Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT02427 (Atropine)
 3,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Atropine, calcium, calcium-channel blockers, beta-adrenergic-receptor blockers, oxygen, morphine, vasodilators, and potent diuretics are frequently used in advanced cardiac life support (ACLS). Since the last AHA conference on ACLS standards, little controversy has arisen regarding the use of oxygen, morphine, vasodilators, or potent diuretics. In 1979, a full vagolytic dose of atropine was recommended for use early in the course of asystolic or bradycardiac arrest. Since then reports suggest that this higher dose of atropine may be of some limited value in treating this highly resistant form of arrest. The routine use of calcium for asystole, bradycardiac arrest, and electromechanical dissociation has come under intense scrutiny. Studies have failed to demonstrate improved survival and have found potentially deleterious levels of serum calcium when calcium was administered according to AHA standards. It is also possible that postanoxic cerebral injury is exacerbated by the use of calcium. No controversy exists, however, concerning the use of calcium for the moribund patient with possible hypocalcemia or with an excess of calcium-channel blockers. The use of calcium-channel blockers has been advocated to prevent or retard the intracellular accumulation of calcium, which may cause irreversible postanoxic tissue damage. Calcium-channel blockers may also be useful in preventing or decreasing cerebral and coronary arteriospasm. These drugs have antianginal properties that may decrease ischemia. The antiarrhythmic effect of verapamil is particularly useful in the treatment of uncomplicated paroxysmal supraventricular tachycardia. Verapamil and diltiazem slow conduction through the atrioventricular node and may be used to slow the ventricular response in atrial fibrillation and flutter.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cardiovascular pharmacology. III: Atropine, calcium, calcium blockers, and beta-blockers. 287 54

The effect of ischemia on phosphatidylinositol (PI) degrading enzymes in brain homogenate, cytosol and synaptosomes was investigated to evaluate the involvement of cholinergic receptor in PI hydrolysis during ischemia. The activity of phospholipase C in cytosol was not changed by ischemic insult. PI degradation in synaptosomes was significantly (60%) enhanced by ischemia. Atropine and gamma-butyrolactone abolished the ischemic effect on PI degradation, suggesting that the cholinergic receptor system mediates breakdown of PI during ischemia.
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PMID:Phosphatidylinositol degradation in ischemic brain specifically activated by synaptosomal enzymes. 358 67

Bradyarrhythmias, with or without hypotension, may be associated with acute myocardial infarction, especially inferior. The early use of atropine in the management of sinus bradycardia, with associated hypotension, spurred a continuing controversy that has found only partial solution in animal models. Experimentally there is increased sensory and autonomic motor activity with acute coronary occlusion. For example, in the cat, increased cholinergic activity was evidenced by the absence of bradycardia with atropinization and vagotomy, although these pretreatments accelerated the onset of significant ventricular arrhythmias. Atropine in experimentally infarcted dogs increased ischemia, while elevated heart rates reduced the threshold for ventricular fibrillation (VF) and vagal stimulation increased the threshold for VF, largely independent of heart rate. Specific clinical studies failed to support much of the animal data, although reports of tachyarrhythmias and VF resulting from the administration of atropine extended the controversy. The animal models, in the main, failed to mimic the clinical situation, for: 1) pentobarbital, with its propensity to alter some autonomic reflexes, dominated earlier work; 2) relatively large doses of atropine were employed; 3) the animals were presumed to be free of coronary and cardiac disease, factors known to influence autonomic reflexes; and 4) vagotomy and atropinization commonly preceded the acute occlusion.
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PMID:Atropine: animal models. 647 48

In a group of 288 patients with acute inferior (diaphragmatic) myocardial infarction, second and third degree atrioventricular (AV) block was diagnosed in 37 (14%). Three of the 37 died. The AV block in the 34 survivors could be differentiated into two distinct types, namely, early and late AV block. In 15 patients, second and third degree AV block developed within 6 hours of the first signs of infarction. In these 15 patients, all signs of AV block disappeared within 24 hours after infarction. Second and third degree AV block appeared suddenly in the vast majority, and first degree AV block could be detected in only a few patients and for a very short time before normalization of conduction. Atropine either abolished AV block completely or caused a marked acceleration of ventricular escape rhythm. In 14 patients, second and third degree AV block developed later than 6 hours (in 12 later than 24 hours) after infarction. It was heralded and followed by relatively long periods of first degree AV block in all cases (except in two patients who were admitted 72 hours after infarction). The total duration of AV block was longer than 40 hours in all of these patients, and the ventricular rate was relatively high. In no patient was abolishment of AV block achieved by atropine, and ventricular acceleration was relatively slight in all. In five patients, early and late AV block could be recognized consecutively. The two types of AV block seem to have different causes. Increased vagal tone is probably operative in the first type, and metabolic changes due to ischemia in the second. Response to atropine and sympathomimetic drugs is much better, and cardiac pacing only rarely indicated, in patients with early than in those with late AV block.
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PMID:Early and late atrioventricular block in acute inferior myocardial infarction. 673 51

