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Fifty-seven patients 14% ; had persistent lymphoblasts 1% ; in the BM on day 15 and 27 patients 5.5% ; had persistent lymphoblasts on days 22 to 25 Table 1 ; . Of the 117 patients who actually received day 25 BM examinations, 14 were outside the acceptable range of days and one was considered to be not evaluable. Of the remaining 102 patients with eligible and evaluable day 25 marrows, 10 9.8% ; were positive for lymphoblasts. Persistence of BM lymphoblasts on day 15 or days 22 to 25 induction was correlated with a number of adverse presenting features Table 2 ; : high WBC count, unfavorable age, and T-cell immunophenotype on day 15, and WBC count, unfavorable age, T-cell immunophenotype, unfavorable DI ie, 1.16 or 1.60 ; and the presence of the Philadelphia chromosome on days 22 to 25. MLL gene rearrangement and CNS status at diagnosis were not associated with persistent disease on either day 15 or 22 25. The day 43 CR rate for patients with any lymphoblasts 1% ; in the day 15 BM was significantly lower than that for other patients 89% versus 99%, P .001 ; . The day 43 CR rate for children with 1% lymphoblasts or more on days 22 to 25 was even lower 59% ; . The CR rates varied according to degree of BM involvement ie, 1% to 4% versus 5% ; : 97% versus 78% for day 15 results and 64% versus 56% for days 22 to 25 results. Persistence of lymphoblasts 1% ; on the day 15 and days 22 to 25 was associated with a poorer treatment result P .001 for both comparisons, Figures 1 and 2 ; . The 5-year EFS rates 1 SE for patients with and without lymphoblasts on day 15 were 40% 6% and 78% 2%, respectively, and on days 22 to 25 they were 4% 3% and 76% 2%, respectively. A worse prognosis was observed even for those patients with a low percentage of persistent lymphoblasts ie, 1%-4% ; at either day 15 5-year EFS 56% 8% ; or days 22 to 25 5-year EFS 0% ; compared to patients who did not have morphologically identifiable persistent lymphoblasts at these times P .001 for both comparisons ; . The EFS for patients with lymphoblasts 1% ; on day 15 that cleared by days 22 to 25 was significantly P .006 ; worse than that for patients with no lymphoblasts on day 15 5-year rate 61% 8% versus 78% 2%, respectively Figure 3 ; . A Cox proportional hazards model revealed the independent prognostic importance of persistent lymphoblasts 1% ; in the day 15 and days 22 to 25 marrow; those with persistent disease on day 15 and day 22 had a 3-fold and 10-fold higher risk of failure, respectively Table 3 ; . These results were significant even after adjusting for age, WBC count, National Cancer Institute NCI.

Dobutamine vasodilation 12. Fink MP, Antonsson JB, Wang H, et al. Increased intestinal permeability in endotoxic pigs: mesenteric hypoperfusion as an etiologic factor. Arch Surg 1991; 126: 211 Deitch EA, Specian RD, Berg RD. Endotoxin-induced bacterial translocation and mucosal permeability: role of xanthine oxidase, complement activation and macrophage products. Crit Care Med 1991; 19: 78591. Oldner A, Goiny M, Ungerstedt U. Splanchnic homeostasis during endotoxin challenge in the pig as assessed by microdialysis and tonometry. Shock 1996; 6: 188 Ohhara H, Ogawa T, Takeda M, et al. Cardiovascular effects of the new cardiotonic agent 1, 2-dihydro-6-methyl-2-oxo-5 imidazo[1, 2-a]pyridin-6-yl ; -3-pyridine carbonitrile hydrochloride monohydrate: 2nd communication--studies in dogs. Arzneimittelforschung 1989; 39: 38 Takaoka H, Takeuchi M, Odake M, et al. Comparison of the effects on arterial-ventricular coupling between phosphodiesterase inhibitor and dobutamine in the diseased human heart. J Coll Cardiol 1993; 22: 598 Rodbard S. Evidence that vascular conductance is regulated at the capillary. Angiology 1966; 17: 539 Haylett DG, Jenkinson DH. The receptors concerned in the actions of catecholamines on glucose release, membrane potential and ion movements in guinea-pig liver. J Physiol 1972; 225: 75172. Fujimoto S, Ohasi M, Hiramoto A, et al. Vasorelaxant effect of olprinone, an inhibitor of phosphodiesterase 3, on mesenteric small artery and vein of rabbits. Eur J Pharmacol 1998; 353: 