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The aim of the present study was to document heart rate HR ; responses during the 6MWT in patients with PAH. The rationale was as follows. Exercising PAH patients exhibit a limited increase in stroke volume [911], such that the increase in cardiac output is mainly achieved through increases in HR. The HR increases could have opposite pathophysiological meanings.
ABSTRACT: We investigated the mechanism of renal tubular secretion of the dopamine D2 receptor agonist pramipexole in rats, focusing on organic cation transporters 1 and 2. The uptake of [14C]pramipexole by Xenopus oocytes injected with complementary RNA of either rat organic cation transporter rOCT ; 1 or rOCT2 was significantly higher than that by water-injected oocytes: the kinetic parameters, Km and Vmax, of pramipexole uptake were 49.5 M and 234 pmol 60 min oocyte for rOCT1, and 16.9 M and 12.8 pmol 60 min oocyte for rOCT2. Pramipexole was taken up into kidney slices in a time- and concentration-dependent manner, and Eadie-Hofstee plots revealed the involvement of two saturable components. The kinetic parameters, Km1 and Vmax1, of the high-affinity component were 12.9 M and 10.7 nmol 15 min g kidney, respectively. The uptake of [14C]pramipexole by rOCT1, rOCT2, and kidney slices was inhibited by procainamide and corticosterone, which are selective inhibitors of rOCT1 and rOCT2, respectively. The IC50 values of procainamide and corticosterone for the uptake of [14C]pramipexole by rOCT1, rOCT2, and kidney slices were 7.7, 167.0, and 47.0 M and 163.7, 10.7, and 47.7 M, respectively. These results demonstrate that both rOCT1 and rOCT2 are involved in the renal uptake of pramipexole across the basolateral membrane of the proximal tubular epithelial cells and procaine.
ACS can give rise to a life-threatening arrhythmia that may be the first manifestation of ischemia. The mechanisms of these arrhythmias may be different from those seen in chronic stable ischemic heart disease. Arrhythmias during acute ischemia may be related to re-entry, abnormal automaticity, or triggered activity and are affected by a variety of endogenous factors such as potassium levels and autonomic states. These arrhythmias may cause many of the reported sudden deaths in patients with ischemic syndromes. VF or sustained VT has been reported in up to 20% of AMIs.346, 347 The incidence of VF occurring within 48 h of the onset of the ACS ; may be decreasing owing to aggressive revascularization limiting infarct size and to increased betablocker use.348 VF occurring early in the ACS has been associated with an increase in hospital mortality but not with increased long-term mortality.346 Prophylaxis with lidocaine may reduce the incidence of VF in the ACS but appears to be associated with increased mortality likely owing to bradycardia and this treatment has largely been abandoned.349 Use of prophylactic beta blockers in the setting of AMI reduces the incidence of VF, and this practice is encouraged when appropriate. Similarly, correction of hypomagnesemia and hypokalemia is encouraged because of the potential contribution of electrolyte disturbances to VF.350 More recent data showed the benefit of the eplerenone, an aldosterone antagonist, in reducing the risk of SCD mortality by 37% p 0.051 ; 30 d after randomization in patients after AMI when initiated at a mean of 7.3 d after AMI ; in addition to conventional therapy in patients with an LVEF less than or equal to 40% and signs of HF.351 7.1.1.1. Pulseless ventricular tachycardia ventricular fibrillation. In the event of pulseless VT or VF ACS, the standard ACLS protocol is initiated including unsynchronized electric shock following basic assessment of airway and initiation of CPR. Energy delivery consists of 1 or more monophasic shocks at 360 J or biphasic shocks at a dose range demonstrated by manufacturer to be effective. If not available, a dose of 200 J is recommended for the first shock and an equal or higher dose for subsequent shocks. The optimal dose for biphasic shocks has not been determined, and no waveform or escalating energy levels recommendations can be made for biphasic defibrillators at this time. If return to normal rhythm is not accomplished by defibrillation, the ACLS protocol for pulseless VT or VF followed. This includes epinephrine 1 mg intravenously every 3 to 5 min ; or vasopressin 40 U intravenously once only; 1 dose of vasopressin intravenously intraosseously may replace either the first or second dose of epinephrine ; , and amiodarone 300-mg or 5-mg kg intravenous push, with a possible repeat 150-mg intravenous push once only ; , or as a second tier, lidocaine 1.0 to 1.5 mg kg with repeat dose of 0.5 to 0.75 mg intravenously intraosseously up to a total dose of 3 mg kg ; . Additional second-tier therapy includes intravenous magnesium 1 to 2 procainamide 30 mg min up to 17 mg kg ; . The latter is considered acceptable but is no longer recommended.334 Following resuscitated VF, prophylactic drug infusion, typically with amiodarone plus a beta blocker, may be continued. The antiarrhythmic should be withdrawn as appropriate to assess the presence of ongoing arrhythmias.
