UMLS:C0151744 - FACTA Search

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Query: UMLS:C0151744 (myocardial ischemia)
31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vagally mediated vasodepressor reflexes are observed in dogs and patients with acute myocardial ischemia or infarction and may be related to the Bezold-Jarisch reflex. To test whether nicotine and bradykinin produced site-specific vagal vasodepressor and sympathetic vasopressor responses, respectively, we compared blood pressure and heart rate responses to these drugs applied topically at six epicardial sites of the canine left ventricle: midanterior, apical anterior, midlateral, apical lateral, midposterior, and apical posterior left ventricle. In alpha-chloralose-anesthetized dogs with open chests a felt pad soaked in bradykinin (25 micrograms) or nicotine (50 micrograms) was applied to the test sites. Previous studies indicated that epicardial application of these drugs elicited a sympathetically mediated pressor response and a vagally mediated depressor response, respectively. Vasopressor response to bradykinin did not differ among six test sites in 10 dogs. However, vasodepressor response to nicotine was greater in the midposterior left ventricular epicardium than at other test sites in 16 dogs. A hypertensive response after the initial hypotensive response to nicotine was observed in the midanterior left ventricle and not in any other site. These data indicate that vagal vasodepressor responses to epicardial nicotine are greater in the canine midposterior left ventricle and are compatible with the higher incidence of bradycardia or hypotension during acute inferoposterior myocardial infarction in patients. Sympathetic vasopressor responses to epicardial bradykinin are not site specific. Half of the dogs showed no response to bradykinin or nicotine.
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PMID:Increased afferent vagal responses produced by epicardial application of nicotine on the canine posterior left ventricle. 366 66

Although arrhythmias caused by myocardial ischemia are a well recognized cause of sudden death, the potential influence of cardiogenic reflexes originating in areas of ischemia has received less attention. In this study, 12 patients with well documented single vessel coronary artery spasm, with a total of 2,240 episodes of transient transmural ischemia, are described. Continuous electrocardiographic and hemodynamic recordings were analyzed to determine possible relations between the anatomic area of ischemia and patterns of change in blood pressure and heart rate. Of seven patients with ischemia of the posterior or inferior left ventricular wall, six had associated bradycardia and hypotension, an apparent Bezold-Jarisch response. Only one of five patients with anterior ischemia had a similar response. A hypertensive, tachycardiac response resembling the James reflex was seen in two of the patients with anterior ischemia, with an increase in blood pressure of 36/22 +/- 12/6 mm Hg and an increase in heart rate of 8 +/- 3 beats/min. This increase began before the onset of chest pain and was seen even in asymptomatic episodes. These reflexly mediated hemodynamic responses may modulate the direct effects of myocardial ischemia and could play a role in sudden cardiac death.
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PMID:Reflexes unique to myocardial ischemia and infarction. 399 36

The concept of depressor reflexes originating in the heart was introduced by von Bezold in 1867 and was later revived by Jarisch. The Bezold-Jarisch reflex originates in cardiac sensory receptors with nonmyelinated vagal afferent pathways. The left ventricle, particularly the inferoposterior wall, is a principal location for these sensory receptors. Stimulation of these inhibitory cardiac receptors by stretch, chemical substances or drugs increases parasympathetic activity and inhibits sympathetic activity. These effects promote reflex bradycardia, vasodilation and hypotension (Bezold-Jarisch reflex) and also modulate renin release and vasopressin secretion. Conversely, decreases in the activity of these inhibitory sensory receptors reflexly increase sympathetic activity, vascular resistance, plasma renin activity and vasopressin. Long regarded as pharmacologic curiosities, it is now clear that reflexes originating in these inhibitory cardiac sensory receptors are important to the pathophysiology of many cardiovascular disorders. This paper reviews the role of inhibitory cardiac sensory receptors in several clinical states including 1) bradycardia, hypotension and gastrointestinal disorders with inferoposterior myocardial ischemia and infarction, 2) bradycardia and hypotension during coronary arteriography, 3) exertional syncope in aortic stenosis, 4) vasovagal syncope, 5) neurohumoral excitation in chronic heart failure, and 6) the therapeutic effects of digitalis.
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PMID:The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. 682 48

