PubMed Health⌕ Search

Biomedical subjects

P Abete

Publications and source records attributed to P Abete.

At least 19 recordsLinked to original sources
PubMed1992

Role of intracellular Na+ activity in the negative inotropy of strophanthidin in cardiac Purkinje fibers.

The relation between intracellular sodium activity (aNai) and different phases of strophanthidin inotropy was studied in sheep cardiac Purkinje fibers superfused in vitro. Strophanthidin (1 microM) progressively increases aNai whereas increases and then decreases contractile force, induces contracture ('mechanical toxicity') and arrhythmias ('electrical toxicity'). Contractile force begins to decrease at approximately 11 mM aNai. Force and aNai show a positive correlation during the increasing and a negative correlation during the decreasing phase of strophanthidin inotropy. In high [K]o (8, 12 and 16 mM), strophanthidin increases aNai and force to a smaller peak and fails to induce toxicity. In high [Na]o (+18.5%), strophanthidin increases aNai and force to a larger peak and induces electrical toxicity below and mechanical toxicity above a higher aNai value (approximately 15 mM). In higher [K]o, high [Na]o restores the ability of strophanthidin to induce mechanical toxicity. Thus, mechanical toxicity begins when aNai increases past a critical value and the continuing aNai increase correlates with decrease in contractile force and contracture. The critical value of aNai is modified by Ca load related to changes in membrane potential or to Na electrochemical gradient.

Animals↗
PubMed1992

Age-related effects of ischemia, lidocaine and verapamil on overdrive-induced suppression of ventricular pacemakers in isolated rat heart.

The effect of age on ventricular automaticity in the isolated perfused rat heart was determined under different conditions. When the ventricle is electrically stimulated at a faster rate, drive cessation is followed by a temporary suppression of ventricular automaticity (overdrive suppression). The effects of ischemia, lidocaine and verapamil on overdrive suppression were studied in isolated perfused adult and senescent rat hearts with complete atrio-ventricular block, by monitoring ventricular escape rate and escape rhythm recovery time after 1 minute of overdrive at a constant multiple (x3) of the spontaneous rate. The results demonstrated that: 1) lidocaine decreases ventricular automaticity especially in senescent hearts; 2) verapamil does not modify ventricular automaticity in basal conditions in either adult or senescent hearts; 3) myocardial ischemia causes a reduction in ventricular automaticity and more markedly in senescent hearts; and 4) lidocaine exaggerates the effect of ischemia, while verapamil seems to antagonize its depressant effect more in adult than in senescent hearts.

Aging↗
PubMed1992

Age-related effects of platelet activating factor (PAF) in the isolated perfused rat heart.

Platelet Activating Factor (PAF) is a phospholipid that has been implicated as an important mediator of anaphylactic cardiac dysfunction and involved in the toxic effects of the ischaemia-reperfusion process. In the elderly, these phenomena are thought to be exaggerated by the age-related changes in response to several chemical factors and myocardial ischaemia. We evaluated the effects of PAF (acetyl-o-alkyl-l-phosphatidylcholine) on left ventricular systolic (LVSP) and diastolic (LVDP) pressure, coronary flow rate (CFR) and heart rate (HR) in adult (6 months, AH) and senescent (24 months, SH) rat hearts. The perfusion of PAF (10(-8), 10(-7) and 10(-6) M) induced a concentration-related reduction of LVSP, CFR and HR and a linear increase in LVDP. Contractile modifications were more pronounced in senescent hearts: LVSP decreased (P < 0.01) and LVDP increased with respect to younger animals (P < 0.01 vs. AH). This negative inotropic effect was also present in electrically paced hearts. PAF produced conduction arrhythmias ranging from second-degree atrio-ventricular conduction block to cardiac standstill both in adult and senescent hearts; at a higher dose (10(-6) M), cardiac standstill appeared after 96.5 +/- 15.3 s in adult hearts and after 45.5 +/- 17.6 s in senescent hearts (P < 0.01). Lyso-PAF did not modify while specific PAF antagonist compounds CV-3988 inhibited all electromechanical responses both in adult and senescent hearts. These data suggest that age influences the effect of PAF on contractile parameters, coronary flow and conduction arrhythmias by acting on receptors, whose function is unaffected by age.

Aging↗
PubMed1991

Mechanisms of lidocaine actions on normal and abnormal rhythms in canine cardiac tissues in vivo and in vitro.