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Mortality In the National Heart, Lung and Blood Institute's Cardiac Arrhythmia Suppression Trial CAST ; , a long-term, multi-center, randomized, doubleblind study in patients with asymptomatic nonlife-threatening ventricular arrhythmias who had had a myocardial infarction more than 6 days but less than 2 years previously, an excessive mortality or non-fatal cardiac arrest rate 7.7% ; was seen in patients treated with encainide or flecainide compared with that seen in patients assigned to carefully matched placebo-treated groups 3.0% ; . The average duration of treatment with encainide or flecainide in this study was 10 months. The applicability of the CAST results to other populations eg, those without recent myocardial infarction ; is uncertain. Considering the known proarrhythmic properties of Norpace or Norpace CR and the lack of evidence of improved survival for any antiarrhythmic drug in patients without life-threatening arrhythmias, the use of Norpace or Norpace CR as well as other antiarrhythmic agents should be reserved for patients with life-threatening ventricular arrhythmias. Negative Inotropic Properties: Heart Failure Hypotension Norpace or Norpace CR may cause or worsen congestive heart failure or produce severe hypotension as a consequence of its negative inotropic properties. Hypotension has been observed primarily in patients with primary cardiomyopathy or inadequately compensated congestive heart failure. Norpace or Norpace CR should not be used in patients with uncompensated or marginally compensated congestive heart failure or hypotension unless the congestive heart failure or hypotension is secondary to cardiac arrhythmia. Patients with a history of heart failure may be treated with Norpace or Norpace CR, but careful attention must be given to the maintenance of cardiac function, including optimal digitalization. If hypotension occurs or congestive heart failure worsens, Norpace or Norpace CR should be discontinued and, if necessary, restarted at a lower dosage only after adequate cardiac compensation has been established. QRS Widening Although it is unusual, significant widening greater than 25% ; of the QRS complex may occur during Norpace or Norpace CR administration; in such cases Norpace or Norpace CR should be discontinued. Q-T Prolongation As with other Type 1 antiarrhythmic drugs, prolongation of the Q-T interval corrected ; and worsening of the arrhythmia, including ventricular tachycardia and ventricular fibrillation, may occur. Patients who have evidenced prolongation of the Q-T interval in response to quinidine may be at particular risk. As with other Type 1A antiarrhythmics, disopyramide phosphate has been associated with torsade de pointes. If a Q-T prolongation of greater than 25% is observed and if ectopy continues, the patient should be monitored closely, and consideration be given to discontinuing Norpace or Norpace CR. Hypoglycemia In rare instances significant lowering of blood glucose values has been reported during Norpace administration. The physician should be alert to this possibility, especially in patients with congestive heart failure, chronic malnutrition, hepatic, renal or other diseases, or drugs eg, beta adrenoceptor blockers, alcohol ; which could compromise preservation of the normal glucoregulatory mechanisms in the absence of food. In these patients the blood glucose levels should be carefully followed. Concomitant Antiarrhythmic Therapy The concomitant use of Norpace or Norpace CR with other Type 1A antiarrhythmic agents such as quinidine or procainamide ; , Type 1C antiarrhythmics such as encainide, flecainide or propafenone ; , and or propranolol should be reserved for patients with life-threatening arrhythmias who are demonstrably unresponsive to single-agent antiarrhythmic therapy. Such use may produce serious negative inotropic effects, or may excessively prolong conduction. This should and procarbazine.
