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PubMed1996

[Evaluation of myocardial viability very early after acute myocardial infarction by ultra-low dose echo-dipyridamole test].

BACKGROUND: After an acute myocardial infarction (AMI), stunned myocardium may cause a reversible left ventricular dysfunction. Dipyridamole echocardiography (0.56 mg*kg-1 over 4' e 0.84 mg*kg-1 over 10') can identify viable myocardium but can also induce ischaemia. AIM OF THE STUDY: To evaluate the usefulness of "Infra-low" dose dipyridamole echocardiography for identification of myocardial viability. METHOD AND RESULTS: Of thirty-four consecutive in-hospital patients, thirty (26 males; mean age 59 +/- 11 years) with AMI separately underwent (40 +/- 12 hours from symptoms onset): 1. a baseline resting echo (BASELINE); 2. a low dose dobutamine (DOB) echotest (5-10 mcg*kg-1*m-1 for 5') (DOB5, DOB10); 3. an "infra-low" dose dipyridamole echotest (0.28 mg*kg-1 over 4') (DIP). A pre-discharge resting echo was performed 7 days after admission (follow-up). No patient developed echocardiographic or electrocardiographic signs of ischaemia after DIP, while 4 patients developed ischaemia after DOB. The systolic blood pressure (112 +/- 18 mmHg) did not change after both DOB and DIP. The heart rate was unchanged after DIP (BASELINE = 73 +/- 18 bpm', DIP = 75 +/- 14 bpm'), while it increased after DOB (BASELINE 69 +/- 11 bpm'; DOB5 = 71 +/- 11 bpm', p = 0.02; DOB10 = 74 +/- 12 bpm', p = 0.001). Wall motion score index (WMSI), in a 16-segment model (from 1 = normal to 4 = diskinetic) (BASELINE = 1.64 +/- 0.3), improved after DIP (1.56 +/- 0.36, p < 0.05 vs BASELINE) and after DOB10 (1.50 +/- 0.36, p < 0.05 vs BASELINE) while did not change after DOB5 (1.59 +/- 0.35, p = n.s.). WMSI decreased at follow-up (1.53 +/- 0.31, p < 0.05 vs BASELINE); DIP and DOB10, but not DOB5, correctly predicted the WMSI decrease observed at follow-up. Results of DOB5, DOB10 and DIP were fully concordant in 118 segments (67%) (kappa = 0.54): 13 (7%) with concordant positivity and 105 (60%) with concordant negativity; 58 (33%) segments showed different results. At follow-up 54 (30%) of the 178 segments with baseline dysfunction, observed in 29 survivors, showed an improvement of grade 1 or more (viable). Two patients did not undergo DOB10; therefore, of the 168 segments with baseline dysfunction, in 27 survivors who underwent all tests, 54 (32%) showed an improvement of grade 1 or more (viable) e 114 (68%) showed no improvement (not viable). Of 25 DOB5 "responders" segments, 11 (44%) showed spontaneous recovery at follow-up (true-positive); of 153 "non responders" segments, 110 (72%) showed no spontaneous recovery at follow-up (true-negative). Of 61 DOB10 "responders" segments, 29 (47%) showed spontaneous recovery at follow-up (true positive); of 107 "non responders" segments, 82 (77%) showed no spontaneous recovery at follow-up (true-negative). Of 36 DIP "responders" segments, 19 (53%) showed spontaneous recovery at follow-up (true positive); of 142 "non responders" segments, 107 (75%) showed no spontaneous recovery at follow-up (true-negative). The sensitivity of DOB5, DIP and DOB10 for predicting short-term spontaneous recovery was 20, 35 and 53% (DOB10 vs DOB5: p < 0.001), respectively; specificity was 88, 86 and 71% (DOB5 vs DOB10: p = 0.002; DIP vs DOB10: p = 0.01); the positive value was 44, 52 and 47% (p = n.s.) and the negative predictive value was 72, 75 and 76% (p = n.s.) while the diagnostic accuracy was 67, 70 and 85% (p = n.s.). CONCLUSIONS: "Infra-low" dose dipyridamole echocardiography appears to be a hemodynamically neutral stress which does not modify either heart rate or blood pressure. It allows to explore selectively the viability of stunned myocardium, without eliciting ischaemia; it shows a good overall concordance with low-dose dobutamine and a low sensitivity but an excellent specificity for predicting spontaneous recovery early after AMI.