1. The actions of lidocaine on cardiac pacemaker rhythms were studied in anaesthetized dogs and in Purkinje fibres from hearts of the same animals. 2. In vivo, lidocaine (1 mg/kg, intravenously) slowed the sino-atrial (SA) node rhythm (-5.0%), and (during vagal stimulation) prolonged ventricular standstill by +25.1% and slowed the idioventricular rhythm (-16.7%). A higher dose (4 mg/kg) had more pronounced effects. 3. Propranolol also slowed sinus (-26.2%) and idioventricular (-27.2%) rhythms, and prolonged ventricular standstill (+36.8%). In the presence of propranolol, the effects of lidocaine on idioventricular rhythm were exaggerated. 4. In Purkinje fibres driven in vitro, lidocaine (10 mumol/L) decreased contractile force (-47.9%) and (during the interruption of drive) prolonged the suppression of (+53.2%) and slowed the escape rhythm (-67.0%). 5. In the presence of lidocaine the threshold potential was shifted to less negative values and diastolic depolarization slope was decreased (-23.6%). 6. Lidocaine slowed spontaneously active Purkinje fibres, abolished early afterdepolarizations in low [K]o and slow responses in high [K]o (by shifting the threshold to less negative values), and antagonized strophanthidin arrhythmias. 7. TTX reduced the hyperpolarization by lidocaine in low [K]o and vice versa. 8. We conclude that lidocaine enhances vagally-induced ventricular standstill by depressing the idioventricular rhythm far more than the sinus rhythm, an action enhanced by beta-blockade. Furthermore, lidocaine depresses normal and different types of abnormal automaticity through direct and indirect effects of the blockade of the fast sodium channel.

Animals↗
PubMed1991

Dipyridamole echocardiography as a useful and safe test in the assessment of coronary artery disease in the elderly.

We prospectively studied the sensitivity, specificity, feasibility, and safety of high-dose dipyridamole echocardiography, compared to exercise electrocardiography in 130 subjects (67 younger and 63 elderly patients) referred for angiographic evaluation of suspected or proven coronary artery disease. Sensitivity, specificity, and feasibility of dipyridamole echocardiography were respectively 75.5%, 100%, and 88.0% in younger patients and 82.9%, 100%, and 79.4% in elderly patients (P = NS). The sensitivity of exercise electrocardiography was 72.7% in young and 66.6% in elderly patients (P = NS); specificity 66.0% vs 60.0% (P = NS); feasibility 83.6 vs 63.5 (P = 0.05). Forty-nine younger and 38 elderly patients performed both tests. Sensitivity of dipyridamole echocardiography compared to exercise electrocardiography was 76.2% vs 73.8% in young patients and 83.3% vs 70% in the older group (P = NS). The feasibility of the two tests was significantly different in the elderly group only (dipyridamole echocardiography 79.4% vs exercise electrocardiography 63.5%; P less than 0.01). The incidence of side effects during dipyridamole echocardiography was similar in the two groups, except for dyspnea which was observed in 20% of older and 5% of younger patients (P less than 0.05). Our data demonstrate that the dipyridamole test combined with echocardiographic monitoring of regional myocardial contractility may be considered a valid non-invasive method for evaluating coronary artery disease in the elderly and that this test is a satisfactory alternative to the exercise stress test.

Aged↗
PubMed1991

The hypothetical role of potassium conductance on the genesis of R-wave amplitude increase during ischemia in the isolated rat heart.

The effect of increased potassium conductance on the genesis of R-wave amplitude increase during acute myocardial ischemia has been studied in the isolated perfused rat heart by simultaneously recording the R-wave amplitude of epicardial electrograms (VEE), heart rate (HR), coronary flow rate (CFR), left ventricular diastolic pressure (LVDP), and left ventricular systolic pressure (LVSP). The experiments were performed during basal and partial or total ischemic conditions at spontaneous or fixed HR. In some experiments, potassium conductance was increased by means of high-calcium (8 mM) or acetylcholine chloride (10(-6) M) perfusion. In the control experiments, partial ischemic perfusion produced an increase in VEE and LVDP and a decrease in HR, CFR, and LVSP; total ischemic perfusion exaggerated these variations. High-calcium perfusion provoked an increase in VEE and LVDP and a decrease in HR, CFR, and LVSP during basal conditions (p less than 0.01 vs. control experiment); these modifications increased progressively during partial ischemic perfusion (p less than 0.01 vs. control experiment) and during total ischemic perfusion (p less than 0.01 vs. control experiment). Perfusion with acetylcholine chloride produced variations similar to those observed in high-calcium solution except that LVDP under basal conditions remained unchanged from control. When the HR was maintained at a constant value by means of atrial pacing the results were similar to those observed in the unpaced hearts. In conclusion, in the isolated perfused rat heart, increasing potassium conductance may influence the genesis of R-wave amplitude increasing during acute myocardial ischemia.

