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In atrial fibrillation flutter, pharmacologic therapy is designed to reduce the ventricular rate and convert maintain normal sinus rhythm. Specific drugs may be more or less effective for these two goals. Intravenous esmolol or diltiazem are both effective at controlling the rate, however esmolol may be more effective at conversion.9 Procainamide may convert the rhythm to sinus but will not control the ventricular response, while amiodarone may do both. Both sotalol and amiodarone are more effective than digoxin for conversion of new onset atrial fibrillation. 10 Ibutilide is a recent addition to the antidysrhythmic pharmacopaea. It is a Vaughan Williams Class III drug prolongation of repolarization ; with a rapid onset and relatively short duration of action, indicated for the conversion of acute atrial fibrillation flutter to sinus rhythm. It appears to be somewhat more effective in atrial flutter than fibrillation, converting 35-60% of patients.11 The drawback to this drug is a significant incidence of proarrhythmia which increases as ventricular function worsens. There are no published studies of the use of ibutilide in anesthetized patients. Direct current synchronized cardioversion is the treatment of choice in patients with tachydysrhythmias associated with hypotension or significant "hemodynamic compromise." During or after major surgery this treatment is likely to be ineffective or only temporarily effective until the underlying cause for the dysrhythmia is addressed eg volume overload, diuretic therapy, or the presence of catecholamine infusions ; . The pathophysiology and treatment of atrial fibrillation after cardiac surgery have recently been reviewed by Hill et al, 12, 13 and surgical options including intraoperative ablation of atria are reviewed by Gillinov et al.14 b ; Ventricular tachydysrhythmias The first line treatment for hemodynamically unstable ventricular tachydysrhythmias is direct current cardioversion. The first line antidysrhythmic drug this rhythm with stable hemodynamics, or to prevent recurrence has historically been lidocaine, administered as a load 1.5 - 2 mg kg ; followed by an infusion 2 mg min ; at the time of the cardioversion. As mentioned above, unless Mg + levels have been documented as elevated or a dose has been given recently, in the cardiac surgical patient a dose of 1-2 grams of Mg + should be given and the serum level of K + measured. Any metabolic abnormalites should be treated, and if catecholamine infusions are running consideration should be given to using the least arrhythmogenic combination of drugs eg, use of norepinephrine and milrinone appears less likely to exacerbate dysrhythmias than epinephrine or dobutamine ; . Second line drug treatment for refractory ventricular dysrhythmias has traditionally been another class 1 drug eg procainamide ; or the class III drug, bretylium. Recent publication of revised guidelines for the treatment of life threatening cardiac dysrhythmias has moved amiodarone from a 3rd line drug to either first line, or second after lidocaine. 15 Amiodarone compares favorably to bretylium in medical patients with refractory ventricular dysrhythmias, being equally effective and less likely to cause.
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AiR 1980; 135: 327-330 Fork F-T. Double contrast enema and colonoscopy in polyp detection. Gut 198122: 971-977 Thoeni AF, Petras A. Detection of rectal and rectosigmoid lesions by double-contrast barium enema examination and sigmoidoscopy. Radiology 1982; 142: 59-62 Teefey SA, Carlson HC. The fluoroscopic barium enema in colonic polyp detection. AJR 1983; 141 : 1279-i 281 Feczko PJ, Halpert RD. Reassessing the role of radiology in hemoccult screening. AJR 1986; 146: 697-701 Ott DJ, Gelfand DW. Colorectal tumors: pathology and detection. AJR 1978; 131 : 69i-695 Gelfand DW, Ott DJ. The economic implications of radiologic screening for colonic cancer. AJR 1991156: 939-943 Kelvin FM, Gardiner A, Vas W, Stevenson GW. Colorectal carcinoma missed on double contrast barium enema study: a problem of perception. AJR 1981; 137: 307-313 Johnson CD, Carison HC, Taylor WF, Weiland LP. Barium enemas of carcinoma of the colon: sensitivity of doubleand single-contrast studies. AJR 1983; 140: i143-1149 Ott DJ, Scharling ES, Chen YM, Wu WC, Gelfand DW. Barium enema examination: sensitivity in detecting colonic polyps and carcinomas. South MedJ 1989; 82: 197-200.