239. Dobutamine side effects RESULTS reduction of the various carriers achieved by The percentage addition of 90 NADH to mung bean mitochondria in the presence of 0.27 mm cyanide can be estimated from the records of Figures 1 and 2. In these experiments, the pulse of 90 , M NADH is allowed to give a full cycle of reduction followed by complete ' Abbreviations: mCLAM: mn-chlorobenzhydroxamic acid; 1799: bis hexafluoroacetonyl ; acetone; TES: tris hydroxymethyl ; methylaminomethyl sulfonic acid; TTFA: 1-thienoyl-3, 3, 3-trifluoroacetone; MBM: mung bean mitochondria. Hormones parathyroid hormone, 1a, 25-dihdroxyvitamin D3, calcitonin ; is unknown. Because soleus weight and soleus weight index were still significantly lower in dobutamine-treated suspended rats than in Sed Con Sal rats, and only minimally different in Ex Sus Dob vs. Ex Sus Sal rats, this b-agonist does not appear to effectively maintain muscle mass per se. Even though electromyographic activity of the soleus returns to normal weight-bearing patterns after 7 days of hindlimb suspension, one can observe continued loss of muscle and bone 1 ; . Even if an adrenergic agonist were to elevate basal contractile activity of suspended muscle or maintain muscle mass, it is unlikely that either factor would help maintain bone mass in the suspended limbs without the loading provided by ground reaction forces incurred during weight-bearing activity. The strong positive relationship between muscle weight and bone area observed in control animals virtually disappeared in suspended rats Fig. 3B ; . Interestingly, dobutamine injections were somewhat effective in ameliorating muscle mass loss in the exercised rats subjected to suspension. The 18% decrease in soleus weight index in these rats was significantly less than the 39% loss observed in the Ex Sus Sal group. Despite this, Ex Sus Dob rats had smaller bone areas than Ex Sus Sal animals. Because MAR did not vary significantly between these two group, whereas B.Dm values were significantly lower in the dobutaminetreated group, we surmise that the Ex Sus Dob rats experienced some larger reduction in bone matrix formation rates at periosteal surfaces during suspension relative to that in Ex Sus Sal rats. In summary, the most significant finding of this study is the prevention of suspension-induced loss of bone mass in sedentary rats by the administration of dobutamine, a synthetic adrenergic agonist, mediated in part by the maintenance of normal mineralization rates at the periosteum during the period of unweighting. Further studies are needed to confirm the mechanism for this response, be it mediated by some indirect effect of dobutamine on limb muscle or via some direct effect on bone cell activities. Vigorous endurance exercise training preceding suspension is not an effective countermeasure for the deleterious effects of unweighting on bone.

Dobutamine dose for stress echocardiography Song RX et al. Effect of long-term estrogen deprivation on apoptotic responses of breast cancer cells to 17beta-estradiol. J Natl Cancer Inst 2001; 93 22 ; : 1714-23. Abstract. Dobutamine tests Insomnia characterizedby difficulty in faDingasleep, frequent nocturnal awakenings.and or early morning awakenings. It is recommended that HALCIONnot be prescribed in quantities exceedinga one-month supply. CONTRAINDICATIONS: Patients with known hypersensitivity to this drug or other and docetaxel. As this paper has demonstrated, there are numerous barriers that exist in Canada, which either delay or block access to needed medicines. This is particularly so for newer drugs. It can also take the form of the dropping of an effective older medication from formulary coverage due to "cost containment." The Common Drug Review has created redundancies in the drug review process by adding another layer of bureaucracy between patients and newer medical therapies. Decision-makers must consider taking the following actions with respect to CDR: Bring drug review times in line with stated targets Revise CEDAC to allow for greater transparency and stakeholder input Eliminate provincial review processes that take place in addition to CDR, or eliminate CDR.