Adult↗
PubMed2004

Dynamic estimation of the myocardial oxygen extraction ratio during dipyridamole stress by MRI: a preliminary study in canines.

The myocardial oxygen extraction fraction (OEF) reflects the balance between myocardial oxygen supply and demand. The feasibility of quantifying myocardial OEF was demonstrated with MRI during pharmacologic vasodilation in dogs. Dipyridamole was infused intravenously to increase blood flow and change in myocardial oxygen content. Arterial and coronary sinus blood sampling was performed during dipyridamole-induced vasodilation to measure the myocardial blood oxygen content. Myocardial T(2) was measured dynamically during the vasodilation, and quantified with a simplified diffusion model as a function of myocardial OEF and blood volume. The results showed a strong correlation (R(2) = 0.89) between myocardial OEF values measured by MRI and those measured by blood sampling. Regional differences in the OEF were demonstrated by direct infusion of dipyridamole into coronary arteries in dogs. Combined with vasodilator stress, dynamic assessments of the OEF may provide a putative measurement of myocardial flow reserve and allow consecutive monitoring of myocardial dose and response.

Animals↗
PubMed1994

Adenosine and dipyridamole mimic the effects of ischemic preconditioning.

The effects of preconditioning, adenosine and dipyridamole in protecting the systolic and diastolic alterations of myocardial stunning in rabbit hearts were studied. Isovolumic left ventricular developed pressure (LVDP), and end diastolic pressure (LVEDP) were measured. The time constant of relaxation (T) was calculated. Isolated rabbit hearts were subject to 15 min of global ischemia (37 degrees C) followed by 30 min of reperfusion. LVDP and LVEDP stabilized to 55 +/- 5% and 320 +/- 28% of control values respectively (stunned group) T increased early in reperfusion (from 48.2 +/- 3.9 to 97.2 +/- 10 ms P < 0.05) but returned to control value late in reperfusion. When hearts were preconditioned by a single cycle of 5 min of ischemia LVDP and LVEDP stabilized at 89 +/- 3% and 162 +/- 34% of preischemic values respectively (P < 0.05 with respect to stunned group). The change in T was attenuated (62 +/- 6 ms at 5 min of reperfusion, P < 0.05 with respect to stunned group). Hearts treated either with adenosine (800 micrograms/min) or the nucleoside transport blocker dipyridamole (4 micrograms/min) previously to the ischemia, recovered their LVDP to 86 +/- 1% and 82 +/- 3% of preischemic values, respectively (P < 0.05 with respect to stunned group). Adenosine and dipyridamole also attenuated the increase in LVEDP (195 +/- 12% and 197 +/- 10% respectively, P < 0.05 with respect to stunned group).(ABSTRACT TRUNCATED AT 250 WORDS)

Adaptation, Physiological↗
PubMed1992

The significance of a dipyridamole induced 99mTc-MIBI perfusion abnormality on single photon emission tomography: a quantitative validation with labelled water and positron emission tomography.