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Desire ; is to this day the supreme spiritual focus for those Tantrics who worship the goddess with the help of Her priestesses, who possess naturally the characteristic talis man of the Goddess. Here at Kamrup the menstruation of the earth occurs, according to Hindu belief. The above examples of divine centres are peculiar to Egypt and India. There is, however, a world-wide complex of centres and they are reflected in miniature in the seven major chakras situated in the subtle counterpart of the human body. To be more precise, the chakras function through the endocrine system and so affect humanity at psycho-physical levels. The macrocosmic centres are widely distributed over the earth's surface; one is located in Cairo, another in Sumer, a third in the British isles, and the most exalted and spiritual centre is located at the southern extremity of India. The remaining three are situated in the trans-Himalayan region of the Gobi desert, in the Andes and in California respectively.
Br j anest 1986; 58 5 ; : 483- somogyi a, bochner dose and concentration dependent effect of ranitidine on procainamide disposition and renal clearance in man.
Ing experience-two years of which were consultative, administrative or teaching. Salary commensurate with experience and education. Attrative fringe benefits. Send resume to: Mr. Gary Williams, Administrator, Las Animas-Huerfano Counties District Health Department, 412 Benedicta Avenue, Trinidad, CO 81082. Equal Opportunity Employer.
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To the Editor: In their excellent article, 1 Kwan et al found that 1 ; the antiarrhythmic effect of procainamide PA ; could not be attributed to the alteration in wavelength because it did not significantly affect wavelength during ventricular fibrillation VF ; , and 2 ; the ability of PA to decrease the number of wavelets by preventing spontaneous wave breaks can represent a novel mechanism of antiarrhythmic drug action. Because PA antiarrhythmic and defibrillating effects in rats2 and guinea pigs3 cannot be explained by prolongation of wavelength, and the mechanisms of preventing wave break are not clear, let us discuss briefly the features required for antiarrhythmic defibrillating compounds. In an attempt to clarify the mechanisms underlying the maintenance of VF, we examined4 the factors involved in transient VF TVF ; versus sustained VF SVF ; . No differences were found between cardiac muscle mass, heart rate, action potential duration, and effective refractory period of animals that exhibited TVF versus SVF. Similar to Kwan et al1 Figure 8 ; , TVF exhibited slow and synchronized electrical fibrillating activity, with a large part of ventricular mass acting in synchrony, whereas SVF exhibited unorganized, less synchronized electrical activity at a higher rate, with small local fibrillating areas. Untreated VF starts as an organized electrical activity resembling TVF, which becomes faster, less organized, and unsynchronized within a few seconds owing to "spontaneous wave break." "Synchronized" fibrillation may occur only in hearts with good functional cell-to-cell coupling, ensuring continuous propagation of electrical signals through the myocardium in a manner that brings the viable cardiomyocytes to act almost in unison. Attenuation of spatial and transmural inhomogeneity of gap junctional alteration by enhancement of intercellular coupling can facilitate conversion of SVF into TVF by preventing spontaneous wave break and decreasing the number of reentry circles via synchronization of small local circles into bigger ones. Spontaneous defibrillation occurs when the viable myocardium acts as a functional syncytium and the majority of myocardial cells are simultaneously in the refractory period.4 Fast fibrillating ; cellular activity associated with temporary hypoxia or ischemia increases junctional resistance, decreases gap junctional conduction, and causes intercellular uncoupling, most likely owing to an increase in cytoplasmic free Ca2 concentration [Ca2 ]i ; and or alteration in intercellular cAMP gradient.5 An excess of diastolic [Ca2 ]i downregulates intercellular communication, impairs intercellular coupling, and thus increases the number of fibrillating microareas by spontaneous wave break. Following this assumption, we hypothesized6 that an antiarrhythmic defibrillating drug should prevent intercellular desynchronization. It should decrease the number of fibrillating circles and thereby slow down the fibrillating rate. It should prevent or attenuate [Ca2 ]i overload-induced electrical uncoupling and thereby enhance or reestablish intercellular coupling and synchronization. It should increase gap junctional conductance, should not decrease conduction velocity, and should preserve excitation-contraction coupling. Recently, it was found2, 3 that PA possesses 1 of the main antiarrhythmic effects: it prevents Ca overload and decreases previously enhanced [Ca2 ]i toward its normal level. In this way.
