H2O and to 197 +/- 4 ms at -60 cm H2O lower body negative pressure. After propranolol, Group I patients had no change in right ventricular effective refractory period despite similar changes in sinus rate and systolic blood pressure. In group II patients, atropine did not alter effective refractory period responses to lower body negative pressure. Thus, reflex adjustments to orthostatic stress result in shortening of right ventricular effective refractory period mediated by way of beta-adrenergic mechanisms. These findings constitute the first evidence that sympathetic influences mobilized by the body can directly modulate ventricular electrophysiologic changes.

Distribution of local repolarization changes produced by efferent vagal stimulation in the canine ventricles.

The purpose of this study was to compare the distribution of effects of right and left efferent vagal stimulation on ventricular recovery properties in the in situ heart. To measure these effects in many areas simultaneously, local repolarization changes (local QT intervals) were recorded with bipolar electrodes in nine ventricular sites from 38 anesthetized dogs. In initial experiments, this method was shown to correlate with effective refractory period changes measured in the same test site after QT recording; vagal nerve stimulation prolonged the local QT interval by 1 ms for each 0.82 ms prolongation in effective refractory period (r = 0.87). Simultaneous local QT recordings during vagal nerve stimulation demonstrated uniform prolongation with two exceptions. First, left vagal efferent stimulation prolonged local QT interval in the posterior left ventricular base more than did right vagal stimulation (5.9 +/- 1.0 mean +/- standard error of the mean versus 3.7 +/- 0.9%, p less than 0.05). This probably resulted from an interaction with the left sympathetic nerves because left stellate ganglionectomy or norepinephrine infusion eliminated differences between effects of right and left vagal stimulation. Second, it was also found that vagal stimulation from either side did not prolong local QT interval time in the anterior right ventricle despite attempts to augment vagal effects with bilateral vagal stimulation alone or during isoproterenol or physostigmine administration. These regional differences in ventricular repolarization exhibited in response to efferent vagal nerve stimulation in the dog may provide a basis for understanding how autonomic influences could contribute to the genesis of ventricular arrhythmias.

Bradycardia and syncope as manifestations of partial epilepsy.

Although transient increases in heart rate typically occur, bradycardia has infrequently been noted in association with partial seizures. Five patients with temporal lobe epilepsy are described in whom sinus bradyarrhythmias and syncope were prominent manifestations of seizure activity. Partial improvement occurred in one of two patients in whom a permanent pacemaker was implanted before a diagnosis of epilepsy was established. Treatment with phenytoin or carbamazepine resulted in nearly complete resolution of symptoms in all five patients. Because pacemaker implantation does not prevent recurrent symptoms, but anticonvulsant therapy does, this experience underscores the importance of considering the diagnosis of partial epilepsy in selected patients with sinus bradyarrhythmias and syncope.

Self-adhesive preapplied electrode pads for defibrillation and cardioversion.

The efficacy of self-adhesive electrode pads for defibrillation and cardioversion was assessed in 80 patients who received 267 shocks from self-adhesive pads. In all but two patients, defibrillation or cardioversion was achieved at least once. The pads were equally effective when used in the apex-anterior or apex-posterior position. The transthoracic impedance using self-adhesive pads was 75 +/- 21 ohms (mean +/- standard deviation), which is similar to previously reported transthoracic impedance in defibrillation, using standard hand-held electrode paddles of 67 +/- 36 ohms. It is concluded that self-adhesive electrode pads are effective for defibrillation and cardioversion.

Exercise and anxiety neurosis: comparison of patients with and without mitral valve prolapse.

It has been hypothesized that mitral valve prolapse may account for a substantial number of patients who have symptoms of chronic anxiety neurosis. In a previous investigation, this hypothesis was confirmed in eight of 21 patients who had anxiety neurosis. In the present investigation, we reevaluated the hypothesis that persons with anxiety neurosis have impaired exercise ability by exercising 20 of the anxiety neurotics according to a standard treadmill exercise protocol. Compared with the control group, the anxiety neurotics required less exercise to achieve an equivalent heart rate and therefore their estimated maximum oxygen consumption was less, thus confirming the hypothesis. However, this difference was due entirely to the anxiety neurotics with mitral valve prolapse, and those without prolapse did not differ significantly from the controls. This suggests that impaired exercise tolerance in anxiety neurotics may be attributable to a subgroup of these patients with mitral valve prolapse.

Inhibition of adrenergic neurotransmission in ischaemic regions of the canine left ventricle.

To test hypothesis that adrenergic neurotransmission is impaired in acute myocardial ischaemia, we studied contractile function of normal and ischaemic myocardium after coronary artery occlusion. For each area we compared the contractile response to left sympathetic nerve stimulation (LSS) with the response to exogenous noradrenaline (NA). Contractile response was measured with intramyocardial sonomicrometers. LSS increased aortic pressure and heart rate. NA was infused to achieve an aortic pressure equivalent to LSS and simultaneous atrial pacing matched the heart rate during LSS. In normal zones both interventions produced increased shortening equivalently. In ischaemic zones systolic expansion was unchanged during LSS, while NA improved contractile function of the same zones by decreasing systolic expansion. These responses occurred during ischaemia produced by either anterior or posterior descending coronary occlusion. Changes in regional blood flow, measured by 8 microns radiolabelled microspheres, could not account for the difference between the ischaemic regional response to LSS or NA. We conclude that acute regional ischaemia impairs adrenergic nerve transmission.

Carotid sinus baroreflex influence on electrophysiologic properties of the canine atrioventricular node and ventricle.