Acetylcholine↗
PubMed1991

[Aging and left ventricular diastolic function].

Several studies have demonstrated that physiological aging significantly affects cardiovascular function. Experimental researches, conducted on cardiac muscle of senescent animals, have shown a prolongation of both contraction and relaxation times. This phenomenon was explained by a reduced Ca(++)-stimulated ATPase pump activity, responsible for the reduced sarcoplasmic reticulum Ca++ uptake rate. The myofilament response to Ca++ in the aging heart is normal as are peak contractile force production and post-extrasystolic twitch potentiation during continual paired stimulation. On the other hand, the inotropic response to cardiac glycosides and beta-adrenoceptor stimulation is diminished in senescent compared to adult myocardium. This decreased contractility could result mainly from mechanisms controlling Ca++ reuptake from sarcoplasmic reticulum and relaxation time (diastolic phase) rather than those determining force generation and contraction time (systolic phase). Age-related physiologic structural changes are not associated with significant variations in left ventricular diastolic and systolic sizes, but they seem a direct consequence of the rising systolic blood pressure observed in these age decades. Myocardial hypertrophy should not be considered a specific marker of the senescent heart, but rather an adaptive response to increased afterload conditions. As regard the relationship between age and diastole, it is important to underline that the alterations in aging cardiac muscle function primarily involve the isovolumic relaxation time and diastolic phase. With age, the early diastolic phase declines while the contribution of atrial contraction to ventricular diastolic filling increases as well as the isovolumic relaxation time.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1990

Acute effects of nisoldipine, propranolol, and their combination in patients with chronic stable angina: a double-blind, randomized, cross-over, placebo-controlled study.

We studied the short-term effects of oral administration of nisoldipine (10 mg) and propranolol (80 mg) alone and in combination in 14 patients with chronic exertional angina pectoris in a double-blind, randomized, cross-over study. The 14 patients (13 men and 1 woman, mean age 56 +/- 7 years) performed symptoms-limited bicycle exercise stress test 3 h after placebo or active substance administration. Maximal work load, exercise duration, and time to 1-mm ST segment depression were significantly increased and ST depression at peak exercise was significantly decreased by drugs alone and in combination. Propranolol and nisoldipine alone improved exercise duration similarly and as well as the combination; however, a different response to the three pharmacologic interventions was found in patients treated with single drugs. The improvement in exercise tolerance was associated with rate-pressure product values at peak exercise, unchanged after nisoldipine and significantly reduced after both propranolol alone and in combination. After placebo, all patients had exercise-induced angina, in 9, 8, and 4 patients after nisoldipine, propranolol, and the combination of the two drugs, respectively. Nisoldipine is effective in the treatment of effort angina and its combination with propranolol may be useful and superior in patients who show poor response to monotherapy.

Aged↗
PubMed1990

Arrhythmogenic age-related effects of lysophosphatidylcholine in the rat heart.

Ventricular arrhythmias are the most common cause of death among patients with coronary artery disease; this is more evident in the elderly, who tend to have more severe coronary artery disease and age-dependent modifications of cardiac electrophysiology. Lysophosphoglycerides, which accumulate in the ischemic myocardium, are responsible for oscillatory after-potentials and may contribute to the development of ventricular arrhythmias. The aim of this study was to examine the effects of lysophosphatidylcholine (5 x 10(-5) M) in the absence or presence of epinephrine (10(-6) M) in isolated, perfused hearts from adult (6-12 months old) and senescent (24 months old) rats. Rat hearts (30/group) were randomly divided into four groups each of which included hearts of 6, 12 and 24-month old rats. The groups comprised a control group, a group treated with epinephrine, a group treated with lysophosphatidylcholine and a group treated with both epinephrine and lysophosphatidylcholine. Analysis of arrhythmias indicated a linear correlation between epinephrine- and lysophosphatidylcholine-induced ventricular arrhythmias and age. The incidence of arrhythmias was higher in the hearts treated with epinephrine and lysophosphatidylcholine together than in those treated with either substance separately (p less than 0.01). The results indicate that age influences the arrhythmogenic action of lysophosphatidylcholine, and that epinephrine contributes to this effect.

