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Biomedical subjects

R Wolk

Publications and source records attributed to R Wolk.

At least 19 recordsLinked to original sources
PubMed2006

Obesity-related cardiovascular disease: implications of obstructive sleep apnea.

Obesity and obstructive sleep apnea (OSA) often coexist. OSA has been linked to cardiovascular disease. Thus, OSA may contribute to the cardiovascular consequences of obesity. In this review, we explore clinical and pathophysiological interactions between obesity, cardiovascular disease and OSA. We discuss the mechanisms whereby OSA may contribute to hypertension, atherosclerosis, insulin resistance and atrial fibrillation associated with obesity, and emphasize the potential implications for understanding why only a subgroup of obese patients develop cardiovascular disease. Identification of the OSA-dependent and OSA-independent pathways in the cardiovascular pathophysiology of obesity may hold clinical and therapeutic promise.

Atherosclerosis↗
PubMed2001

Clinical characteristics of patients with increased urinary excretion of adrenaline in mild to moderate heart failure.

BACKGROUND: We have previously demonstrated that adrenaline (AD) is released into the circulation during acute myocardial infarction and is associated with a more severe clinical course. The role of elevated AD levels in congestive heart failure is not known. HYPOTHESIS: The study aimed to determine whether increased daily AD excretion is associated with more severe clinical symptoms and a more complicated clinical course in patients with exacerbation of congestive heart failure (CHF). METHODS: Urinary excretion of AD, noradrenaline, magnesium (Mg), and potassium (K), serum levels of aldosterone, K, and Mg, as well as the incidence of arrhythmias (24-h Holter) were assessed in 49 patients with CHF New York Heart Association (NYHA) class II-III. The patients were allocated to two groups, with normal (Group 1) and increased (Group 2) excretion of AD. RESULTS: Groups 1 and 2 did not differ in respect of age, etiology of CHF, or the medication used. Also, left ventricular ejection fraction was similar in the two groups. However, left ventricular end-diastolic dimension was greater in Group 2 (61+/-9 vs. 55+/-11 mm, p<0.05), as was the proportion of patients in NYHA class III (74 vs. 40%). Group 2 was also characterized by increased urinary excretion of Mg (60+/-24 vs. 43+/-16 mg/24 h, p < 0.007) and the presence of more complex and numerous ventricular arrhythmias (74 vs. 37% and 68 vs. 33% of patients, respectively). CONCLUSIONS: Urinary excretion of AD is increased only in a subgroup of patients with CHF. These patients are characterized by a more advanced NYHA class, increased end-diastolic left ventricular diameter, and increased urinary excretion of magnesium. It is likely that all these factors contribute to the presence of more complex and numerous ventricular arrhythmias in this subgroup of patients.

Aged↗
PubMed2001

Event-free survival in patients after an acute coronary event with exercise-induced normalization of the T-wave.

BACKGROUND: Risk stratification of patients with unstable angina or non-Q-wave myocardial infarction (MI) is an unresolved clinical problem. The prognostic value of T-wave normalization (TWN) during exercise has not been studied in this group of patients. HYPOTHESIS: Event-free survival in clinically stable patients after an acute coronary event without ST-segment elevation can be predicted by the presence of exercise-induced TWN. METHODS: Sixty-five patients (43 men and 22 women, mean age 62+/-10 years) entered the study. The diagnosis of unstable angina and non-Q-wave MI was made in 40 and 25 patients, respectively. A treadmill exercise test was performed in all patients after clinical stabilization. The patients were divided into three groups: those with negative baseline T waves and exercise-induced TWN (Group 1); those with negative baseline T waves, but without TWN (Group 2); and those with positive baseline T waves (Group 3). The patients were followed up for 6 months. RESULTS: During follow-up, serious cardiovascular complications occurred in 15 (23%) patients. These included exacerbation of ischemic heart disease (14 patients) and acute MI (1 patient). Event-free survival was greater in patients in Group 1 (95%) than in those in Group 2 (68%, p < 0.034) or Group 3 (71%, NS). Among all patients studied, exercise-induced TWN was predictive of event-free survival with a sensitivity of 38% and a specificity of 93%. CONCLUSIONS: In clinically stable patients after an acute coronary event without ST-segment elevation, exercise-induced TWN is a specific but n ot sensitive predictor of event-free survival after 6 months.

