Abdominal İskemi-Reperfüzyon Sonrası Papiller Kas Aksiyoon Potansiyelinde Meydana Gelen Değişiklikler (original) (raw)
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Papillary Muscle Action Potential Alterations After Abdominal Ischemia-Reperfusion
OSMANGAZİ JOURNAL OF MEDICINE
Abdominal aortic aneurysm (AAA) has a high prevalence and surgical treatment is still the best option for many reasons. Surgical treatment needs abdominal blood flow to be discontinued, which leads to secondary complications caused by ischemiareperfusion (I/R) in different organs. Since distant organ damages are seen after surgery, abdominal ischemia reperfusion results in post-treatment deaths especially due to heart based problems. In this study, we aimed to investigate the possible alterations in action potential parameters of papillary muscle after abdominal I/R injury. Adult Wistar-Albino rats were divided into two groups randomly: SHAM group (only laparotomy was performed) and I/R group (abdominal aorta was clamped for 1 hour and reperfused for 2 hours). After the operational period, left ventricle papillary muscles were isolated and action potential (AP) recording experiments were carried out in-vitro. Significant hyperpolarization was seen in resting membrane potential in I/R group. There was no alteration in the general shape of the action potential after I/R. Some delayed-after-depolarizations were recorded, that suggests an impaired persistent Na+ channel activity when interpreted with resting membrane potential findings.This study shows that I/R does not affect the AP parameters except for resting membrane potential. However, it is also likely that the sodium-calcium exchanger (NCX) causes delayed arrhythmias after depolarization due to dysfunction of unknown causes.
Electrophysiological alterations in diaphragm muscle caused by abdominal ischemia-reperfusion
Respiratory Physiology & Neurobiology, 2017
Ischemia-reperfusion injury is the major complication of abdominal aortic surgery, and it mainly affects the lower extremities and remote organs. In the present study, the electrophysiological alterations in diaphragm that underlie the post-operative respiratory dysfunction were investigated. Wistar Albino rats were randomly divided into two groups: SHAM (only laparotomy was performed) and IR (abdominal aorta was clamped for 30 min and reperfused for 2 h). Following the operational period diaphragm muscles were isolated and electrophysiological experiments were carried out in-vitro. 3 nM Ryanodine application, Na + and K + current blockage (0.3 mM 4-Aminopyridine and 127 mM N-methyld-glukamine) experiments were also conducted to further reveal any alterations. Twitch and tetanic force were decreased significantly. Action potential overshoot, amplitude and area were increased while diaphragm muscle cells were found to be hyperpolarized significantly. Mechanical alterations were shown to be caused by deterioration of Ca ++ homeostasis. At resting state, a decrease in persistent Na + current was found. The reshaping of action potential, on the other hand, was shown to be due to altered kinetics of Na + channels and delayed activation of voltage dependent K + channels.
1992
The effects of platelet activating factor (PAF) were studied on the electromechanical properties and 45Ca2 + fluxes of guinea-pig isolated atria. 2 Both in spontaneously beating and electrically driven atria, PAF (10-1210-7M) increased atrial rate but produced a biphasic effect on contractile force. At low concentrations (up to 10-10 M) it produced a positive inotropic effect, while at higher concentrations PAF exerted a negative inotropic effect. A similar biphasic effect was observed in the slow contractions elicited by isoprenaline in K+-depolarized atrial fibres. 3 The positive inotropic effect of PAF was prevented by verapamil, whereas pretreatment of atria with propranolol, phentolamine, indomethacin or atropine did not modify its positive and negative inotropic actions. BN 52021, a specific PAF antagonist, abolished both the positive and negative inotropic effects. 4 PAF had no effect on the characteristics of the action potentials recorded in either normally polarized or K+-depolarized (slow action potential) atrial fibres. 5 At concentrations at which it increased contractile force, PAF potentiated the contractile responses to Ca2+ (0.9-9mM), whereas at negative inotropic concentrations it inhibited them. The negative inotropic effect of PAF was partially reversed in 70% Na+ medium. 6 At 10-M, PAF increased 45Ca2 + uptake and reduced the rate coefficient (k,.) for the 4'Ca2 + efflux. This increase in 4'Ca2+ uptake was abolished in atria pretreated with verapamil or BN 52021. However, 10-7M PAF modified neither 4'Ca2 + uptake nor efflux in atrial muscle. 7 These results suggest that in guinea-pig atria the biphasic inotropic effects of PAF cannot be explained through modifications in the slow inward Ca2+ current or in Na'-Ca2+ exchange, but may be related to changes in trans-sarcolemmal Ca2 + entry mediated by specific PAF receptors.