0 CARDIAC continued ; CPR Defibrillation - Date of Cert. Renewal CVP - Manometer Readings Maintenance EKG Monitoring - Recognition of Basic Arrhythmias Nursing Intervention IABP Kontron ; Pacemaker - Insertion Care of Temporary - Failure to Capture Failure to Sense Care of Permanent - Failure to Capture Failure to Sense Streptokinase TPA Therapy Swan Ganz - Recognition of Normal Waves PAP, PAWP, CVP ; Trouble-Shooting C.O. Drugs Familiarity, Ability to Titrate ; Dopamine Levaphed Lidocaine Nipride Bretylium Pronestyl Aramine Dobutamine Insulin Heparin CHEMOTHERAPY Drugs and Agents Protocols and docusate Ex: i perform chemical dobutamine ; cardiac stress testing.

Response to injury: assessment of the work-length relationship in the intact heart. Circulation 76: 717727, 1987. Nakano K, Sugawara M, Ishihara K, Kanazawa S, Corin WJ, Denslow S, Biederman RW, and Carabello BA. Myocardial stiffness derived from end-systolic wall stress and logarithm of reciprocal of wall thickness. Contractility index independent of ventricular size. Circulation 82: 13521361, 1990. Neumann T, Ravens U, and Heusch G. Characterization of excitation-contraction coupling in conscious dogs with pacinginduced heart failure. Cardiovasc Res 37: 456466, 1998. Pellikka PA, Roger VL, McCully RB, Mahoney DW, Bailey KR, Seward JB, and Tajik AJ. Normal stroke volume and cardiac output response during dobutamine stress echocardiography in subjects without left ventricular wall motion abnormalities. J Cardiol 76: 881886, 1995. Power TP, Kramer CM, Shaffer AL, Theobald TM, Petruolo S, Reichek N, and Rogers WJ Jr. Breath-hold dobutamine magnetic resonance myocardial tagging: normal left ventricular response. J Cardiol 80: 12031207, 1997. Rademakers FE, Rogers WJ, Guier WH, Hutchins GM, Siu CO, Weisfeldt ML, Weiss JL, and Shapiro EP. Relation of regional cross-fiber shortening to wall thickening in the intact heart. Three-dimensional strain analysis by NMR tagging. Circulation 89: 11741182, 1994. Ross J, Linhart JW, and Braunwald E. Effects of changing heart rate in man by electrical stimulation of the right atrium. Circulation 32: 549558, 1965. Scott CH, Sutton MS, Gusani N, Fayad Z, Kraitchman D, Keane MG, Axel L, and Ferrari VA. Effect of dobutamine on regional left ventricular function measured by tagged magnetic resonance imaging in normal subjects. J Cardiol 83: 412 417, Teichholz LE, Kreulen T, Herman MV, and Gorlin R. Problems in echocardiographic volume determinations: echocardiographic-angiographic correlations in the presence or absence of asynergy. J Cardiol 37: 711, 1976. Urheim S, Edvardsen T, Torp T, Angelsen B, and Smiseth OA. Myocardial strain by Doppler echocardiography. Validation of a new method to quantify regional myocardial function. Circulation 102: 11581164, 2000. Voigt JU, Arnold M, Karlsson M, Hubbert L, Kukulski T, Hatle L, and Sutherland GR. Assessment of regional longitudinal strain rate derived from Doppler myocardial imaging indices in normal and infarcted myocardium. J Soc Echocardiogr 13: 588598, 2000. Weidemann F, Jamal F, Kowalski M, Kukulski T, D'hooge J, Bijnens B, Hatle L, De Scheerder I, and Sutherland GR. Can strain rate and strain quantify changes in regional systolic function during dobutamine infusion, -blockade and atrial pacingimplications for quantitative stress echocardiography. J Soc Echocardiogr. In press and dofetilide.

The o2 extraction ratio was decreased following norepinephrine and dobutamine treatments.