The gastric microvascular changes in reserpine (RES 6 mg/kg s.c.)-induced ulcer in Wistar male rats were studied. Two kinds of water paints were injected through the superior mesenteric vein and celiac artery. Excised stomachs were frozen instantly by cooled methanol (-70 degrees C) and were put into methylsalicylate after 24 hr in order to make transparent preparations. RES caused constriction of the vein from the middle layer till the muscularis mucosae and congestion with ischemia in the gastric mucosa after 1 hr. Even after 3 hr, these vascular changes remained and were accompanied by erosion. After 6 and 9 hr, the erosion became more severe, while ischemia was no longer found and the vessels were rather dilated. These lesions initiated from the fundic-antral border area in the lesser curvature and gradually extended to the greater curvature. The early changes up to 3 hr were inhibited by phentolamine, isoproterenol, C6, metiamide and methysergide, but not by carbachol, atropine, vagotomy and propranolol. Atropine, vagotomy, isoproterenol, propranolol and C6 inhibited erosion in the late stage. Phentolamine, carbachol, diphenhydramine, metiamide and methysergide were not effective. From these results and the gastric movement caused by RES, it is suggested that the vascular changes of the early stage in RES-induced ulcer are due not only to the autonomic nervous system but also to the endogenous biogenic amines, and the erosions in the late stage depend on the hypermotility of the stomach rather than on the hypersecretion of the stomach.
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PMID:[Changes of gastric mucosal vessels in reserpine-induced ulcer (author's transl)]. 708 19

Attenuated cholinergic vasodilatation has been suggested as an endothelium-related mechanism involved in essential hypertension. We investigated the role of muscarinic (M) receptor subtypes in the forearm resistance vasculature. In eight white men with essential hypertension and eight matched normotensive control subjects (age of both groups, 47 +/- 4 years; mean +/- SEM), we infused the nonselective agonist methacholine in the presence of saline and the antagonists atropine (nonselective), pirenzepine (M1-selective), and AF-DX 116 (M2-selective) into the brachial artery and measured forearm blood flow and forearm vascular resistance using venous occlusion plethysmography. Affinity constants (pKb values) were determined from calculated plasma concentrations of the infused compounds and EC50 values. Sodium nitroprusside was given as an endothelium-independent control, and minimal forearm vascular resistance after 10 minutes of ischemia was used as a marker of structural vascular changes. Hypertensive patients showed higher minimal forearm vascular resistance, indicating structural vascular changes. However, sodium nitro-prusside- and methacholine-induced vasodilatation was similar in both groups, with apparent EC50 values (log moles per liter; mean +/- SEM) of -7.32 +/- 0.13 and -7.51 +/- 0.21 in hypertensive patients and -7.37 +/- 0.13 and -7.45 +/- 0.02 in control subjects, respectively. Atropine, pirenzepine, and AF-DX 116 caused a shift to the right of the concentration-response curve of methacholine, with apparent pKb values of 8.63 +/- 0.08, 6.81 +/- 0.13, and 5.51 +/- 0.29 in hypertensive individuals and 8.62 +/- 0.10, 6.98 +/- 0.08, and 5.49 +/- 0.09 in control subjects, respectively. Again, there were no statistically significant differences in these pharmacological parameters between hypertensive patients and normotensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:In vivo characterization of muscarinic receptor subtypes that mediate vasodilatation in patients with essential hypertension. 760 35

1. Cerebral ischemia of 5 min duration was induced in unanesthetized gerbils by bilateral occlusion of the carotid arteries. 2. The extent of cerebral damage was assessed by the elevation of motor activity in comparison with control animals and by a histological assessment of the extent of neuronal degeneration in the CA1 area of the hippocampus. 3. Atropine, an antagonist of ACh, at either a low (1 mg/kg) or a high (10 mg/kg) dose administered 15 min prior to the ischemic episode, did not confer protection against cerebral ischemic damage. 4. This finding suggests that ACh does not play a critical role in the generation of ischemia reperfusion injury.
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PMID:Atropine and cerebral ischemic injury in the Mongolian gerbil. 795 34