Characteristics and possible mechanisms of low - Na+ induced contractions in rat aorta
Naunyn-Schmiedeberg's Archives of Pharmacology, 1995
The influence of reducing external Na + concentration ([Na+] ex) upon vascular smooth muscle contractility was investigated using the rat isolated aorta. NaC1 from the physiological saline solution (PSS) was replaced with either choline-C1, sucrose, or LiC1 to give the following [Na+]ex (mM): 115, 85, 55, and 25 (ll5NaPSS to 25NaPSS). Small reductions in [Na+]ex (ll5NaPSS) induced a biphasic contraction, comparable in amplitude with the control one induced by phenylephrine 10 -6 M. Elimination of the endogenous catecholamine participation using either phentolamine 10-SM or guanethidine 3.10-6 M similarly reduces these contractions to 25% (sucrose replacement). A similar relaxing effect was obtained with D600 10-5 M, an antagonist of the voltage operated Ca 2 + channels (25-30% residual tension for all the substitutes). Large reductions in [Na+]ex (25NaPSS) induced contractions comparable in amplitude and shape, but less sensitive to phentolamine and guanethidine (residual tension 65-75 %, sucrose replacement) and insensitive to D600 (all the substitutes). The Na+/K + ATPase inhibitor ouabain (10-4 M) elicited slowly developing contractions, the amplitude being 115% of the phenylephrine 10-6 M control.
1996
Background. The mechanisms underlying repetitive activity during reperfusion of ischemic myocardium are thought to include triggered responses elicited at short pacing cycle lengths. The potential to generate repetitive responses at longer pacing cycle lengths under similar conditions, however, has not been explored. Thus, the present study examined the role of cycle length on the cellular electrical changes produced during recovery from ischemic-like conditions and identified the major component precipitating nondriven, repetitive activity. Methods and Results. Transmembrane potentials were recorded in vitro from isolated rabbit Purkinje fibers exposed to hypoxia (defined as Po2<30 mm Hg, high [K'],, and zero glucose) plus lactic acidosis (pH 6.7) for 45 minutes and during recovery in normal Tyrode's solution (pH 7.4). Compared with control, action potential duration (90% repolarization) during recovery increased transiently by 40.9±+11.8 and 241.0±51.1 msec at respective basic cycle lengths of 1,000 and 3,000 msec (both p<0.005). In 81% of preparations, action potential prolongation was accompanied by early afterdepolarizations and triggered activity generated from low (positive to-40 mV) or high (negative to-40 mV) membrane potentials. In 62% of experiments, brief periods of abnormal automaticity also occurred. Triggered responses were 1) unaffected by 1 ,M ryanodine, 2) abolished by pacing at short basic cycle lengths or by exposing tissues to 2.5 ,g/ml lidocaine, and 3) more easily induced at long basic cycle lengths or by superfusing 2.5 ,ag/ml quinidine. When tissues were conditioned with hypoxia alone (pH 7.4), action potential prolongation on recovery was comparatively small, and nondriven responses did not develop. Conversely, addition of 10-20 ,uM amiloride to the hypoxic, acidic test solution augmented recovery-induced action potential prolongation. Conclusions. We conclude that acidosis, as a component of ischemia, plus slow pacing frequencies may mediate the genesis of early afterdepolarizations and triggered activity in Purkinje fibers on recovery, long after extracellular pH has been restored to normal. These data may have clinical relevance to the mechanisms of reperfusion arrhythmias in the intact human heart. (Circulation 1991;83:1352-1360) M yocardial ischemia and hypoxia elicit complex changes in the electrophysiological properties of cardiac cells that are thought to underlie the genesis of tachyarrhythmias in the intact heart. These include reduction of membrane potential,1,2 changes in active and passive electrical properties,3,4 and perturbations in cation homeosta-From the
Ischemia Alters Sensitivity of Action Potential to the Sodium-Potassium Pump
Ischemia increases extracellular concentration of potassium, [K + ] o , reduces the cytosolic ATP concentrations, and reduces cytosolic pH. The sodiumpotassium pump, I NaK , is an ATPase that maintains the ionic gradients across the cell membrane required to drive the action potential (AP) and depends on these parameters. The suitability of biophysically detailed mathematical models to study pathophysiological conditions is in their capability to produce physiological responses to parameter alterations. This study evaluated the sensitivity of INaK parameters and of [K + ] o to AP in a human ventricle cell model using forward sensitivity analysis. The derivative based forward sensitivity of the O'Hara et al. model AP to [K + ] o , ATP, and pH was estimated using difference quotient algorithms. The FSA was verified by computing I NaK-concentration curves for each of the three parameters. AP alterations under small and large alterations of the parameters were also computed. The model's AP has sensitivity to the ischemic parameters in agreement with experimental data. The sensitivity of the AP to pH, however, was found to be small. This could be improved by further developing the INaK formulation. FSA is a straightforward method serving as a first port of call to evaluate model suitability.
