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Childrens Hospital of Los Angeles, University fornia School of Medicine, Los Angeles. Manuscript received April 12; revision accepted Reprint requests: Dt Garg, Division ofNeonatology, Sunset Bled, Los Angeles 9fXl27.

Reserpine agonist Uation mended warrants for use potential risk. in children. Precautions: Psychotic symptoms may be exacerbated in schizophrenic patients. Increased anxiety and agitation may occur in overactive or agitated patients. Manicdepressive patients may experience shift to manic phase. Hostility may be aroused. Concomitant administration of reserpine may produce a "stimulating" effect. Watch for possible epileptiform seizures during treatment. Use cautiously with anticholinergic or sympathomimetic drugs. Concurrent electroconvulsive therapy may increase hazards associated with nortriptyline HC1. When possible, discontinue drug several days prior to surgery. Potentially suicidal patients require supervision and protective measures during therapy. Prescriptions should be limited to the least possible quantity. Both elevation and lowering of blood sugar levels have been reported. Adverse Reactions: Note: The pharmacologic similarities among the tricyclic antidepressant drugs require that each of the following reactions be considered when nortriptyline is administered. Cardiovascular: t-lypotension, hypertension, tachycardia, palpitation, myocardial infarction, arrhythmias, heart block, stroke. Psychiatric: Confusional states especially in the elderly ; with hallucinations, disorientation, delusions; anxiety, restlessness, agitation; insomnia, panic, nightmares; hypomania; exacerbation of psychosis. Neurologic: Numbness, tingling, paresthesias of extremities; incoordination, ataxia, tremors; peripheral neuropathy; extrapyramidal symptoms; seizures, alteration in EEG patterns; tinnitus. A nticholinergic: Dry mouth and rarely, associated sublingual adenitis; blurred vision, disturbance of accommodation, mydriasis; constipation, paralytic ileus; urinary retention, delayed micturition, dilation of the urinary tract. Allergic: Skin rash, petechiae, ing, photosensitization avoid exposure to sunlight edema face and tongue ; , drug fever, ity with other tricyclic drugs. Hematologic: Bone-marrow including agranulocytosis; pura; thrombocytopenia. Gastrointestinal: Nausea and anorexia, epigastric distress, urticaria, itchexcessive general or of cross-sensitivGynecomastia in the male, breast and galactorrhea in the female; or decreased libido, impotence, swelling; elevation or depression sugar levels. Moreover, the risk of severe incontinence increased up to threefold for subjects who had been diagnosed with type 2 diabetes for at least 5 years. Federici et al. were filled with a standard internal solution containing 145 mM K-gluconate, 0.1 mM CaCl2, 2 mM MgCl2, 10 mM HEPES, 0.75 mM EGTA, 2 mM Mg2-ATP, 0.3 mM Na3-GTP, or 145 mM potassium methylsulfate, 8 mM KCl, 10 mM HEPES, 2 mM Mg-ATP, and 0.3 mM Na3GTP, pH 7.35 with KOH. The extracellular perfusate consisted of ACSF plus tetrodotoxin 1 M ; , sulpiride 13 M ; , and SCH23390 310 M ; . Access-resistance was monitored at regular intervals. A 10-mV hyperpolarizing step 250 ms ; was applied to measure membrane resistance. The current-voltage relationship was measured with a step protocol 1 s per sweep, four sweeps, 60 to 120 mV ; executed after the GIRK conductance was completely activated GTP S baclofen ; and in the presence of the trace amine at steady-state. All membrane potentials were corrected for the calculated liquid junction potential 1315 mV ; . Ca2 Imaging. The fluorescent ion indicator Fura-2 was loaded into the cell via the patch pipette, and the fluorescence emitted at excitation wavelengths of 340 to 380 nm was detected by a chargecoupled device camera Photonic Science, Millham, UK ; at 6-s intervals and then stored. Fluorescence values from selected regions of the neuron that included the cell body were then analyzed offline in term of ratio value changes R ; . Drugs. -Phenylethylamine, p-tyramine, phentolamine, reserpine, dopamine hydrochloride, AP-5, bicuculline methiodide, staurosporine, Rp-cAMPS, and SQ22, 536 were purchased from Sigma Milan, Italy baclofen, CNQX, prazosin, sulpiride, SCH23390, carbidopa, U73122, and S ; -3, 5- dihydroxyphenylglycine DHPG ; from Tocris Cookson Inc. Bristol, UK tetrodotoxin was from Alomone Labs Jerusalem, Israel ; , CGP55845 was a kind gift from Novartis Basel, Switzerland phosphatidylinositol-3, 4-biphosphate PtIns 4, 5 ; P2 ; was purchased from Calbiochem Sa Diego, CA and Fura-2 was from Molecular Probes Leiden, the Netherlands ; . All drugs were bath-applied at known concentrations by switching the perfusion using a three-way tap. Baclofen or DHPG 100 M ; was applied in extracellular solution through a glass pipette whose open end approximately 2 m in diameter ; was positioned 20 to 30 from the cell body of the patched neuron. The local application of baclofen or DHPG was performed at 20 psi with a pneumatic picopump Picospritzer; WPI ; . PtIns 4, 5 ; P2 was dissolved in pipette solution at a nominal concentration of 500 M. The solution was sonicated intermittently on ice for 30 min. Sonication was repeated each time before filling a new pipette. PtIns 4, 5 ; P2 solutions were used for 1 day only. In addition, the PKA inhibitor c-AMPS-Rp triethylammonium salt was applied by intracellular dialysis. A series of rats were treated with reserpine 5 to 8 mg kg injected 15 to 24 before the electrophysiological experiments. These dosages produced profound hypokinesias and ptosis. Reserpine derivative