The purpose of this study was to establish the safety of high-dose dobutamine-atropine stress echocardiography in patients with suspected or proven coronary artery disease. Six hundred fifty consecutive examinations were completed. Mean age of patients was 61 years; 300 had a previous myocardial infarction. Heart rate increased from 73 to 129 beats/min during stress testing, blood pressure did not change significantly (from 140/81 to 150/80 mm Hg). Atropine was added to dobutamine in 239 patients when no ischemia was induced with dobutamine alone and the peak heart rate was < 85% of the theoretical maximal heart rate. Atropine was more frequently administered to patients taking beta blockers (77 vs 27%, p < 0.001). New wall motion abnormalities developed in 243 patients (37%). Significant or symptomatic cardiac tachyarrhythmias, or both, developed during 24 examinations: 1 patient developed ventricular fibrillation, 3 patients developed sustained ventricular tachycardia, 12 patients experienced nonsustained ventricular tachycardia (< 10 beats) and 8 patients had paroxysmal atrial fibrillation. Cardiac arrhythmias were more frequent in patients with a history of ventricular arrhythmias (ventricular tachycardia and fibrillation) (odds ratio 9.9, 2.0 to 45) or left ventricular dysfunction at rest (wall motion score > 1.12) (odds ratio 2.9, 1.1-7.6), but not associated with atropine addition. No death or myocardial infarction occurred. The full dose was not given to 13 patients despite absence of signs or markers of ischemia for limiting side effect, yielding an overall feasibility of the stress test of 98%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Safety of dobutamine-atropine stress echocardiography in patients with suspected or proven coronary artery disease. 814 Oct 86

Temporal changes in cholinergic functions following transient cerebral ischemia (10 min) were studied in the hippocampus of awake unrestrained gerbils using in vivo microdialysis. These data were compared with the results for temporal change in the area of each CA1 cell soma, measured with a microcomputer imaging device. KCl-induced release of acetylcholine (ACh) tended to be lower within 1 day after recirculation, and was significantly lower on the 4th, 7th and 14th days. Atropine-induced release of ACh gradually decreased over the test period. In histological estimation, no differences were observed within the 1st day, but a significant decrease of the area of CA1 cell soma was observed from the 4th to 14th days. Moreover, ischemia over 2 min decreased KCl- and atropine-induced ACh release on the 14th day without significant changes of hippocampal CA1 pyramidal cell. From these results, it is clear that ischemia produced dysfunction of hippocampal cholinergic neurons, and that dysfunction of the hippocampal cholinergic system following transient ischemia precedes pyramidal cell damage in the hippocampal CA1 subfield.
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PMID:Temporal changes in extracellular acetylcholine and CA1 pyramidal cells in gerbil hippocampus following transient cerebral ischemia. 818 Aug 40

Ischemia in active skeletal muscle induces reflex increases in systemic arterial pressure (SAP) and heart rate (HR), termed the muscle metaboreflex. When metaboreflex activation is maintained during postexercise muscle ischemia, SAP remains elevated; however, HR decreases. Why the HR responses differ with metaboreflex activation during exercise vs. during postexercise ischemia while the SAP responses are similar in each setting remains unclear. Two hypotheses were tested: 1) the increase in HR with muscle ischemia occurs predominantly via an increase in sympathetic activity, and 2) sympathetic activity to the heart remains elevated during post-exercise ischemia; however, HR decreases because of an increase in parasympathetic outflow. The muscle metaboreflex was activated in conscious dogs during treadmill exercise (3.2 kph, 0% grade) by progressively decreasing perfusion to the hindlimbs. Experiments were performed before and after muscarinic (atropine) or beta- (atenolol or propranolol) receptor blockade. In control experiments, once beyond the threshold for the reflex, the HR sensitivity of the muscle metaboreflex averaged -2.4 +/- 0.3 beats.min-1.mmHg-1 and the reflex open-loop gain averaged -3.2 +/- 0.3 (calculated as the ratio of the increase in HR or SAP to the decrease in hindlimb perfusion pressure beyond threshold). Atropine had no effect on either HR sensitivity (-2.7 +/- 0.4 beats.min-1.mmHg-1) or open-loop gain (-3.3 +/- 0.5, both P > 0.05 vs. control). However, pretreatment with beta-receptor antagonist significantly decreased both HR sensitivity (-0.7 +/- 0.1 beats.min-1.mmHg-1, P < 0.001) and open-loop gain (-1.9 +/- 0.3, P < 0.01). During postexercise ischemia, HR decreased while SAP remained elevated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Autonomic mechanisms of muscle metaboreflex control of heart rate. 851 92


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