Aging↗
PubMed1988

Electrical and ionic mechanisms of early reperfusion arrhythmias in sheep cardiac Purkinje's fibers.

The mechanisms of induction of early reperfusion arrhythmias were studied in sheep cardiac Purkinje's fibers superfused in vitro. Transmembrane potentials, intracellular sodium activity (aiNa), and contractile force were recorded. Stoppage of the flow of Tyrode's solution (ischemia) for 1 hour initially decreased slightly aiNa (-0.57 mmol -7.2%), increased the action potential amplitude (+6.1%) and duration (+7.8%), and decreased diastolic depolarization slope (-45.2%). As the ischemia continued, aiNa increased progressively (to 12.53 mmol, +56.2%), whereas force peaked (+395%) after about 30 minutes and then began to decrease. By the end of ischemia, there was a decrease in action potential amplitude (-14.9%) and duration (-39.6%), whereas diastolic depolarization slope reincreased again almost to control value (-7%). When the flow of Tyrode's solution was resumed (reperfusion), force markedly increased (+211.1%) and oscillatory potentials initiated arrhythmias (extrasystoles and repetitive fast discharge) in 64% of tests. Force and aiNa decreased relatively rapidly. The arrhythmias initiated after 58.4 +/- 1.8 seconds of reperfusion and lasted 101.5 +/- 3.2 seconds. When [Na]o was increased by +19.2%, reperfusion arrhythmias occurred after only 30 minutes of ischemia. Thus, in Purkinje's fibers superfused in vitro, early reperfusion arrhythmias are induced by oscillatory potentials caused by calcium overload, which is enhanced by the increase in aiNa during ischemia.

Animals↗
PubMed1988

Regional left ventricular mechanical function during isometric exercise in patients with coronary artery disease: correlation with regional coronary blood flow changes.

The effects of isometric exercise on regional left ventricular mechanical function and regional coronary blood flow were evaluated in 17 patients with significant proximal stenosis of the left anterior descending coronary artery and 10 patients with normal coronary arteriograms. All patients had normal myocardial contractility in the basal condition. All performed isometric handgrip exercise at 50% of the maximal voluntary contraction for 3 min during two-dimensional echocardiographic monitoring and hemodynamic evaluation of great cardiac vein flow by thermodilution technique. During isometric exercise, 7 of the 17 patients with left anterior descending coronary stenosis developed asynergy in the anterior territory (anterior or septal segment, or both) (group I); the remaining 10 showed normal myocardial contraction during the test (group II). The 10 normal subjects manifested no regional asynergy during the test (control group). The increase in great cardiac vein flow at peak isometric exercise was significantly smaller (p less than 0.01) in group I (+15 +/- 8%) than that in group II (+98 +/- 48%) and the control group (+64 +/- 22%). Anterior coronary vascular resistance decreased in group II (-32 +/- 13%) and in the control group (-25 +/- 8%) but increased in group I (+6 +/- 8%, p less than 0.01 versus group II and control group). These data demonstrate that handgrip-induced myocardial asynergy is associated, in our study patients, with an abnormal response of the regional coronary circulation. The increase in coronary vascular resistance in group I patients with asynergy demonstrates that functional mechanisms play a dominant role in left ventricular mechanical dysfunction induced by isometric exercise.

Aged↗
PubMed1988

Relation between Na+-K+ pump, Na+ activity and force in strophanthidin inotropy in sheep cardiac Purkinje fibres.

