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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Epoxyeicosatrienoic acids (EETs), products of the cytochrome P-450 monooxygenase metabolism of arachidonic acid, can regulate the activity of ion channels. We examined the effects of EETs on cardiac L-type Ca2+ channels that play important roles in regulating cardiac contractility, controlling heart rate, and mediating slow conduction in normal nodal cells and ischemic myocardium. Our experimental approach was to reconstitute porcine L-type Ca2+ channels into planar lipid bilayers where we could control the aqueous and lipid environments of the channels and the regulatory pathways that change channel properties. We found that 20 to 125 nM EETs inhibited the open probability of reconstituted L-type Ca2+ channels, accelerated the inactivation of the channels, and reduced the unitary current amplitude of open channels. There was no selectivity among different EET regioisomers or stereoisomers. When 11,12-EET was esterified to the sn-2 position of phosphatidylcholine, restricting it to the hydrophobic phase of the planar lipid bilayer, the reconstituted channels were similarly inhibited, suggesting that the EET interacts directly with Ca2+ channels through the lipid phase. The inhibitory effects of EET persisted in the presence of microcystin, an inhibitor of protein phosphatases 1 and 2A, suggesting that dephosphorylation was not the mechanism through which these eicosanoids down-regulate channel activity. This inhibition may be an important protective mechanism in the setting of cardiac ischemia where arachidonic acid levels are dramatically increased and EETs have been shown to manifest preconditioning-like effects.
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PMID:Inhibition of cardiac L-type calcium channels by epoxyeicosatrienoic acids. 992 20

Two types of sinus nodal cells were responsible for the main differences in the literature concerning the ultrastructure of the sinuatrial node: the intercalated clear cells and pale cells. Canine hearts were arrested by (1) aortic cross clamping, (2) coronary perfusion with the cardioplegic solution St. Thomas, and (3) coronary perfusion with the cardioplegic solution HTK (Custodiol(R)). After fixation by immersion or perfusion the sinus node tissue was prepared for electron microscopy. Following cardioplegic arrest and perfusion fixation, three nodal cell types in the non-ischemic sinuatrial node were observed: typical nodal cells, transitional cells, and intercalated clear cells. Less than 1% of the non-ischemic sinuatrial cells were intercalated clear cells, surrounded by typical nodal cells or transitional cells. The contractile apparatus of the intercalated clear cells was extremely poorly developed. Great structural variations in the mitochondria were observed in intercalated clear cells, variations that would not appear under conditions of ischemia. In contrast, after 15-25 min of ischemia at 25 degrees C the appearance of the sinus nodal cells was strikingly different from that of the non-ischemic sinuatrial cells. More than 10% of the nodal cells showed typical ischemic alterations, e.g., mitochondrial swelling, clumping of nuclear chromatin, loss of glycogen particles, and cell swelling in varying degrees. Because they look very pale, these nodal cells have been described as pale cells in the literature. Intercalated clear cells appear mainly in non-ischemic nodal tissue. Pale cells are ischemically damaged sinus nodal cells.
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PMID:Intercalated clear cells or pale cells in the sinus node of canine hearts? An ultrastructural study. 1096 34

We report on a 62 year old female patient treated with paroxetine, a selective serotonin reuptake inhibitor, because of an anxiety neurosis undergoing a vaginal hysterectomy in general anesthesia. Apart from a dietary treated diabetes mellitus there were no other diseases. There were no complications during the operation. At the end of the anesthesia an A-V nodal tachycardia appeared which spontaneously changed to a sinus rhythm ten hours after the end of the operation. No clinical or laboratory findings indicated a cardiac ischemia and an additional Holter ECG-Recording showed no further cardiac arrhythmias. No other complications occurred afterwards and the patient was discharged after two weeks. This case report demonstrates clearly that despite a reduced rate of cardiovascular complications compared to other types of antidepressants selective serotonin reuptake inhibitors can lead to perioperative cardiac arrhythmias.
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PMID:[A patient with nodal tachycardia after general anesthesia during medication with a selective serotonin reuptake inhibitor]. 1132 55