This study examines the efferent mechanisms of carotid sinus baroreflex influence on ventricular repolarization and refractory period compared with effects on atrioventricular (AV) nodal conduction. Pressure was controlled in both carotid sinuses by the Moisejeff technique in 16 chloralose-anesthetized dogs. Increases in carotid sinus pressure during pacing produced graded prolongation of AV nodal conduction, ventricular repolarization and refractory period with a threshold at a carotid sinus pressure of 120 mm Hg and a peak response at 200 mm Hg. Atropine, 0.4 mg/kg, attenuated the peak percent change in ventricular repolarization interval by only 12 +/- 14% (+/- standard error of the mean) despite a significantly greater attenuation (48 +/- 11%, p less than 0.05) in peak percent change in AV nodal conduction. However, stellate ganglionectomy attenuated the peak percent change in ventricular repolarization (42 +/- 19%), similar to effects on AV nodal conduction (59 +/- 21%, p greater than 0.25). Changes in mean arterial pressure, ventricular end-diastolic segment length or segment length shortening with systole (sonomicrometer technique) did not account for the electrophysiologic responses. Latency to peak effect on ventricular repolarization (43 +/- 7 seconds) was slower than that on AV nodal conduction (23 +/- 6 seconds, p less than 0.05). This difference in time course was not abolished by atropine. Thus, the carotid sinus baroreflex prolongs ventricular repolarization and refractoriness mainly by withdrawal of sympathetic influence; AV nodal conduction is prolonged by both vagal activation and sympathetic withdrawal. In addition, differences in time course between ventricular and AV nodal electrophysiologic responses are not explained by different efferent autonomic mechanisms.

Usefulness of isoproterenol facilitation of ventricular tachycardia induction during extrastimulus testing in predicting effective chronic therapy with beta-adrenergic blockade.

Previous studies indicate that programmed extrastimulus testing (PES) during isoproterenol infusion facilitates induction of clinical ventricular tachycardia (VT) in some patients. This study attempts to determine if VT inducible only during isoproterenol infusion predicts suppression of VT with chronic oral beta-adrenergic blockade. Nine patients, aged 23 to 77 years, with symptomatic VT or syncope not necessarily provoked by exercise or stress were evaluated. Extrastimuli did not induce VT in any patient. However, during isoproterenol infusion (1 to 4 micrograms/min), all patients had reproducibly inducible VT corresponding to their spontaneously occurring VT (recordings available in 7 patients). Coupling intervals inducing tachycardia during isoproterenol were similar to intervals that did not induce VT without isoproterenol. No patient had VT with isoproterenol infusion alone (without extrastimuli). In only 4 of 8 patients who underwent exercise tests while not taking medications was VT provoked. With propranolol therapy (160 mg/day) or its equivalent, only 1 patient had recurrent symptoms during a mean follow-up of 39 months (range 23 to 52). VT inducible with extrastimuli only during isoproterenol infusion predicts that oral beta-adrenergic blockade will prevent spontaneous VT or syncope long term. These data suggest that occurrence of VT in some patients depends on premature depolarizations in the setting of beta-adrenergic influence.

Effect of direct, reflex and exercise-provoked increases in sympathetic tone on idiopathic ventricular tachycardia.

Exercise treadmill testing and direct enhancement of sympathetic influence with agents such as isoproterenol are often used to reproduce ventricular tachycardia (VT). The cardiac effects of, and arrhythmia responses to, graded exercise, isoproterenol infusion and lower body negative pressure (the latter 2 with and without atrial and ventricular stimulation) were studied in 11 patients with idiopathic VT. During maximal exercise, substantial increases in heart rate and blood pressure occurred, but only 2 of 9 exercised patients had VT (during recovery in both). During programmed stimulation alone, VT was initiated in 6 patients. During maximum levels of lower body negative pressure (-60 cm of water in most), mean systolic blood pressure decreased by 10 mm Hg, heart rate increased by 15 beats/min, and ventricular refractory period decreased by 10 ms. In 4 patients VT occurred spontaneously during lower body negative pressure; in 2, lower body negative pressure was the only intervention producing VT. During isoproterenol infusion VT occurred spontaneously in 2 patients; both had VT initiated during other interventions. Lower body negative pressure and isoproterenol increased VT rate, but did not prolong it. It is concluded that there is significant variability in arrhythmia responses to sympathetic augmentation, suggesting that additional covariables such as parasympathetic input and ventricular volume may also have a role in arrhythmia occurrence.

Sympathetic denervation limited to a region of acutely ischemic canine myocardium increases excitability threshold and duration of bipolar electrograms.

This study determines the direct effects of sympathetic denervation on excitability threshold and bipolar electrograms in acutely ischemic myocardium. Regional denervation was performed by application of phenol to the epicardium surrounding the ischemic zone in order to eliminate the possible hemodynamic effects that global cardiac denervation may exert on the ischemic zone. Data were obtained during serial occlusions (less than or equal to 6 minutes in duration) of left anterior coronary artery in open-chest dogs with sympathetic denervation performed before the last occlusion. Late diastolic threshold was measured every 5 seconds by a constant voltage pacemaker which automatically registered threshold in stimulus duration. During ischemia, regional denervation (n = 9) increased peak excitability threshold from 240 +/- 51 (standard error of the mean) to 552 +/- 182 mus (p less than 0.05) and prolonged electrographic duration in epicardium from 19 +/- 3 to 25 +/- 4 ms (p less than 0.025) and in endocardium from 20 +/- 3 to 25 +/- 4 ms (p less than 0.01). Phenol application did not alter aortic pressure, ischemic wall motion (sonomicrometer technique), or ischemic zone blood flow (microsphere technique). Thus, acute sympathetic denervation when limited to ischemic myocardium increases the peak excitability threshold and concomitantly prolongs duration of bipolar electrograms.