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C. One-two years experience D 4. Care of the patient with a. Abdominal aortic aneurysm repair b. Acute MI c. Cardiac arrest d. Cardiac temponade e. Congestive heart failure CHF ; f. EP study & ablation g. Heart transplant h. Immediate post open-heart surgery i. Infective endocarditis j. Myocardial contusion k. Pericarditis l. Post AICD insertion m. Post arthrectomy DCA ; n. Post, valve repair replacement o. Post intracoronary stent placement p. Post percutanious balloon valvuloplasty q. Post rotoblade r. Pre post angioplasty s. pre post cardiac cath 5. Medications a. Amiodarane Cardarone ; b. Aropine c. Bretylium Bretrylol ; d. Digoxin Lanoxin ; f. Ditiazem Dardizem ; g. Dobutamine Dobutrex ; h. Dopamine Intropin ; i. Epinephrine Adrenalin ; j. Esmolol Brevibloc ; k. Inocor Brevibloc ; l. Lidocaine Xylocaine ; m. Metropolol Lopressor ; n. Nipride Nitroprusside ; o. Nitroglycerine Tridil ; p. Procainamide Pronestyl ; q. Reteplase recombinant Retavase ; r. Streptokinase s. TPA Alteplase ; t. Verpamil Calan, Isoptin, VerelanA ; 4. Care of the patient with a. Abdominal aortic aneurysm repair b. Acute MI c. Cardiac arrest d. Cardiac temponade e. Congestive heart failure CHF ; D. More than 2 yrs experience A B C and procarbazine.
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Ringer's injection, USP; 5% dextrose and ringer's injection; 5% lactated ringer's and 5% dextrose injection; 5% dextrose injection, USP; 0.9% sodium chloride injection, USP; 5% dextrose and 0.2% sodium chloride injection, USP; 2.5% dextrose and 0.45% sodium chloride injection, USP; 5% dextrose and 0.9% sodium chloride injection, USP; and 5% dextrose and 0.33% sodium chloride injection, USP. TRANDATE Injection was NOT compatible with 5% sodium bicarbonate injection, USP. Care should be taken when administering alkaline drugs, including furosemide, in combination with labetalol. Compatibility should be assured prior to administering these drugs together. HOW SUPPLIED: TRANDATE Injection, 5 mg mL, is supplied in 20mL 100mg ; vials, box of one NDC 0173035058 ; and 40mL 200mg ; vials, box of one NDC 0173035057 ; . STORE BETWEEN 2 DEG AND 30 DEG C 36 DEG AND 86 DEG F ; . DO NOT FREEZE. PROTECT FROM LIGHT. May 1997 RL426 Shown In The Product Identification Guide Of Current PDR. as significant adverse effects are not produced by the antiarrhythmic drug. Benefits from treatment of long term ventricular ectopy in asymptomatic individuals with underlying heart disease are less clear. Although such individuals are at increased risk of sudden cardiac death, antiarrhythmic therapy has not been shown to prolong survival. In contrast, survival may be improved by comprehensive evaluation and treatment of survivors of outofhospital cardiac arrest not associated with AMI see Section 11E, Survivors of Cardiac Arrest: Options for Management ; . Clinical concerns regarding the management of patients with newonset PVCs that occur in association with acute ischemic heart disease are very different than the concerns posed by longstanding ventricular ectopy. Because the risk of developing malignant ventricular arrhythmias i.e., sustained ventricular tachycardia or ventricular fibrillation ; is much greater in the acute setting, much greater consideration should be given to active antiarrhythmic therapy. If the decision is made to treat, IV lidocaine is the drug of choice. Patients who are at the greatest risk for developing malignant ventricular arrhythmias with AMI are those who are seen within the first few hours of the onset of symptoms. Consequently, patients with new onset chest pain in whom there is a high index of suspicion for acute infarction would seem to be the group most suited for consideration of lidocaine prophylaxis, especially if they are seen within the first 6 hrs of the onset of symptoms. However, because the incidence of primary ventricular fibrillation is less in patients over 70 years of age and the risk for developing lidocaine toxicity is significantly greater ; , antiarrhythmic prophylaxis is less likely to be beneficial in elderly subjectsand may not be worth the risk. Overall, the issue remains controversial. Therapeutic decisionson whether to initiate lidocaine prophylaxis and or treatmentmust therefore be individualized, and are usually based on clinical circumstances and the judgment beliefs of the health care team. Detailed discussion on the use of lidocaine for patients with suspected AMI including the rationale for treatment and dosing recommendations ; is covered in Sections 12B and 12E, and summarized in Table 12B2. We limit discussion here to emphasis of several key points in management: 1. IV lidocaine should NOT be used to treat chronic PVCs that occur in an asymptomatic patient who is not having an acute ischemic syndrome. In most instances, this general rule should be followed even if PVCs are frequent and short runs of repetitive forms are present. 