Acute inferior wall infarction is frequently complicated by conduction disturbance, but the relationship between ischemia and atrioventricular (AV) conduction disturbance is not well understood. The present experiments were made on cats with heart efferent completely denervated. A, H and V waves were picked up by a template-machine algorithm from His bundle electrogram, AA interval (cardiac cycle length), AH interval (AV conduction time), HV and AV intervals were measured. Of 20 cats, 14 showed prolongation of AH interval (Group A), while not in 6 cats (Group B) after ligation of right coronary artery. A fast pacing of right atrium (AA interval = 267 ms) was produced in Group B and AH interval was also prolonged after ligation of the artery. By multiple-step pacing, the curve of AV nodal function shifted to the right, AH interval which induced AV nodal block was prolonged after ischemia. After reperfusion, AH interval was shortened both in Group A and B. The above results show that myocardial ischemia may cause abnormality of AV conduction and accommodation function. The abnormality appears to be a potential danger which will induce AV conduction block during tachycardia.
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PMID:[Atrioventricular conduction changes in acute ischemic and reperfused coronary artery of cats]. 1149 88

The cardiac pacemaker is a sino-atrial (SA) nodal cell. The signal induced by this pacemaker is distributed over the heart surface by a specialised conduction system and is clinically recorded as the ECG. The SA nodal cells are highly resistant to cardiac failure and ischemia. Under calcium overload conditions, some dysrythmias of SA nodal cells occur easily. Morphological analysis under these conditions shows swelling of the cisternae of the Golgi apparatus, with little or no other histological change or damage being observed. The rate of sinus rhythm is quite different between various species. The investigations of SA nodal cells have so far clarified the pacemaker mechanisms involved. A number of ionic channel currents or pacemaker currents, contribute to the depolarization of the pacemaker potential (phase 4). This will not occur with a single current. Recent experiments have identified several novel pacemaker currents and have also revealed several differences in the pacemaker currents between species. The marked hyperpolarization-activated inward current (I(f)) appears in SA nodal cells of most species, while the inwardly rectifying K+ current (I(K1)) with masked I(f) current is found in those of the rat and monkey. In addition, the rapidly activated current (I(Kr)) and slowly activated current (I(Ks)) of the delayed rectifier K+ current (I(K)) contribute to the pacemaker potential in guinea pig SA nodal cells, with only the I(Ks) current in porcine SA nodal cells and only the I(Kr) current in the rat and rabbit. These differences in ionic channels presumably result from differences in gene expression. Some smooth muscle cells also possess the capacity to beat spontaneously. Uterine smooth muscle cells also exhibit an I(f) current. The basal mechanism for spontaneous activity in both SA nodal cells and smooth muscle cells is almost the same, but some differences in the ionic channels and their genetic expression may contribute to their respective pacemaker currents.
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PMID:Sino-atrial nodal cells of mammalian hearts: ionic currents and gene expression of pacemaker ionic channels. 1469 28

Hypoxic/ischemic and traumatic injury to central nervous system myelinated axons is heavily dependent on accumulation of Ca ions in the axoplasm, itself promoted by Na influx from the extracellular space. Given the high density of nodal Na channels, we hypothesized that nodes of Ranvier might be particularly vulnerable to Ca overload and subsequent damage, as this is the expected locus of maximal Na influx. Adult rat optic nerves were exposed to in vitro anoxia and analyzed immunohistochemically for the presence of spectrin breakdown. Cleavage of spectrin became detectable between 15 and 30 mins of anoxia, and increased homogeneously along the lengths of fibers; localized breakdown was not observed at nodes of Ranvier at any time point analyzed. Spectrin breakdown was also found in glial processes surrounding axons. Confocal imaging of axoplasmic Ca also revealed a gradual and nonlocalized increase as anoxia progressed, without evidence of Ca 'hot-spots' anywhere along the axons at any time between 0 and 30 mins of anoxic exposure in vitro. Calculations of Ca diffusion rates indicated that even if Ca entered or was released focally in axons, this ion would diffuse rapidly into the internodes and likely produce diffuse injury by activating Ca-dependent proteases. Western blot analysis for voltage-gated Na channel protein revealed that key functional proteins such as these are also degraded by anoxia/ischemia. Thus, proteolysis of structural and functional proteins will conspire to irreversibly injure central axons and render them nonfunctional, eventually leading to transection, degradation, and Wallerian degeneration.
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PMID:Spatiotemporal distribution of spectrin breakdown products induced by anoxia in adult rat optic nerve in vitro. 1616 97