Acute Disease↗
PubMed2001

Extrasystolic beats affect transmural electrical dispersion during programmed electrical stimulation.

BACKGROUND: Experimental studies suggest that the electrocardiographic Tpeak-Tend (TpTe) interval reflects transmural dispersion of repolarization (TDR). The genesis and role of the TpTe interval in a clinical setting have not been established. This study aimed to assess the clinical usefulness of the TpTe interval as an index of TDR and a pro-arrhythmic marker. MATERIALS AND METHODS: Endocardial monophasic action potential (MAP) duration and electrocardiographic QTp, QTe and TpTe intervals were assessed in 13 patients undergoing an electrophysiological study. Surface electrocardiograms were recorded during right ventricular pacing (Basic Cycle Length = 600 ms) before and after single extrastimuli. RESULTS: Ventricular arrhythmia was induced in six patients. During ventricular pacing, MAP duration and QTp intervals shortened in response to extrastimuli applied at progressively shorter coupling intervals. In contrast, QTe intervals increased in response to premature stimulation and QTe dispersion increased at short coupling intervals. During sinus rhythm, the TpTe interval was greater in the inducible group in leads V3-V4. Premature stimulation increased the duration of TpTe intervals, suggesting an increase in TDR. The maximum TpTe interval was greater in the inducible than in the noninducible group, both during baseline ventricular drive pacing (163 +/- 22 vs. 130 +/- 27 ms, respectively, P < 0.03) and after application of shortly coupled extrastimuli (263 +/- 66 vs. 200 +/- 47 ms, respectively, P < 0.05). CONCLUSIONS: The TpTe interval of surface ECG is likely to represent TDR. TDR is increased by premature ventricular stimulation and the magnitude of the maximum TpTe interval (i.e. maximum TDR) during ventricular pacing is greater in patients with inducible arrhythmias.

Action Potentials↗
PubMed2001

Left ventricular hypertrophy increases transepicardial dispersion of repolarisation in hypertensive patients: a differential effect on QTpeak and QTend dispersion.

BACKGROUND: Ventricular arrhythmias in left ventricular hypertrophy (LVH) are related to regional electrical heterogeneity. The significance of noninvasive electrocardiographic indices of electrical heterogeneity in LVH has not been established. The aim of the study was to investigate changes in the Tpeak-Tend interval (an index of transmural dispersion of repolarisation) in addition to other traditional electrocardiographic indices of electrical dispersion in patients with hypertensive LVH. METHODS: Consecutive patients were screened for the presence of hypertensive echocardiographic LVH and compared with a control group. LVH was identified as left ventricular mass > 134 g m-2 in men and > 110 g m-2 in women. Twelve-lead ECGs were analysed in respect of various indices of electrical dispersion. RESULTS: Left ventricular mass was greater in the LVH than in the control group (174 +/- 39 vs. 101 +/- 18 g m-2, P < 0.0001). The Tpeak-Tend interval was not affected by LVH. The main effect of LVH was an increase in QTpeak dispersion (40 +/- 13 vs. 53 +/- 21 ms, P < 0.05), which resulted from an increase in the maximum QTpeak interval (337 +/- 24 vs. 358 +/- 30 ms, P < 0.04), without any change in the minimum QTpeak interval. There was a significant correlation between the left ventricular mass index and QTpeak dispersion (r = 0.40; P < 0.01). In contrast, LVH did not exert any effect on QTend dispersion (65 +/- 21 vs. 65 +/- 16 ms, ns), because LVH increased both the maximum QTend interval (430 +/- 30 vs. 449 +/- 28 ms, P < 0.05) and the minimum QTend interval (365 +/- 29 vs. 384 +/- 27 ms, P < 0.04). CONCLUSIONS: Hypertensive LVH exerts a differential effect on QTpeak and QTend interval dispersion. The most likely explanation is that these changes reflect a nonuniform prolongation of action potential duration across the epicardium, leading to an increase in transepicardial dispersion of repolarisation.

Action Potentials↗
PubMed2001

Effects of glucose-insulin-potassium infusion on QT dispersion in patients with acute myocardial infarction.