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Drug Antihypertensive effects Pharmacokinetics Indications Adverse effects Centrally acting sympatholytics These drugs act by inhibiting sympathetic outflow from vasomotor centers in the brain stem. They do not affect the sensitivity of these centers for baroreceptor control, thus their antihypertensive and adverse effects are independent of the posture of the patient i.e. blood pressure is controlled whether the pt is lying or standing and postural hypotension almost never occurs. Disadvantage of their use is Rebound hypertension. Used as second or third -Reduces peripheral and renal Methyldopa -MOA: P O or IV. -Sedation, lassitude, vertigo, nightmares, line drugs b c of their vascular resistance. -Half life is about 2 hours. headache, depression, involuntary movements -Reduces cardiac output and -Effect persist for 24 hours. adverse effects ; in extrapyramidal effects ; moderate to severe heart rate. -Lactation, black tounge, + ve coombs test, hypertension. hemolytic anemia, leucopenia & hepatitis. -Dry mouth, sedation, fluid retention. -MOA: P O & via a transClonidine -Abrupt withdrawal may cause life-threatning dermal patch hypertensive crisis manifested as nervouness, -Half life is 8-12 hrs, effect tachycardia, headache, & sweating. persists for 2-3 days. Ganglion-blocking drug These drugs competitively block nicotinic cholinoreceptors in both sympathetic & parasympathetic system. Their antihypertensive and adverse effects are dependent on the posture of the patient and thus may cause orthostatic hypotenison. Almost all of these drugs have been withdrawn from clinical practice b c of their intolerable side effects. Trimethaphan Increases capacitance of venules -MOA: I V Previously used for acute These are same for sympatholytics causing pooling of blood. -Very rapid onset of action hypertensive emergencies. orthostatic hypotension, sexual dysfunction etc ; & parasy- mpatholytics dry mouth, blurred vision etc ; Peripheral adrenergic neuron blocker These drugs act by preventing normal physiologic release of nor-epinepherine from postganglionic sympathetic neurons. Their effect is also dependent on the posture of the patient. Their use in treating hypertension has now become very limited. Guanethedine -Reduces cardiac output and -MOA: P O Previously used for mild Sympatholytic effects sexual dysfunction, increases capacitance of venules. -Very long half-life so hypertension & to reduce orthostatic hypotension etc ; , Diarrhea, muscle -Long term therapy may decrease maximal effect develop in intraocular pressure in aches & weakness. No effect on CNS dose peripheral vascular resistance. 1-2 wks. glaucoma. not cross blood brain barrier ; . Drug depleting neurotransmitter These drugs act by depleting nor-adrenaline in adrenergic neurons by blocking the storage mechanism in the nerve endings. They do not affect sympathetic reflex and thus their hypotensive action is independent of posture. Postural hypotension occurs rarely. Now used only in cases of High doses may cause sedation, lassitude, Reserpine -Reduces cardiac output & -MOA: P O, rarely I V. decreases peripheral vascular -It has a short t1 2, but has a hypertension, unresponsive nightmares & severe depression. May cause diarrhea, abd cramps & acid secretion. May to other drugs Refractory resistance. long duration of action also produce extrapyramidal effects may be due to retention of hypertension ; resembling Parkinson's disease. drug at its site of action.