Authors report a left colon ischemia six days after laparoscopic para-aortic lymphadenectomy in the staging of advanced cervical carcinoma. Before surgery, positron emission tomography scanning was performed: there were no para-aortic nodal metastasis. The histologic examination confirmed the radiological staging. Positron emission tomography scanning could avoid surgery in the case of patients with high risks morbidity factors.
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PMID:[Left colon necrosis after endoscopic para-aortic lymph node exploration in a cervical carcinoma stage IIB]. 1662 20

Accompanying the clear benefits, there are certain risks of tachyarrhythmias in percutaneous coronary interventions (PCI), including serious ventricular arrhythmias and atrial fibrillation (AF). Ventricular arrhythmias may result from excess catheter manipulation, intracoronary dye injection, new ischemic events, or reperfusion. In patients with heart failure such kind of arrhythmias can occur more frequently. Atrial dysfunction, sino-atrial and nodal ischemia, congestive heart failure, sympathetic stimulation, iatrogenic factors are the possible causes of AF especially in patients undergoing primary PCI. Atrial fibrillation, on the other hand, can cause clinical squeal in the setting of a rapid ventricular response or if the loss of atrial systole results in hypotension, as in a patient with mitral stenosis or diastolic ventricular dysfunction. Majority of the ventricular arrhythmias and AF tend to revert spontaneously. However, the special treatment must be given, when necessary.
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PMID:Tachyarrhythmias in percutaneous coronary interventions. 1669 2

Resveratrol (trans-3, 4', 5-trihydroxystilbene), a natural antioxidant derived from grapes, has beneficial effects against coronary heart disease. Its electrophysiological characteristics for antiarrhythmic efficacy are largely unknown; thus, this study aims to explore the resveratrol's antiarrhythmic effects and conduction system in isolated hearts as well as its electrophysiological effects on cardiac myocytes. In the experiment, resveratrol suppressed the ischemia/reperfusion-induced ventricular arrhythmias in Langendorff-perfused rat hearts. In the current clamp study of the experiment, resveratrol prolonged the action potential duration (APD(50) and APD(90)) and suppressed the upstroke velocity of the action potential (V(max)). In the voltage clamp study, resveratrol inhibited sodium inward current (I(Na)) in a concentration-dependent manner and negative-shifted the voltage-dependent inactivation curve. Resveratrol also reduced the calcium inward current (I(Ca), 51.2+/-13.3% at 100 microM). Furthermore, the transient (I(to)) and sustained (I(ss)) outward potassium currents were decreased 60.2+/-5.7% and 42.3+/-5.2% after exposure to resveratrol (100 microM), respectively. The inward rectifier potassium current (I(K1)) was also reduced 24.2+/-7.0% in the presence of resveratrol (100 microM). In the isolated heart perfusion model, resveratrol (100 microM) prolonged AV nodal refractory period, the Wenckebach cycle length and the conduction through AV node and His-Purkinje system. In conclusion, resveratrol increased the cardiac effective refractory period mainly through inhibiting the ionic channels including I(Na), I(to) and I(ss) which could contribute to the conversion of ischemia/reperfusion-induced lethal arrhythmias.
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PMID:In vitro electrophysiological mechanisms for antiarrhythmic efficacy of resveratrol, a red wine antioxidant. 1710 72

Ischemia-reperfusion injury of the myocardium has long been a subject of intense research. Cardiac preconditioning, an associated phenomenon, has also been critically investigated over the past two decades. Although the biochemistry of ischemia-reperfusion and its association with oxidative metabolism has long been established, recent studies have further revealed a more intricate role of a number of reactive oxygen-nitrogen species in those processes. Emerging evidence suggests that an elaborate network of enzymes (and other biomolecules) dedicated to the generation, utilization, and diminution of reactive oxygen-nitrogen species maintains the redox homeostasis in the myocardium, and any perturbation of its status has distinctive effects. It thus appears that while excessive generation of reactive species leads to cellular injury, their regulated generation may cause transient and reversible modifications of cellular proteins leading the transmission of intracellular signals with specific effects. Taken together, generation of reactive oxygen-nitrogen species in the myocardium plays a nodal role in mediating both ischemic injury and cardioprotection.
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PMID:Ischemia-reperfusion and cardioprotection: a delicate balance between reactive oxygen species generation and redox homeostasis. 1755 99


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