Myocardial ischemia and reperfusion can evoke excitation of cardiac vagal afferent nerve endings and activation of a cardiogenic depressor reflex (Bezold-Jarisch effect). We postulate that oxygen-derived free radicals, which are well known to be produced during prolonged ischemia and reperfusion, contribute to this excitation. Hydroxyl radicals derived from hydrogen peroxide (H2O2) activate abdominal sympathetic afferents and produce reflex excitation of the cardiovascular system. However, it is not known whether inhibitory vagal cardiac afferents are activated by oxygen-derived free radicals. We recorded activity from 52 single vagal afferent fibers in 29 rats; the endings of these fibers were located in the walls of all four chambers of the heart. Thirty-three (63%) of these fibers were classified as chemosensitive C-fiber endings because of their irregular discharge under resting conditions, their activation in response to the topical application of capsaicin (1 to 10 micrograms) to the surface of the heart encompassing the receptive field, and their conduction velocities. Fourteen (27%) of the remaining fibers were found to be mechanoreceptors. Topical application of H2O2 to the heart activated 50% of the chemosensitive endings and did not directly affect cardiac mechanoreceptors. Activity increased by 498% at a dose of 3 mumol (P < .001). This effect was reproducible and dose dependent and was not due to [H+]. Topical application of xanthine/xanthine oxidase (20 mmol/0.03 mU) activated 8 of the 12 chemosensitive fibers tested and had no direct effect on mechanosensitive fibers. Activity increased by 287% (P < .001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Activation of cardiac vagal afferents by oxygen-derived free radicals in rats. 815 36

Myocardial ischemia and reperfusion can evoke excitation of cardiac vagal nerve endings and activation of a cardiogenic depressor reflex (Bezold-Jarisch effect). We postulate that oxygen-derived free radicals, which are known to be produced during prolonged ischemia and reperfusion, contribute to this afferent excitation. We recorded activity from 47 chemosensitive vagal afferent fibers in 31 rats; the endings of these fibers were located in the left ventricle. Chemosensitive endings were identified with topical applications of capsaicin (10 micrograms) to the surface of the heart. Reactivity of the endings to oxygen-derived free radicals was assessed by topical application of H2O2 (3 to 9 mumol). Activity of the vagal fibers was recorded during 30 minutes of occlusion of the left anterior descending coronary artery (LAD) and 10 minutes of subsequent reperfusion. The activity of chemosensitive endings within the ischemic zone increased in the first 2 minutes of LAD occlusion from 2.2 +/- 0.4 to 4.3 +/- 0.9 impulses per second (107 +/- 30% increase, P < .05). This increased activity waned after 3 to 5 minutes of occlusion. Endings outside the ischemic zone did not increase, their activity at the beginning of ischemia. Reperfusion caused a rapid elevation of activity only in chemosensitive fibers whose endings were found to respond to topical H2O2. The reperfusion-sensitive endings were located both within and outside the ischemic zone of the left ventricle. Indomethacin (5 mg/kg i.v., 20 minutes before occlusion) effectively prevented activation of chemosensitive afferent endings at the beginning of LAD occlusion regardless of their sensitivity to H2O2 but had no effect on the activation at reperfusion.
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PMID:Activation of cardiac vagal afferents in ischemia and reperfusion. Prostaglandins versus oxygen-derived free radicals. 815 37