M strate was 2 m oxaloacetate, and antimycin A 0.36 p ~ ; Deamino-NADH Can Cenerate a Membrane Potential was present. The concentration of each of the nicotinamide Only in the Presence of UQ-1 dinucleotides was 0.2 mM. The effect of UQ-1 on the membrane potential of intact Protein determinations were made according to the mitochondria with NADH and deamino-NADH as submethod of Lowry et al. 1951 ; using BSA as the standard. strates was measured using safranine as a probe. NADH The concentration of UQ-1 in the stock solution was detercaused the rapid formation of a membrane potential, which mined by the method of Lawford and Garland 1972 ; . The increased only slightly in magnitude by the subsequent final concentration of UQ-1 was 60 p~ in a11 experiments. addition of UQ-1 Fig. 1A ; . This experiment was performed without added Ca2 + , but there is sufficient Ca2 + in the RESULTS AND DISCUSSION standard reaction medium to allow close to maximum activity Rasmusson and Msller, 1991b ; . Clearly, a rate of UQ-1 lnduces Deamino-NADH Oxidation by approximately 250 nmol O, min-l mg-' Table I ; is suffilntact Mitochondria cient to give a maximum membrane potential. In the presIntact potato tuber mitochondria did not oxidize ente of EGTA, the oxidation of NADH could also generate deamino-NADH Table I ; , confirming that the external a full membrane potential, but this took much longer than NADH dehydrogenase does not accept this substrate unwith Ca2 + Fig. 1B ; . This result is consistent with the much der normal conditions Rasmusson and Msller, 1991a ; . lower rate of oxidation with EGTA than with Ca2 + Table However, the addition of 60 p~ UQ-1 induced deaminoI ; . The relationship between rate of oxidation and size of NADH oxidation Table I ; , the rate of which was about 20% the membrane potential as monitored with safranine is of the maximum rate of NADH oxidation observed in the shown in Figure 2 for intact potato tuber mitochondria. A presence of Ca2 + .In contrast to normal external NAD P ; H rate greater than 50 m o min-' mg-' is required to oxidation Table I; Arron and Edwards, 1979; M ~ l l and give a full membrane potential under the conditions used, Palmer, 1981; Msller et al., 1981 ; , the UQ-1-induced but very little decrease is seen unless the rate is less than 30 deamino-NADH oxidation by intact mitochondria was not nmol O, min-l mg-'. sensitive to Ca2 + addition Table I ; . The oxidation of The addition of deamino-NADH to intact mitochondria NADH by intact mitochondria was also stimulated by the did not give rise to a membrane potential. However, the presence of UQ-1 and in this state became less dependent subsequent addition of UQ-1 led to the rapid formation of on Ca2 + Table I ; . a membrane potential, the size of which could not be The UQ-1-induced deamino-NADH oxidation was comsubstantially increased by the addition of NADH Fig. 1C ; . pletely sensitive to antimycin A Table I ; , as was the memThis is consistent with the observation that a rate of 60 brane potential generated by this oxidation see below ; . nmol O, min-' mg-' Table I ; is sufficient to give a full membrane potential Fig. 2 ; . Thus, UQ-1-induced, Ca2'This indicates that the enzyme involved is part of the electron transport chain. It should be noted that in the independent Fig. 1C ; and Ca2 + -dependent not shown ; presence of UQ-1 and absence of Ca2 + 1 m EGTA M oxidation of deamino-NADH was coupled to the generapresent ; the effect of antimycin A is slower about 1 min tion of a membrane potential. This membrane potential rather than 20 s ; and more antimycin A is required to give was completely collapsed by the addition of antimycin A full inhibition we used 0.9 instead of 0.36 p ~ ; . Fig. 1C ; or carbonyl cyanide p- trifluoromethoxy ; phenylhydrazone not shown ; , showing that proton pumping by complexes I11 and IV was involved in its generation. We Table 1. The effect of UQ-1 on deamino-NADH and NADH oxidaconclude that UQ-1 induces oxidation of deamino-NADH tion by potato tuber mitochondria and inside-out SMPs through the electron transport chain, giving rise to a memRotenone was used a t a final concentration of 20 p~ and antimybrane potential. cin was used at 0.9 PM. Similar results were observed on four independent preparations and representative data are presented and dolasetron.

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