1. The effects of different concentrations of strophanthidin on intracellular sodium activity (aiNa), membrane potential and contractile force have been studied in cardiac sheep Purkinje fibres under conditions (overdrive) that stimulate Na+-K+ pump activity. 2. In fibres driven at 1 Hz, a 5 min overdrive at 2 Hz in the steady state increased force by +74.2%, aiNa by +10.9% and the maximum diastolic potential (Emax) by 3.32 +/- 0.52 mV. 3. During the recovery from overdrive (the fibres being driven again at 1 Hz), both contractile force and aiNa transiently undershot the control value by -10.5 and -3.7%, respectively. When the fibres were quiescent during the recovery from overdrive, no aiNa undershoot was present. 4. During overdrive, force and aiNa were closely correlated when plotted either on linear (correlation coefficient, R = 0.98) or logarithmic (R = 0.98) co-ordinates. 5. A low concentration of strophanthidin (0.01 microM) decreased force (-31.7%) and aiNa (-7.2%): overdrive increased force and Emax more and aiNa less than in the absence of strophanthidin. During the recovery, the undershoot in force (-12.9%) and aiNa (-5.4%) was larger and longer than in the absence of strophanthidin. 6. An intermediate concentration of strophanthidin (0.05 microM) increased force (+43.5%) and aiNa (+6.4%): overdrive increased force and aiNa as usual, but during the recovery the force remained above the value prior to overdrive and there was no aiNa undershoot. 7. A high concentration of strophanthidin (0.1 microM) increased force (+91.4%) and aiNa (+11.7%): overdrive further increased force and aiNa more than in control but there was no increase in Emax. During the recovery, both force and aiNa remained well above the values prior to overdrive. 8. Force and aiNa were closely correlated whether aiNa decreased in 0.01 microM-strophanthidin (R = 0.99 both on linear and logarithmic co-ordinates) or increased in 0.05-microM- (R = 1.00 on both co-ordinates) and in 0.1 microM- (R = 0.98 and 0.99, respectively) strophanthidin. The two parameters were well correlated also during overdrive in the three strophanthidin solutions. However, the slope of the relation was less steep in the low- than in the higher-strophanthidin solutions. 9. For a 1 mM change in aiNa, force decreased less in the low- than it increased in the intermediate-strophanthidin solution. Also, in low-strophanthidin solution, at the end of overdrive the aNao/aNai ratio was similar to that in Tyrode solution but force was well above control (+73.2%).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Diagnostic value of the ratio of recovery systolic blood pressure to peak exercise systolic blood pressure for the detection of coronary artery disease.

It has been previously reported that at treadmill exercise testing an abnormal ratio of recovery systolic blood pressure (SBP) to peak exercise SBP is more sensitive than exercise-induced angina or ST segment depression for diagnosing coronary artery disease (CAD). To investigate whether the SBP ratio keeps its diagnostic value during upright bicycle exercise, we evaluated the ratio of postexercise SBP to peak SBP in 73 patients with angiographically documented CAD and in 48 patients with normal coronary arteries (OV group) undergoing maximal stress testing on a bicycle ergometer. Three minutes after exercise ended, SBP ratio was significantly higher in the CAD than in the OV group (0.79 +/- 0.1 vs 0.71 +/- 0.08; p less than .001). Setting the upper normal limits of the recovery SBP ratio at 2 SDs from the mean for the OV group (SBP ratio = 0.98 and 0.88 at 1 and 3 min after exercise, respectively), with an increase or no change in SBP ratio at between 1 and 3 min of recovery considered an abnormal response, the sensitivity of SBP ratio was 30%, the specificity was 83%, and the accuracy was 51%. The respective values for ST depression were 81% (p less than .0001 vs SBP ratio), 48% (p less than .001 vs SBP ratio), and 67% (p less than .01 vs SBP ratio). Thus, for bicycle ergometer exercise testing, ST segment depression seems to be more accurate than SBP ratio in diagnosing CAD.

Adult↗
PubMed1988

[Action of magnesium salts on the toxic effects of calcium overload in the isolated and perfused rat heart].

The toxic effect of calcium overload and the action of magnesium sulfate (4 mM) and magnesium chloride (4 mM) on heart rate, coronary flow rate, left ventricular systolic pressure, dp/dt max and voltage epicardial electrogram were studied in the isolated and perfused rat heart. Increasing calcium load by increasing [Ca]o from 1 to 6 mM we observed a progressive increase in heart rate coronary flow rate, left ventricular systolic pressure, dp/dt max and a decrease in voltage epicardial electrogram. During the exposure to [Ca]o 8 mM the toxic manifestations of calcium overload developed and we observed a reduction in heart rate, coronary flow rate, left ventricular systolic pressure, dp/dt max and an increase in voltage epicardial electrogram. Magnesium sulfate and magnesium chloride had similar effect: in fact, in both procedures we observed a decrease in heart rate, left ventricular systolic pressure, dp/dt max, voltage epicardial electrogram and an increase in coronary flow rate at [Ca]o 2 mM. When magnesium salts were administered at the same time as the heart was exposed to [Ca]o 8 mM, we observed a reduction in the toxic effect of calcium overload. When magnesium salts were administered after the appearance of the calcium overload, they did not revert the toxic effect of calcium overload but prevented the insurgence of cardiac standstill. Thus, in the isolated perfused rat heart, the toxic manifestations of calcium overload develop at [Ca]o 8 mM and magnesium salts are able to reduce the toxic effects of calcium overload and the appearance of cardiac standstill according to their calcium-antagonism mechanism.

Animals↗