Circular lesions were deployed around each PV ostium at the atrial level and isolation was defined by the achievement of low bipolar potentials 0.1 mV ; inside the circular lesions and local activation time delays of 30 ms between contiguous points across the line 15 ; . Using these criteria, isolation was achieved in 75% of the patients. Interestingly, Pappone et al. 15 ; clearly pointed out that no significant relationship between lesion completeness and clinical outcome was observed and discussed that PV foci isolation might not have been the sole mechanism responsible for the cure of AF. Instead, the therapeutic efficacy was discussed as being related in part to an alteration of the substrate, changes in autonomic innervation, or atrial debulking 4, 15 ; . Furthermore and in contrast to the classic PV disconnection 8 ; , high success rates could be achieved in both subgroups i.e., in patients with paroxysmal as well as persistent AF ; 15 ; . comparison to the data reported by Pappone et al., the patients in our series needed more antiarrhythmic drugs and second procedures, which might be related to the learning curve of our group. In the present study, circular and linear left atrial lesions were combined and placed with guidance of the electromagnetic mapping system, thereby combining elements of the intraoperative IRAAF study 7 ; and the Pappone et al. 4 ; approach. Instead of encircling each PV, one big circle was placed around the PVs of each side, and linear lesions connected the two circles and also connected the left circle to the mitral annulus. Thereby, our approach theoretically targeted both the initiation as well as the perpetuation of AF. From a practical point of view, one big circle around the veins of each side protects from ablation in the transition zone between the upper and lower PVs, which often are separated only by a small fold instead of a linear atrial wall intersection. Furthermore, the addition of the linear lesions may have contributed to the very low incidence of stable left atrial flutter after ablation. Analysis of rhythm outcome after interventional therapy of AF. The analysis of the rhythm outcome after intraoperative ablation of AF already has indicated that early relapses of AF after ablation for substrate modification did not predict long-term treatment failure 7 ; . In the IRAAF study, twothirds of patients with persistent and one third of patients with paroxysmal AF were treated transiently with antiarrhythmic drugs because of early recurrences; however, stable sinus rhythm was achieved during follow-up in 90% of both patient subgroups 7 ; . To analyze the short- and long-term rhythm response after catheter ablation of AF, we used repetitive 7-day ECG recordings in the present study. Our results clearly indicate that the arrhythmia response after catheter ablation of AF using the current technique is far from being "all or nothing." In many patients, early AF recurrences were observed but stepwise passed away over time, indicating toward a reverse remodeling of the atria, although the percentage of patients on antiarrhythmic drugs decreased over time substantially from 90% directly after ablation to 40% after 12 months. The significant stepwise reduction of the relative time spent in.

1. Grahmann H, Suchenwirth R. Thrombosis hazard in chlorpromazine and reserpine therapy of endogenous psychoses [in German]. Nervenarzt. 1959; 30: 224-225. Haefner H, Brehm I. Thromboembolic complications in neuroleptic treatment. Compr Psychiatry. 1965; 58: 25-34. Varia I, Krishnan RR, Davidson J. Deep-vein thrombosis with antipsychotic drugs. Psychosomatics. 1983; 24: 1097-1098. Thorogood M, Cowen P, Mann J, Murphy M, Vessey M. Fatal myocardial infarction and use of psychotropic drugs in young women. Lancet. 1992; 340: 10671068. Zornberg GL, Jick H. Antipsychotic drug use and risk of first-time idiopathic venous thromboembolism: a case-control study. Lancet. 2000; 356: 1219-1223. Parkin L, Skegg DC, Herbison GP, Paul C. Psychotropic drugs and fatal pulmonary embolism. Pharmacoepidemiol Drug Saf. 2003; 12: 647-652. Kapur S, Remington G. Atypical antipsychotics. BMJ. 2000; 321: 1360-1361. Walker AM, Lanza LL, Arellano F, Rothman KJ. Mortality in current and former users of clozapine. Epidemiology. 1997; 8: 671-677. Ihde-Scholl T, Rolli ML, Jefferson JW. Clozapine and pulmonary embolus. J Psychiatry. 2001; 158: 499-500. Hgg S, Spigset O, Sderstrm TG. Association of venous thromboembolism and clozapine. Lancet. 2000; 355: 1155-1156. Knudson JF, Kortepeter C, Dubitsky GM, Ahmad SR, Chen M. Antipsychotic drugs and venous thromboembolism. Lancet. 2000; 356: 252-253. Hgg S, Tatting P, Spigset O. Olanzapine and venous thromboembolism. Int Clin Psychopharmacol. 2003; 18: 299-300. Waage IM, Gedde-Dahl A. Pulmonary embolism possibly associated with olanzapine treatment. BMJ. 2003; 327: 1384. Hamanaka S, Kamijo Y, Nagai T, et al. Massive pulmonary thromboembolism demonstrated at necropsy in Japanese psychiatric patients treated with neuroleptics including atypical antipsychotics. Circ J. 2004; 68: 850-852. Ray JG, Mamdani MM, Yeo EL. Antipsychotic and antidepressant drug use in the elderly and the risk of venous thromboembolism. Thromb Haemost. 2002; 88: 205-209 and restasis.

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