2. When used prophylactically i.e., in the absence of PVCs ; , aggressive loading with IV lidocaine is probably not needed and may unnecessarily increase the risk for drug toxicity. In most cases, 1 to 2 boluses of lidocaine and constant infusion at a rate of 2 mg min is perfectly adequate to ensure the drug's protective effect. Even if some ventricular ectopy persists, additional boluses and higher infusion rates may still not be needed as long as repetitive forms i.e., ventricular couplets or salvos ; are infrequent. Elimination of every PVC is NOT essential for protection against ventricular fibrillation. 3. Lidocaine toxicity is prone to develop in patients with congestive heart failure or shock who are likely to have difficulty clearing the drug ; , the elderly, patients with lower body weights, and with concomitant use of propranolol or cimetidine. Use of lower infusion rates i.e., 0.5 to 1 mg min ; and monitoring with lidocaine levels if available ; should be considered for such patients. 4. Although still the subject of controversy, lidocaine has been recommended as a drug of choice for treatment of refractory ventricular fibrillation. Studies to date have not demonstrated a significant difference in clinical efficacy between this drug and bretylium in this situation. Because lidocaine may be a safer agent, and most emergency care providers are more comfortable with its use, this drug is favored over bretylium for treatment of refractory ventricular fibrillation. Because of the markedly decreased clearance of lidocaine during cardiac arrest, 1 to 2 boluses of the drug with or without initiation of a maintenance infusion ; is usually all that is needed to achieve therapeutic levels during this lowflow state. Once the patient has been converted out of ventricular fibrillation, however, clearance of the drug markedly increases. Resumption of a normal dosing schedule i.e., rebolus and institution of a maintenance infusion ; is essential at this time to minimize the chance that ventricular fibrillation will recur. Practically speaking, it may be far simpler to always initiate a maintenance infusion at 2 mg min ; at the same time the decision is made to administer IV loading boluseseven during the low flow state of cardiac arrest see Section 12E ; . 5. Although lidocaine may be administered by the endotracheal route, absorption of the drug is unreliable during cardiac arrest. Peak concentrations of lidocaine may be delayed for up to 10 minutes following intratracheal instillation. Therefore, if IV access is available, this route is definitely preferred for administration of lidocaine. 6. Lidocaine will not always be successful in terminating sustained ventricular tachycardia. However, because the drug is rapidly administered, well tolerated by most patients, associated with relatively few adverse effects, and does not impair the ability to subsequently give other drugslidocaine remains the firstline agent for medical treatment of this arrhythmia. If at any time the patient becomes hemodynamically unstable, immediate cardioversion becomes the treatment of choice. 7. Lidocaine is most likely to be effective in the treatment of acute ventricular arrhythmias that develop as a result of ischemia. It appears to be much less effective in the treatment of longstanding arrhythmias that arise from a fixed anatomic substrate such as commonly occurs under nonischemic conditions Wesley et al, 1991 ; . If such nonischemicrelated arrhythmias are to be treated at all, other antiarrhythmic agents such as procainamide ; are more likely to be effective than lidocaine.
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Amiodarone HCL Amiodarone HCL CORDARONE I.V. Amiodarone HCL Disopyramide Phosphate Disopyramide Phosphate ETHMOZINE Moricizine HCL Flecainide Acetate Lidocaine HCL Mexiletine HCL NORPACE CR PACERONE Disopyramide Phosphate Amiodarone HCL Procainamide HCL Procainamide HCL Procainamide HCL PROCANBID PRONESTYL PRONESTYL PRONESTYL-SR Procainamide HCL Procainamide HCL Procainamide HCL Procainamide HCL Propafenone HCL Quinidine Gluconate Quinidine Gluconate Quinidine Sulfate Quinidine Sulfate RYTHMOL SR TIKOSYN XYLOCAINE IV FOR CARDIAC Propafenone HCL Dofetilide Lidocaine HCL and procrit.