BACKGROUND: Increased QT dispersion during acute myocardial infarction (AMI) has been associated with the occurrence of ventricular arrhythmias. Also, serum potassium levels have been shown to be relevant to the arrhythmic risk in this group of patients. The aim of the present study was to assess changes in QT dispersion during infusion of glucose-insulin-potassium (GIK) during AMI. METHODS: Patients from the Pol-GIK study were analyzed retrospectively. The patients were selected from the placebo (1000 mL of 0.89% NaCl) and the GIK (1000 mL of 10% dextrose, 20-32 units of insulin, 80 mEq K(+)) groups (18 and 24 patients, respectively). QT interval duration and dispersion (the difference between the longest and shortest QT intervals) were measured at baseline, 18-24 hours into placebo/GIK infusion and 24 hours after the end of infusion. RESULTS: In the placebo group, plasma potassium levels changed from 4.1 +/- 0.5 mmol/L at baseline to 4.6 +/- 0.8 mmol/L during infusion (P < 0.05) and 4.6 +/- 0.4 mmol/L after infusion, whereas in the GIK group the respective values were 4.0 +/- 0.4, 4.6 +/- 0.3 (P < 0.0001), and 4.5 +/- 0.5 mmol/L. QT interval duration was stable throughout the study and there was no difference between the groups. The two groups did not differ in respect to QT dispersion at any time point, the respective values were 79 +/- 28, 65 +/- 25, and 77 +/- 27 ms in the placebo group, and 61 +/- 35, 60 +/- 26, and 76 +/- 43 ms in the GIK group. The incidence of arrhythmias was also similar in both groups. CONCLUSIONS: GIK, at the dose used, is unlikely to affect heterogeneity of ventricular repolarization during AMI.

Aged↗
PubMed2000

Effects of oral L-arginine supplementation on exercise-induced QT dispersion and exercise tolerance in stable angina pectoris.

We assessed the effects of L-arginine (an endogenous precursor of nitric oxide) on the magnitude of exercise-induced QT dispersion in patients with coronary artery disease. The study had a randomized double-blind cross-over design. Twenty-five patients with stable coronary artery disease underwent two separate exercise tests: after oral administration of L-arginine (6 g/24 h for 3 days) or placebo. Indications for cessation of exercise included: pulse limit, exhaustion, chest pain, ST segment depression >2 mm. We found that arginine significantly increased exercise duration from 604+/-146 to 647+/-159 s (P<0.03). However, it had no effect on the sum of exercise-induced ST segment depressions (1.9+/-2.3 and 2.4+/-3.3 on and off arginine, respectively, NS). Exercise shortened QT interval to a similar extent in patients treated with placebo or arginine. QT dispersion changed during exercise from 55+/-21 to 60+/-19 ms (NS) and from 60+/-21 to 53+/-17 ms (NS), respectively. We conclude that, in patients with coronary artery disease, oral supplementation of L-arginine does not affect exercise-induced changes in QT interval duration, QT dispersion or the magnitude of ST segment depression. However, it significantly increases exercise tolerance, most likely due to improved peripheral vasomotion. These results may be of clinical and therapeutic importance.

Aged↗
PubMed2000

Congenital pleuroperitoneal communication in a patient with pseudomyxoma peritonei.

BACKGROUND AND OBJECTIVES: Pseudomyxoma peritonei syndrome is a rare disease arising from a perforated appendiceal adenoma. The syndrome is characterized by progressive accumulation of mucinous ascites and tumor within the peritoneal cavity. Direct extension of pseudomyxoma peritonei to the pleural cavity is uncommon and has been associated with surgical penetration of the diaphragm at the time of cytoreduction. METHODS: We review the case of a patient who presented with mucoid peritoneal and pleural fluid consistent with spontaneous pleural spread of pseudomyxoma peritonei. RESULTS: Surgical exploration confirmed direct pleuroperitoneal communication by macroscopic diaphragmatic fenestration. CONCLUSIONS: This is a rare phenomenon. We outline a therapeutic approach to be applied when pleural involvement is suspected in patients with pseudomyxoma peritonei syndrome.

Female↗
PubMed2000

Isosorbide dinitrate inhibits platelet adhesion and aggregation in nonthrombolyzed patients with acute myocardial infarction.