To relate technetium-99m 2-methoxy-isobutyl-isonitrile (99mTc-MIBI) uptake to regional myocardial blood flow (rMBF), 99mTc-MIBI single photon emission tomography (SPET) and H2(15)O positron emission tomography (PET) scans were obtained at rest and after dipyridamole infusion in six patients with single vessel coronary artery disease. 99mTc-MIBI and H2(15)O data sets were created for each segment perfused by the stenotic vessel and for a normal reference area, assigning regions on the SPET tomograms to comparable regions on the PET by similar transaxial image reconstructions. All patients demonstrated post-dipyridamole 99mTc-MIBI perfusion defects in the territories supplied by the stenotic arteries. Resting rMBF in these regions was slightly lower than that in the normal areas (0.82 +/- 0.05 vs 0.90 +/- 0.09 ml/g/min, P = NS). A 43% +/- 14% reduction in 99mTc-MIBI activity in the area at risk was coupled with on average a 60% +/- 9% reduction in post-dipyridamole rMBF compared with control regions (0.98 +/- 0.08 vs 2.52 +/- 0.51 ml/g/min, P < 0.001). Thus, SPET assessment of 99mTc-MIBI uptake tends to underestimate the perfusion contrast between areas with normal and areas with low coronary vasodilatory reserve when compared to PET. However, these findings may still not affect the clinical usefulness of 99mTc-MIBI and more extensive studies are required to confirm these results in the clinical environment.

Contrast Media↗
PubMed1992

Dipyridamole stimulates types II cAMP-dependent protein kinase in vitro.

Dipyridamole activates in vitro type II cAMP-dependent protein kinase. This agent stimulates the autophosphorylation of the regulatory subunit in the presence of cAMP but not so in the absence of the cyclic nucleotide. The activation was also observed with exogenous substrates such as casein, histone 2A and MAP2. This stimulation did not seem to be related to the cAMP binding to the R II subunit of the enzyme. Competition binding experiments showed that dipyridamole does not compete with adenosine for the A1 receptor. The results suggest that the reported regulatory properties of dipyridamole on lipid metabolism (González-Nicolás et al. Int J Biochem 21: 883-888, 1989) might be mediated through a direct action--an activation--on the catalytic subunit of a cAMP-dependent protein kinase.

Adipose Tissue↗
PubMed1981

Evaluation of myocardial perfusion and left ventricular function by 201T1 scintigraphy after dipyridamole.

201T1 myocardial imaging was performed at rest and after dipyridamole (0.44 mg/kg) on 50 patients with known or suspected ischemic heart disease. The dipyridamole had no effect in 14 patients (group Dip.0). In 17 patients (group Dip +/-) it significantly modified the contrast of the rest image (by increasing or decreasing a rest perfusion defect). In 19 patients (group Dip - Steal) the drug induced a paradoxical response interpreted as a coronary steal effect (an active region at rest becomes hypoactive after dipyridamole while an underperfused region at rest improves). All patients underwent coronary arteriography and left monoplane ventriculography; results were interpreted in relation to these angiographic data. The mean percentage of stenoses (per patient) was about the same in the three groups but it was found that, despite these stenoses, the patients of the group Dip - Steal had a good left ventricular function (EF = 0.62 +/- 0.12). On the other hand, the ejection fraction was very poor in the two other groups (0.50 +/- 0.17 and 0.48 +/- 0.17). Moreover it was found that: (1) the frequency of high grade or even complete obstruction was notably less in group Dip - Steal (P less than 0.05); (2) the frequency of angiographically visible collaterals was higher in group Dip - Steal (P less than 0.05); (3) the left anterior descending artery was less diseased than the right coronary artery in group Dip - Steal (P less than 0.05). These results have a real prognostic value for the assessment of the preserved cardiac performance in Dip - Steal patients despite severe stenoses, and are discussed in terms of compensatory collateral circulation and preservation of the coronary-flow reserve in the myocardium distal to a critical stenosis.

Coronary Circulation↗
PubMed1987

Phase I trial of combination therapy of cancer with N-phosphonacetyl-L-aspartic acid and dipyridamole.