1. Myocardial ischaemia and reperfusion can evoke excitation of cardiac vagal afferent nerve endings and activation of a cardiogenic depressor reflex (Bezold-Jarisch effect). We postulate that oxygen free radicals, which are well known to be produced during ischaemia and reperfusion, contribute to this excitation. 2. Activity from vagal afferent fibres in rats, whose endings were located in the walls of all four chambers of the heart, was recorded in response to topical application of pro-oxidant chemicals to the surface of the heart. Activity was also recorded from vagal afferent fibres, whose endings were located in the left ventricle, in response to occlusion of the left anterior coronary artery (LAC) for 30 min and subsequent reperfusion. A majority of the recorded fibres were classified as chemosensitive C-fibre endings due to their irregular discharge under resting conditions, their activation in response to the topical application of capsaicin (1-10 micrograms) to the surface of the heart encompassing the receptive field and their conduction velocities. 3. Topical application of either H2O2 or xanthine/xanthine oxidase to the heart activated 50% of the chemosensitive endings and did not directly affect cardiac mechanoreceptors. This effect was reproducible, dose-dependent and was not due to [H+]. 4. Administration of the superoxide radical scavenging enzyme, superoxide dismutase (20000 U/kg, i.v.), decreased the response of fibres to xanthine/xanthine oxidase but had no effect on the activation caused by H2O2. The antioxidants deferoxamine (20 mg/kg, i.v.) or dimethylthiourea (10 mg/kg, i.v.), which scavenge the hydroxyl radical, abolished the responses to xanthine/xanthine oxidase and H2O2. Administration of indomethacin (5 mg/kg, i.v.) had no effect on the afferent response to H2O2. 5. In response to ligation of the left anterior coronary (LAC), the activity of chemosensitive endings within the ischaemic zone increased within the first 2 min of occlusion. Endings outside the ischaemic zone were not affected at the beginning of ischaemia. Reperfusion activated only chemosensitive endings responsive to topical H2O2. These reperfusion-sensitive endings were located both within and outside the ischaemic zone of the left ventricle. 6. Indomethacin (5 mg/kg, i.v.) prevented activation of chemosensitive endings at the beginning of LAC occlusion regardless of their sensitivity to H2O2 but had no effect on the response to reperfusion. Conversely, deferoxamine (20 mg/kg, i.v.) had no effect on the activation of chemosensitive fibres at the onset of ischaemia, whereas it completely prevented activation at reperfusion. 7. We propose that there are two different mechanisms that activate chemosensitive afferent vagal fibres in the rat heart during ischaemia and reperfusion. The first causes excitation of these endings at the onset of ischaemia and is mediated by prostaglandin synthesis within the ischaemic zone. The second mechanism leads to a more widespread activation of chemosensitive afferents in the left ventricle during prolonged ischaemia and at the moment of reperfusion and is mediated by oxygen free radical formation.
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PMID:Cardiac vagal afferent stimulation by free radicals during ischaemia and reperfusion. 888 94

In fetal sheep, severe hypotension causes heart rate (HR) slowing. Studies during development have also shown that a reflex bradycardia and hypotension can be elicited after chemostimulation with veratridine and is dependent on the age of the animal. In adults, a vagally mediated depressor reflex characterized by bradycardia, hypotension, and withdrawal of efferent sympathetic activity can be observed after stimulation of chemosensitive or mechanosensitive cardiac receptors with veratridine or in circumstances of reduced cardiac filling. This reflex, known as the Bezold-Jarisch reflex, plays a role in disease states such as myocardial ischemia and hemorrhage. The objectives of our study were to determine whether a sympathoinhibitor depressor reflex, along with the bradycardia, is observed during pharmacologically induced hypotension in fetal and newborn lambs. In both fetal and newborn lambs, HR and renal sympathetic nerve activity (RSNA) initially increased (p < 0.05) in response to nitroprusside infusion to reach a maximum value. The range (or "plateau") of mean arterial blood pressure over which maximum RSNA was maintained constant before withdrawal of sympathetic tone started to be observed was significantly (p < 0.05) smaller in fetuses (0.3 +/- 0.3 mm Hg) than newborn (6 +/- 1 mm Hg) lambs. Similarly, the plateau over which maximum HR was maintained before onset of bradycardia was significantly smaller in fetuses (4 +/- 1 versus 11 +/- 2 mm Hg). The mean arterial blood pressure level ("threshold") at which a depressor reflex was triggered was significantly (p < 0.05) lower in fetal than newborn sheep (35 +/- 2 versus 53 +/- 3 mm Hg for HR and 35 +/- 2 versus 57 +/- 2 mm Hg for RSNA). The rates of fall (slopes) for both HR and RSNA were also significantly (p < 0.05) more pronounced in fetuses (1.85 +/- 0.27 and 6.08 +/- 2.45%/mm Hg) than in newborns (1.21 +/- 0.16 and 1.97 +/- 0.32%/mm Hg). Bilateral vagotomy significantly increased the plateau of mean arterial blood pressure over which maximum RSNA and HR were maintained constant. Vagotomy also decreased the threshold for both RSNA and HR and the slope of the RSNA response to the nitroprusside infusion in newborn lambs. Results from this study show that activation of the arterial baroreflex during nitroprusside-induced hypotension is followed by withdrawal of sympathetic tone and bradycardia and that this depressor reflex is more pronounced in late-gestation fetuses than newborn lambs and is significantly attenuated after bilateral vagotomy in newborn lambs.
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PMID:Autonomic adjustments to severe hypotension in fetal and neonatal sheep. 1113 92