BACKGROUND: Apart from their vasodilatatory properties, nitrates have been shown to inhibit platelet aggregation. The effects of nitrates on platelet adhesion have not been studied. Nonselected patients with acute myocardial infarction (AMI) have been suggested to gain no benefit from administration of nitrates. However, the importance of nitrates may be greater in a subgroup of nonthrombolyzed patients with AMI. HYPOTHESIS: Isosorbide dinitrate (ISDN) decreases platelet adhesion and aggregation in nonthrombolyzed patients with AMI. METHODS: Consecutive 48 men with AMI, not eligible for thrombolytic therapy because of late presentation (> 12 h), were prospectively randomized 2:1 to double-blind ISDN (mean dose 2.4 +/- 0.9 mg/h) (n = 33) or placebo (0.9% sodium chloride) (n = 15) infusion. All patients received aspirin. Blood samples were taken at baseline (no study medication) and 3 h into ISDN or placebo infusion. Platelet adhesion to collagen was measured in the ethylene diamine tetraacetic acid (EDTA)-platelet rich plasma by recording changes in light transmission with an optical aggregometer. Platelet aggregation was measured using the Born's method. RESULTS: Isosorbide dinitrate significantly decreased both platelet adhesion and aggregation. No effect was seen in the placebo group. CONCLUSIONS: In patients with AMI who do not receive thrombolytic therapy, ISDN effectively inhibits platelet adhesion and aggregation. These effects of nitrates may be of therapeutic and prognostic significance in this group of patients.

Adult↗
PubMed2000

Regional electrophysiological effects of left ventricular hypertrophy in isolated rabbit hearts under normal and ischaemic conditions.

OBJECTIVES: Left ventricular hypertrophy (LVH) has been reported to produce differential electrophysiological effects in isolated epicardial and endocardial cells. This study aimed to examine regional electrophysiological effects of LVH in normal and ischaemic conditions in the whole heart. METHODS: LVH was secondary to perinephritis-induced hypertension. Monophasic action potential duration (MAPD(90)), effective refractory period (ERP) and conduction delay were measured in paced, isolated working rabbit hearts either at one right ventricular and two left ventricular sites (apical and basal epicardium) or at three left ventricular sites (apical and basal epicardium, apical endocardium). The hearts were subjected to 30 min of regional ischaemia and 15 min of reperfusion. RESULTS: In non-ischaemic conditions, LVH produced uniform prolongation of MAPD(90) and ERP in the left ventricular epicardium, but not in the endocardium. After coronary artery occlusion, LVH significantly increased ischaemia-induced transepicardial dispersion of repolarisation, but not refractoriness. LVH did not affect arrhythmogenesis in either non-ischaemic or ischaemic conditions. CONCLUSIONS: Differential effects of LVH on epicardial and endocardial electrophysiological parameters are also observed in the whole heart. In addition, the sensitivity of hypertrophied myocardium to ischaemia is increased and leads to an increase in ischaemia-induced dispersion of repolarisation. However, neither dispersion of refractoriness nor arrhythmogenesis are affected by LVH in non-ischaemic or ischaemic conditions in this experimental model.

Action Potentials↗
PubMed2000

Hypomagnesemia in heart failure with ventricular arrhythmias. Beneficial effects of magnesium supplementation.

OBJECTIVE: To assess the role of electrolyte imbalance in cardiac arrhythmias associated with congestive heart failure. DESIGN: Serum magnesium and potassium levels, urine magnesium excretion and the incidence of ventricular arrhythmias were assessed throughout the study. The patients who displayed complex arrhythmias after the first week of hospital medication were randomized 2:1 to double-blind magnesium supplementation or placebo. SETTING: The study was carried out in one municipal hospital, providing primary care. SUBJECTS: A total of 588 consecutive patients were screened for eligibility (clinical heart failure >/=6 months; NYHA class II-IV; left ventricular ejection fraction </=40%; sinus rhythm; serum creatinine </=2 mg dL-1). A total of 78 patients entered and 68 patients completed the study. INTERVENTIONS: Intravenous administration of magnesium (magnesium sulphate 8 g in 250 mL of 5% glucose) or placebo (250 mL of 5% glucose) over 12 h. MAIN OUTCOME MEASURES: (i) Incidence of ventricular arrhythmias in patients with hypomagnesemia; (ii) effects of magnesium supplementation on ventricular arrhythmias. RESULTS: On admission, hypomagnesemia was found in 38% and excessive magnesium loss in 72% of patients. Serum magnesium levels were lower and urine magnesium excretion was greater in patients with complex ventricular arrhythmias, both on admission and after treatment for heart failure. Intravenous administration of magnesium caused a significant decrease in the number of ventricular ectopic beats (P < 0.0001), couplets (P < 0.003) and episodes of nonsustained ventricular tachycardia (P < 0.01). CONCLUSIONS: Hypomagnesemia, probably related to increased urine magnesium excretion, is an essential feature of heart failure associated with complex ventricular arrhythmias. These arrhythmias can be alleviated/abolished by magnesium supplementation.