Pulmonary disease had an acute myocardial infarction complicated by congestive heart failure with persistently high filling pressures and low cardiac output in late August 1978. One w-eek later, ventricular fibrillation occurred. The patient was resuscitated, but continued to have severe ventricular arrhythmias, with recurring episodes of ventricular tachycardia refractory to all standard antiarrhythmic drugs and to the investigational agents encainide and aprindine. On October 24 he was started on amiodarone, 600 mg day, without a loading dose. Over the ensuing 3 weeks good control of ventricular tachycardia was attained and he was discharged on the same dose on November 13. Two days later, however, syncope and sustained ventricular tachycardia recurred, and procainamide was added to his regimen. On December 14 he complained of increasing shortness of breath. The chest x-ray showed a diffuse alveolar pattern bilaterally, felt to be consistent with acute pulmonary edema. Despite treatment with diuretics and antibiotics, the patient's status worsened and intubation and mechanical ventilation were required. Amiodarone and procainamide were both discontinued on December 18. Because of continuing respiratory failure despite therapy, an open lung biopsy was performed on December 20. Microscopic examination revealed fibrosing interstitial pneumonitis with hyaline membrane formation and atypical alveolar lining cell hyperplasia. No eosinophilia was noted and no cause determined. The patient's respiratory status did not improve despite aggressive therapy, and on December 23 the patient suffered a cardiac arrest unresponsive to resuscitation.
Tiguous regions for habitat needs. The Office of Natural Lands Management maintains a database of threatened and endangered species of plants and animals, as well as natural vegetative communities of statewide significance. These are compiled in a Natural Heritage Sites database and map Map 7 ; . The compilation cites 28 species of threatened endangered animals, 82 plants, and 16 Natural Heritage Sites in Hunterdon County. Natural Heritage Sites are some of New Jersey's best habitats for rare and endangered species and natural communities. The Landscapes Project: : High Priority Habitats Forests High priority forested areas encompass much of the Highlands region in Hunterdon County. Other notable forests occur on the Sourland Mountain, Cushetunk Mountain and along the Delaware River. Ecologists at the NJDEP have identified the Sourland Mountain as the only remaining large forest patch within the entire Piedmont region in New Jersey. Grasslands Grasslands are open fields dominated by grasses, sedges, rushes and herbaceous plants. In Hunterdon County, they are either abandoned farm fields, actively farmed fields or other managed fields like airports. High priority grasslands occur throughout Hunterdon County. Notable areas include the Amwell Valley in East Amwell Township, adjacent lands in Raritan Township, the southeastern reaches of Franklin and Alexandria Townships, the Musconetcong River valley in Bethlehem Township, and the eastern half of Tewksbury Township. Among these notable grasslands is one that extends from Frenchtown to Everittstown along County Route 513 in Alexandria Township. Like many others, it supports a healthy diversity of habitats. Wetlands Among the more prominent wetlands considered high priority conservation areas are the South Branch of the Raritan River along the Franklin Clinton Township border; headwaters to the Wickecheoke Creek; portions of the Mulhockaway Creek and tributaries to Spruce Run Reservoir in Union Township; portions of Spruce Run in Lebanon Township; and portions of the Rockaway Creek and prohibit.