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Figure 6 Effect of procainamide on the electrocardiogram and on conduction time in an isolated Purkinje fiber bundle. Temp 360 C; cycle length 630 msec. The left panels show donor ECG, the right show conduction time CT ; between two microelectrodes impaled at different sites in a Purkinje fiber bundle. A ; Control. Heart rate upper trace ; 100 min; QRS duration lower trace ; 35 msec; interelectrode CT 2.3 msec. B ; Recorded 40 min after an intravenous injection of PA, 25 mg kg plasma concentration 7 ug ml heart rate 100 min; QRS duration 45 msec; interelectrode CT 3.6 msec. See text for discussion.
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Physiology department faculty of health sciences ben gurion university, beer sheva, cardiac arrhythmia research laboratory, soroka university medical center, beer sheva, 3 cardiology department barzilai medical center, ashkelon and prohibit.
Rosen MR, Merher C, Gelband H, Hoffman BF 1973 ; Effects of procainamide on the electrophysiological properties of the canine ventricular conduction system. J Pharmacol Exp Ther 185: 438446 Sasyniuk BI, Kus T 1973 ; Alterations in electrophysiological properties of cells from infarcted ventricular tissue. Pharmacologist 15: 178 Sasyniuk BI, Kus T 1974 ; Comparison of the effect of lidocaine on electrophysiological properties of normal Purkinje fibers and those surviving acute myocardial infarction abstr ; . Fed Proc 33: 476.
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Have longer time constants "slower" drugs ; . However, if the time constant of the slower drug becomes too long e.g., flecainide ; , the fraction of channels that can be competitively displaced i.e., block and unblock per cycle ; is very small and hence little antagonism is possible. Actually, in clinical concentrations quinidine blocks and unblocks too little for significant displacement to occur. Hence, as described above addition of lidocaine to quinidine in clinically relevant doses will mostly result in extradiastolic block, with little or no reduction of block for the regular heartbeat. Since bupivacaine can readily be displaced by lidocaine, '2 I predict that agents with similar time constants of recovery e.g., amiodarone [1.6 sec]; procainamide [2.3 sec] ; or shorter time constants e.g., mexiletine [360 msec]; tocainide [550 msecl ; could also be readily displaced by lidocaine, at least under conditions in which they produce substantial use-dependent block. It should be noted that blockers of open channels will inherently be better able to reverse sodium-channel block than blockers of inactivated channels with identical time constants of recovery. Indeed, openchannel blockers can sequester channels first opening precedes inactivation ; and deprive the blocker of inactivated channels from an equal opportunity to block channels. For the same reason, a faster blocker of inactivated channels will have an advantage over a slower blocker. A special case of drug interactions, but perhaps a very important one, relates to metabolites interacting with the parent compound. A metabolite with slower kinetics of recovery from block than the parent compound may elicit synergistic interactions. Conversely, a faster metabolite might competitively antagonize the parent compound. It has been demonstrated recently that glycylxylidide exhibits both synergistic and antagonistic interactions with lidocaine for the sodiumchannel receptor. 13 Although until a study in patients is finished it cannot be proven that these interactions are clinically very important for glycylxylidide and lidocaine, it is nevertheless probable that competitive displacement of a parent compound by a metabolite is an important principle to consider for any drug. "No effect" drugs. No-effect drugs may increase selectivity of antiarrhythmic drugs. Drugs with very fast time constants of recovery tau c 10 msec; figure 3, left ; could have little effect on their own; they block the sodium channel for too little time. Actually, the effects of these chemicals are so small that they probably would be missed as sodium-channel blockers by common tests. However, agents with these properties.
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T. : Procainamide-induced lupus erythematosus, New Eng. I. Med., 267: 1357, 1962. HAHN, A. L. : Systemic lupus erythematosus associated with procainamide therapy, Missouri Med., 61: 19, 1964. COLMAN, R. W., AND STURGILL, B. C. : Lupus-like syndrome induced by procaine amide, Arch. Intern. Med and propylthiouracil.
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