Aged↗
PubMed2000

Arrhythmogenic mechanisms in left ventricular hypertrophy.

An important mechanism contributing to the high mortality and sudden death in patients with left ventricular hypertrophy (LVH) is ventricular arrhythmia. Part of the risk is associated with the pro-arrhythmic electrophysiological phenotype of the hypertrophied myocardium. The most consistently observed abnormality is prolongation of the action potential duration and refractoriness, which sets the stage for arrhythmias based on early or delayed afterdepolarizations and triggered activity. In addition, non-uniform prolongation of the action potential in LVH may be pro-arrhythmic by leading to increased dispersion of repolarization or refractoriness and favouring re-entry. The occurrence of delayed after depolarization-induced triggered activity and other ventricular arrhythmias are also related to the impaired ability to handle intracellular calcium due to changes in the density of ryanodine receptors and the Ca2+-ATPase of the sarcoplasmic reticulum. Slowing and fractionation of ventricular conduction, creating the conditions for micro-reentry and arrhythmogenesis, are characteristic of severe LVH, as is the expression of the I(f) current (which may be a source of increased automaticity). The pro-arrhythmic potential of LVH is also related to the presence of coexisting 'extrinsic' factors. The most important and pro-arrhythmic association of LVH is that with myocardial ischaemia. Other conditions include neuroendocrine factors, ventricular wall stress or electrolyte disturbances. The electrophysiological mechanisms of the interactions between these 'extrinsic' factors and LVH have not been fully elucidated. Further research into these mechanisms is required and may have important implications for our understanding of the mechanisms of cardiac arrhythmias in LVH and the appropriate use of antiarrhythmic drug therapy.

Arrhythmias, Cardiac↗
PubMed1999

Facilitation of spontaneous defibrillation by moxonidine during regional ischaemia in an isolated working rabbit heart model.

Moxonidine has been shown to be antiarrhythmic during ischaemia in vivo. This study aimed to investigate its electrophysiological effects in isolated working rabbit hearts in vitro. Monophasic action potential duration, effective refractory period and conduction delay were measured at three ventricular sites. The hearts were treated before and during ischaemia and reperfusion with vehicle, moxonidine (0.01, 0.1 and 1 microM) or labetalol (1 microM). In all groups, ventricular fibrillation was always induced during ischaemia. Only 0.1 microM moxonidine decreased the incidence of sustained ventricular fibrillation from 86 to 17%, although it did not affect any electrophysiological parameters measured. Similarly, labetolol, an adrenoceptor blocker, facilitated spontaneous defibrillation without any electrophysiological effects. In conclusion, moxonidine directly facilitates spontaneous defibrillation of ventricular fibrillation during ischaemia. Since the same effect is observed with labetalol, it is possible that the defibrillatory action of moxonidine is related to its peripheral antiadrenergic activity, although other mechanisms cannot be excluded.

Action Potentials↗
PubMed1999

Functional, structural, and dynamic basis of electrical heterogeneity in healthy and diseased cardiac muscle: implications for arrhythmogenesis and anti-arrhythmic drug therapy.

The electrophysiological properties of the ventricular myocardium are extremely heterogeneous. There are intrinsic electrical differences between the myocytes from different regions of the heart (most notably between the epicardium, midmyocardium, and endocardium), which are the result of different contributions of ionic currents to the transmembrane action potential. Sources of local anisotropy include directional differences in the distribution of gap junctions between adjacent myocytes and the presence of intercalated non-myocytes (e.g., fibroblasts), propagation boundaries, and wavefront collisions, which can lead to local variability of electrical load and, therefore, to nonuniform depolarisation and repolarisation. In addition, the complex anatomical arrangement of the myocardial fibres and nonuniform distribution of transmural mechanical stresses also contribute to electrical heterogeneity. Finally, dispersion of repolarisation is dynamically modified by the restitution properties of individual myocytes, stimulation rate, and the direction of conduction. All aspects of this electrical heterogeneity can be affected by different pathological conditions, such as myocardial ischaemia and cardiac hypertrophy. In particular, differential responses of various myocyte populations to these pathological stimuli and a marked increase in nonuniform anisotropy may be responsible for increased pro-arrhythmic potential in these conditions. In addition, the clinical effectiveness of anti-arrhythmic drugs may be related to their effects on electrical heterogeneity.