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In addition to dose and presence of sustained VT, other risk factors for Torsade de Pointes were gender females had a higher incidence ; , excessive prolongation of the QTc interval and history of cardiomegaly or congestive heart failure. Patients with sustained ventricular tachycardia and a history of congestive heart failure appear to have the highest risk for serious proarrhythmia 7% ; . Of the ventricular arrhythmia patients experiencing Torsade de Pointes, approximately two-thirds spontaneously reverted to their baseline rhythm. The others were either converted electrically D C cardioversion or overdrive pacing ; or treated with other drugs see OVERDOSAGE ; . It is not possible to determine whether some sudden deaths represented episodes of Torsade de Pointes, but in some instances sudden death did follow a documented episode of Torsade de Pointes. Although sotalol therapy was discontinued in most patients experiencing Torsade de Pointes, 17% were continued on a lower dose. Use with Drugs that Prolong QT Interval and Antiarrhythmic Agents: The use of BETAPACE AF in conjunction with other drugs that prolong the QT interval has not been studied and is not recommended. Such drugs include many antiarrhythmics, some phenothiazines, bepridil, tricyclic antidepressants, and certain oral macrolides. Class I or Class III antiarrhythmic agents should be withheld for at least three half-lives prior to dosing with BETAPACE AF. In clinical trials, BETAPACE AF was not administered to patients previously treated with oral amiodarone for 1 month in the previous three months. Class Ia antiarrhythmic drugs, such as disopyramide, quinidine and procainamide and other Class III drugs e.g., amiodarone ; are not recommended as concomitant therapy with BETAPACE AF because of their potential to prolong refractoriness see WARNINGS ; . There is only limited experience with the concomitant use of Class Ib or Ic antiarrhythmics. Congestive Heart Failure: Sympathetic stimulation is necessary in supporting circulatory function in congestive heart failure, and betablockade carries the potential hazard of further depressing myocardial contractility and precipitating more severe failure. In patients who have heart failure controlled by digitalis and or diuretics, BETAPACE AF should be administered cautiously. Both digitalis and sotalol slow AV conduction. As with all beta-blockers, caution is advised when initiating therapy in patients with any evidence of left ventricular dysfunction. In a pooled data base of four placebocontrolled AFIB AFL and PSVT studies, new or worsening CHF occurred during therapy with BETAPACE AF in 5 1.2% ; of 415 patients. In these studies patients with uncontrolled heart failure were excluded i.e., NYHA Functional Classes III or IV ; . other premarketing sotalol studies, new or worsened congestive heart failure CHF ; occurred in 3.3% n 3257 ; of patients and led to discontinuation in approximately 1% of patients receiving sotalol. The inci and propylthiouracil.
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DISOPYRAMIDE, QUINIDINE, AND MUSCARINIC RECEPTORS MtVro et al. method originally described by Yamamura and Snyder 1974 ; . Unless otherwise noted, homogenate 100-200 fig protein ; was incubated in 1-5 ml of medium containing 0.05 M sodium potassium phosphate buffer pH 7.4 ; , 80 [3H]quinuclidinyl benzilate [3H]QNB ; , and relevant drugs. Incubations were for 60 minutes at 37C, which allowed complete equilibration of binding. Specific binding was measured as that radioactivity displaceable by 1 fiM atropine. Bound [3H]QNB was separated from free [3H]QNB by filtration through Whatman GF C filters. The [3H]QNB binding assay was used to examine directly the interaction of antiarrhythmic agents with muscarinic receptors. A series of [3H]QNB competition curves were generated with antiarrhythmic drugs as well as conventional muscarinic antagonists. Binding studies were performed in homogenates of guinea pig right atria, allowing direct comparison of binding data with results of electrophysiological studies. To strengthen the analysis of drug-receptor interaction, all results obtained for crude homogenates were confirmed with a wellcharacterized sarcolemmal-enriched membrane vesicle fraction isolated from canine ventricle. Beta-adrenergic receptors were assessed directly with [3H]dihydroalprenolol [3H]DHA ; as previously reported Jones et al., 1979; Watanabe et al., 1978 ; . Briefly, cardiac membrane vesicles 60-100 fig protein ; were incubated for 10 minutes at 37C in 200 jul of medium containing Tris 50 HIM ; , MgCl2 9 mM ; , [3H]DHA 14 nM ; , and relevant drugs. Specific binding was measured as that radioactivity displaceable by 2 X 10~5 M d -propranolol. Bound [3H]DHA was separated from free [3H]DHA by filtration through Whatman GF C filters. All assays for both receptors were performed in triplicate. Radioactivity was counted on a liquid scintillation counter Beckman Instruments ; at a counting efficiency of 34%. Drugs Atropine sulfate, physostigmine sulfate, quinidine sulfate, quinine sulfate, and -- ; scopolamine sulfate were purchased from Sigma Chemical Company. Procainamide HC1 was purchased from E.R. Squibb and Sons, Inc. Racemic disopyramide, + ; disopyramide, and -- ; disopyramide were gifts from G.D. Searle Company and Roussel Laboratories. Unlabeled and tritiated ; quinuclidinyl benzilate QNB ; were obtained from New England Nuclear. Analysis of Data Analysis of electrophysiological data was designed to allow quantitative correlation with results of direct receptor binding studies. In the electrophysiological model, concentration-dependent drug effects were analyzed as follows: The mean slowing of spontaneous rate observed with 10~6 M physostigmine was arbitrarily designated as 100% cholin.
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