Membrane potassium currents in human radial artery and their regulation by nitric oxide donor
Cardiovascular Research, 2006
Objective: The human radial artery has demonstrated superior long-term results as a graft in coronary bypass surgery, but undesirable postsurgical spasm limits its clinical application. Few have examined its excitatory properties, especially the underlying ion channel mechanisms. In this study, we investigated the kinetic and pharmacological properties of the smooth muscle membrane potassium currents of this important artery. Methods and results: Using whole cell patch-clamp techniques, we found the K + current to be voltage-dependent and outwardly rectifying. Voltage-dependent inactivation was observed, being half-maximal at +28.0 mV but incomplete even at + 40 mV. The K + currents were predominantly sensitive to the K Ca blocker tetraethylammonium (TEA; 63.9 T 12.1% inhibition, p < 0.05), less sensitive to the Kv blocker 4aminopyridine (4-AP; 32.8 T 4.4% inhibition, p < 0.05), and the K ATP blocker glibenclamide (28.7 T 8.5% inhibition), at À 20 mV testing potential. Resting membrane potential was À 52.0 T 6.8 mV (n = 5), and suppression of K + currents by TEA and iberiotoxin (IbTx) caused membrane depolarization. Western blot analysis with channel-specific antibodies confirmed the presence of K Ca and Kv channel proteins. TEA evoked 20.7 T 9.9% of the contractile response to 60 mM KCl, whereas IbTx caused about 10% of the above response at 10 À 7 M. The nitric oxide donor SNAP augmented membrane K + currents in a concentration-dependent fashion; the augmentation was completely suppressed by TEA, but was relatively insensitive to the guanylate cyclase inhibitor ODQ. Conclusions: The radial artery manifests mainly Ca 2+-dependent K + currents at rest; this current is augmented by nitric oxide through a cGMP-and protein kinase G-independent action. The relatively depolarized membrane potential, as well as its muscular structure, predisposes the radial artery to spasm. Agents that activate the Ca 2+-dependent K + current could be of therapeutic value in preventing postsurgical vasospasm.
New Insights in the Contribution of Voltage-Gated Nav Channels to Rat Aorta Contraction
PLoS ONE, 2009
Background: Despite increasing evidence for the presence of voltage-gated Na + channels (Na v ) isoforms and measurements of Na v channel currents with the patch-clamp technique in arterial myocytes, no information is available to date as to whether or not Na v channels play a functional role in arteries. The aim of the present work was to look for a physiological role of Na v channels in the control of rat aortic contraction.
Resting and Action Potentials of Nonischemic and Chronically Ischemic Human Ventricular Muscle
Journal of Cardiovascular Electrophysiology, 1994
Membrane Potentials in Human Ventricle. Introduction: The effect of chronic ischemia on the electrical properties of human cardiac tissue is not well understood. Methods and Results: Membrane potentials were studied using microelectrode techniques in isolated human ventricular tissues obtained from nonischemic (n = 17) or chronically ischemic (n = 71 myocardium. In normal Tyrode's solution, resting potential (Vr) was lower in ischemic (−70.1 · 2.12 mV) than in nonischemic muscles (−77.6 · 0.93 mV; mean · SKM; P < 0.051. In high [K]0 (> 10 mM) media, V, was of similar magnitude in both types of tissue (in 21.6 mM [K]0 Vr was −53.1 · 2.24 mV in nonischcmic and −49.6 · 2.03 mV in ischemic preparations; n = 7 each; P > 0.05). Lowering [K]0. caused persistent Hyperpolarization in nonischemic muscles, but caused depolarization in chronically ischemic preparations (in 2,7 mM [K]0 Vr was −84.9 · 2.74 mV and –61.7 · 7.72 mV, respectively; n = 7; P < 0.05). Pinacidil (100 μM) ...