Action Potentials↗
PubMed1999

Relevance of inter- and intraventricular electrical dispersion to arrhythmogenesis in normal and ischaemic rabbit myocardium: a study with cromakalim, 5-hydroxydecanoate and glibenclamide.

This study aimed to investigate the role of electrical dispersion in arrhythmogenesis by using K(ATP) channel modulating agents. Monophasic action-potential duration (MAPD90), effective refractory period (ERP), and conduction delay were measured at three ventricular sites in isolated working rabbit hearts. Cromakalim (10 microM), glibenclamide (3 microM), or 5-hydroxydecanoate (100 microM) were administered before and throughout 30 min of regional ischaemia and 15 min of reperfusion. Before ischaemia, cromakalim reduced MAPD90 and ERP in all areas and facilitated induction of ventricular fibrillation in five of 12 hearts. In these hearts, cromakalim increased interventricular ERP dispersion from 17 +/- 5 to 38 +/- 5 ms. During ischaemia, cromakalim decreased MAPD90 dispersion within the left ventricle from 84 +/- 5 to 44 +/- 4 ms, but did not affect ERP dispersion and arrhythmogenesis. 5-Hydroxydecanoate had no effect on MAPD90 and ERP shortening or dispersion during ischaemia and reperfusion and was not antiarrhythmic. Glibenclamide reduced forward flow to zero, preventing further electrophysiologic studies. In conclusion, in this model, an increase in interventricular ERP dispersion predisposes to ventricular fibrillation in normoxic conditions after cromakalim administration. However, a decrease in ischaemia-induced MAPD90 dispersion by cromakalim does not affect arrhythmogenesis. A lack of effect of 5-hydroxydecanoate on electrical dispersion during ischaemia is accompanied by a lack of antiarrhythmic activity.

Action Potentials↗
PubMed1998

Regional electrophysiological effects of hypokalaemia, hypomagnesaemia and hyponatraemia in isolated rabbit hearts in normal and ischaemic conditions.

OBJECTIVE: The aims of this study were to establish an isolated working heart model for electrophysiological recordings from the epicardium and endocardium and to examine regional effects of changes in ion concentrations in normal and ischaemic conditions. METHODS: Monophasic action potential duration (MAPD90), effective refractory period (ERP) and conduction delay were measured simultaneously in the epicardium and endocardium of rabbit hearts paced at 3.3 Hz, subjected to 30 min of regional ischaemia and 15 min of reperfusion. The hearts were exposed before and throughout ischaemia and reperfusion to hypokalaemia (K+ = 2 mM), hypomagnesaemia (Mg2+ = 0.5 mM) or hyponatraemia (Na+ = 110 mM). RESULTS: In the control hearts, no regional electrophysiological differences were seen before ischaemia, but ischaemia-induced MAPD90 shortening and postrepolarisation refractoriness were greater in the epicardium than in the endocardium and conduction delay increased only in the epicardium. Hypokalaemia shortened ERP in the epicardium (but not endocardium) and increased conduction delay in all areas before ischaemia, but it had no effects during ischaemia. During reperfusion hypokalaemia increased the incidence of recurrent tachyarrhythmias. Hypomagnesaemia had no effect before ischaemia, increased epicardial (but not endocardial) MAPD90 shortening during ischaemia, although it had no pro-arrhythmic action. Hyponatraemia increased conduction delay in all areas before ischaemia and produced asystole or severe bradycardia in all hearts. During ischaemia, hyponatraemia decreased ERP shortening and inducibility of arrhythmias in the epicardium (but not endocardium). CONCLUSIONS: We conclude that the more pronounced effect of ischaemia upon the epicardium than the endocardium can be explained by the contact of the endocardium with intracavitary perfusate. We also conclude that changes in ion concentrations may have differential regional electrical effects in normal or ischaemic conditions.

Animals↗