While N-phosphonacetyl-L-aspartic acid (PALA), an inhibitor of de novo pyrimidine biosynthesis, demonstrated a unique spectrum of activity during preclinical drug evaluation, multiple clinical trials have shown it to possess minimal clinical activity. One explanation for the disappointing results is the possibility that tumor cells are able to utilize circulating uridine in the synthesis of pyrimidines (salvage pathway). Dipyridamole, an inhibitor of nucleoside transport, has been demonstrated experimentally to potentiate the cytotoxicity of PALA significantly. In addition, this agent has a long safety record when used clinically in man. A phase I trial of this two-drug combination was therefore conducted, with a fixed oral dose of dipyridamole (50 mg/m2 every 6 h) and an escalating i.v. dose of PALA administered every 3 weeks. The dose-limiting toxicity with this schedule was diarrhea and abdominal cramping pain at a PALA dose of 3900-4200 mg/m2. Among the 65 patients participating in this trial 4 objective responses (2 partial, 2 minimal) were observed. Because of the potential for unique clinical synergy between PALA and dipyridamole further investigation should be considered.

Adult↗
PubMed1982

Bioavailability of acetylsalicylic acid and salicylic acid from rapid-and slow-release formulations, and in combination with dipyridamol.

Acetylsalicylic acid (ASA) is a strong, irreversible inhibitor of platelet aggregation, but loses this activity following first-pass deacetylation to salicylic acid (SA). In order to compare the bioavailability of unchanged ASA from rapid- and slow-release formulations, the single-dose concentration profiles of ASA and SA were studied in healthy volunteers following intake of two different rapid-release (conventional and effervescent tablets) and three different slow-release (microencapsulated ASA in tablets and in capsules, and enteric-coated tablets) formulations of ASA, and of one slow-release formulation of sodium salicylate. Since anti-platelet therapy with ASA is often combined with dipyridamol, the influence of this drug was also examined. The concentrations of ASA and SA were measured by high-pressure liquid chromatography. While the bioavailability of SA from the 5 ASA formulations was essentially equal and similar to that of the salicylate formulation, the bioavailability and peak concentrations of ASA appeared to be the much greater after rapid-release than after slow-release formulations. Indeed, ASA was only rarely detected in systemic blood following intake of slow-release ASA. Co-administered dipyridamol did not significantly influence the kinetics of ASA or SA. It appears that rapid-release formulations of ASA should be prefered in anti-platelet therapy, either alone or in combination with dipyridamol.

Adult↗
PubMed1977

Studies on the lithium transport across the red cell membrane. II. Characterization of ouabain-sensitive and ouabain-insensitive Li+ transport. Effects of bicarbonate and dipyridamole.

In studies on Li+ net-transport across the human red cell membrane following results were obtained: 1. In K+- and Na+-free choline chloride media, Li+ is transported into the erythrocytes against an electrochemical gradient. This Li+ uphill transport as well as Li+ downhill transport into the cells is inhibited by ouabain, ATP-depletion, and by external K+ and Na+. The effects of K+ and Na+ are relieved at high Li+ concentrations. 2. Ouabain-sensitive Li+ uptake, determined at 10 mM external Na+, does not obey simple Michaelis-Menten kinetics and exhibits a maximum at about pH 7. 3. Ouabain-resistant Li+ downhill transport into erythrocytes increases with rising pH. It is comprised of a saturating component and a component linearly dependent on external Li+. The linear component is partly inhibited by dipyridamole and accelerated by bicarbonate. The bicarbonate effect can be completely blocked by dipyridamole, phlorizin and phenylbutazone. 4. Li+ release is not inhibited by ouabain, ATP-depletion and external K+. It increases with external Na+ concentration, tending to saturate at 150 mM Na+. Na+-independent Li+ release is stimulated by bicarbonate. It is concluded that ouabain-sensitive Li+ uptake is mediated at the K+-site(s) of the Na+-K+ pump. Li+, K+ and Na+ appear to compete for a common site (or sites). The stimulation of Li+ transfer by bicarbonate and the inhibition by dipyridamole suggest a participation of anionic species in ouabain-resistant Li+ transfer. The Na+-dependent Li+ release and the "saturating component" of Li+ uptake are ascribed to the Na+-dependent Li+ countertransport system.