Stimulation of cardiac vagal afferent endings evokes reflex hypotension and bradycardia, also known as a Bezold-Jarisch effect. The physiological importance of this reflex pathway remains uncertain today, but it is increasingly apparent that cardiac vagal afferents can play an important role in modulating cardiovascular control in pathophysiological states, particularly myocardial ischemia. The afferent endings that compose this vagal input are functionally diverse. Ventricular endings exist that are stimulated by wall motion. However, cardiac chemosensitive endings, stimulated by a variety of metabolically active substances known to be produced by the stressed myocardium (e.g., bradykinin, prostaglandins, reactive oxygen species), play a major role in mediating reflex adjustments during myocardial ischemia. Data are presented highlighting the importance of arachidonic acid metabolites and oxygen radicals in activating cardiac vagal endings during myocardial ischemia and reperfusion, and their role in modulating cardiac afferent sensitivity in the disease states of heart failure and insulin-dependent diabetes.
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PMID:Cardiac vagal chemosensory afferents. Function in pathophysiological states. 1145 8

Although acute myocardial ischemia or infarction may induce the Bezold-Jarisch (BJ) reflex through the activation of serotonin receptors on vagal afferent nerves, the mechanism by which the BJ reflex modulates the dynamic characteristics of arterial pressure (AP) regulation is unknown. The purpose of this study was to examine the effects of the BJ reflex induced by intravenous phenylbiguanide (PBG) on the dynamic characteristics of the arterial baroreflex. In seven anesthetized rabbits, we perturbed intracarotid sinus pressure (CSP) according to a white noise sequence while renal sympathetic nerve activity (RSNA), AP, and heart rate (HR) were recorded. We estimated the transfer function from CSP to RSNA (neural arc) and from RSNA to AP (peripheral arc) before and after 10 min of intravenous administration of PBG (100 microg. kg-1. min-1). The intravenous PBG decreased mean AP from 84.5 +/- 4.0 to 68.2 +/- 4.7 mmHg (P < 0.01), mean RSNA to 76.2 +/- 7.0% (P < 0.05), and mean HR from 301.6 +/- 7.7 to 288.4 +/- 9.0 beats/min (P < 0.01). The intravenous PBG significantly decreased neural arc dynamic gain at 0.01 Hz (1.06 +/- 0.08 vs. 0.59 +/- 0.17, P < 0.05), whereas it did not affect that of the peripheral arc (1.20 +/- 0.12 vs. 1.18 +/- 0.41). In six different rabbits without intravenous PBG, the neural arc transfer function did not change between two experimental runs with intervening interval of 10 min, excluding the possibility that the cumulative effects of anesthetics had altered the neural arc transfer function. In conclusion, excessive activation of the BJ reflex during acute myocardial ischemia may exert an adverse effect on AP regulation, not only by sympathetic suppression, but also by attenuating baroreflex dynamic gain.
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PMID:Bezold-Jarisch reflex attenuates dynamic gain of baroreflex neural arc. 1271 25

Although the Bezold-Jarisch (BJ) reflex is potentially evoked during acute myocardial ischemia or infarction, its effects on the static characteristics of the arterial baroreflex remain to be analyzed in terms of an equilibrium diagram between the neural and peripheral arcs. The neural arc represents the static input-output relationship between baroreceptor pressure input and efferent sympathetic nerve activity (SNA), whereas the peripheral arc represents that between SNA and arterial pressure (AP). In 8 anesthetized rabbits, we increased carotid sinus pressure stepwise from 40 to 160 mmHg in increments of 20 mmHg at one-minute intervals while measuring renal SNA and AP under control conditions and during the activation of the BJ reflex by intravenous administration of phenylbiguanide (PBG, 100 microg.kg(-1).min(-1)). The neural arc approximated a sigmoid curve whereas the peripheral arc approximated a straight line. PBG decreased AP at the operating point from -91.3 +/- 2.4 to -71.7 +/- 3.1 mmHg (P < 0.01), and attenuated the total loop gain at the operating point from -1.31 +/- 0.44 to -0.51 +/- 0.14 (P < 0.05). The equilibrium diagram indicated that PBG caused a parallel shift of the neural arc toward lower SNA such that the maximum SNA was reduced to approximately 60% of control. PBG decreased neural and peripheral arc gains at the operating point to approximately 43% and 77%, respectively. In conclusion, the BJ reflex blunts arterial baroreflex via the shift of the neural arc toward lower SNA.
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PMID:Bezold-Jarisch reflex blunts arterial baroreflex via the shift of neural arc toward lower sympathetic nerve activity. 1563 95

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