Adenosine Triphosphate↗
PubMed1982

Dipyridamole treatment in chronic obstructive airways disease: effect on platelet regeneration time.

The platelet regeneration time (PRT) determined in a group of hypoxaemic patients with chronic obstructive airways disease (COAD), before and after treatment with dipyridamole 150 mg tid, was compared with a group of control subjects. The PRT was computed by a modified non-radioisotope technique and was expressed as t1/2 in days. The patient group showed a significantly shortened PRT as compared to controls of the same age and sex (2.10 +/- 0.16 vs 3.65 +/- 0.26 days; p less than 0.001). One month of dipyridamole administration resulted in prolongation of the PRT in COAD patients (2.10 +/- 0.16 days pre-treatment vs 2.75 +/- 0.20 post-treatment; p less than 0.01), without affecting the platelet cyclo-oxygenase system. This study indicates that dipyridamole may be beneficial in pathological conditions, which are characterized by increased platelet turnover, possibly leading to frequent thromboembolic complications.

Adult↗
PubMed1981

Enhanced prostacyclin production by dipyridamole in man.

The effects of some phosphodiesterase (PDE) inhibitors (dipyridamole, theophylline, papaverine and SH-869) on prostacyclin (PGI2) production have been studied in vitro and in vivo. PGI2 was bioassayed by Vane's superfusion technique. In rabbit aortic rings, only dipyridamole in concentrations from 1 to 12 microM was able to stimulate PGI2 biosynthesis in a dose-dependent manner. This effect was also detected with so-called "exhausted" rabbit aortic rings. The other PDE inhibitors used, both in microM and mM concentration, did not affect PGI2 biosynthesis. Dipyridamole was found to increase PGI2 production in healthy volunteers, when given both by infusion (8 micrograms/kg/min x 2h) and by oral administration (375 mg/day for seven days). Circulating PGI2 and PGI2 production induced by a 3-min period of ischaemia were increased by an average of 137% (p less than 0.001) and 30.8% (p less than 0.001) respectively. Saline and theophylline (as aminophylline) infusions used as controls did not affect PGI2 production.

Adolescent↗
PubMed1995

Dipyridamole thallium-201 single-photon emission tomography in aortic stenosis: gender differences.

Dipyridamole single-photon emission tomography (SPET) is used for the detection of coronary artery disease (CAD) and the method has also been applied in patients with aortic stenosis. This study was undertaken to establish the gender-specific normal limits of thallium-201 distribution in patients with aortic stenosis and to apply these normal limits in a larger group of patients with aortic stenosis to obtain the sensitivity and specificity for coexisting CAD. A low-dose dipyridamole protocol was used (0.56 mg/kg during 4 min). Thallium was injected 2 min later and tomographic imaging was performed. Following image reconstruction a basal, a midventricular and an apical short-axis slice were selected. The highest activity in each 6 degree segment was normalised to the maximal activity of each slice. The normal uptake for patients with aortic stenosis was obtained from ten men and ten women with aortic stenosis and a normal coronary angiography. Eighty-nine patients were prospectively evaluated. An area reduction of at least 75% in a coronary artery was considered to be a significant coronary lesion and was found in 57 (64%) patients. With gender-specific curves (-2.5 SD) sensitivity for detecting CAD was 100% and specificity was 75% in men, while sensitivity was 61% and specificity 64% in women. It is concluded that the gender-specific normal distribution of 201Tl uptake in patients with aortic stenosis, using dipyridamole SPET, yields a high sensitivity and specificity for coronary artery lesions in men but a lower sensitivity and specificity in women with aortic stenosis.

Aged↗
PubMed1992

Phase II trial of 5-fluorouracil, high-dose leucovorin calcium, and dipyridamole in advanced prostate cancer.

To examine the effect of altering intracellular folate pools on the efficacy of 5-fluorouracil (FUra) in the treatment of advanced prostate cancer, we performed a phase II trial of FUra (300-370 mg m-2 day-1 x 5 as an i.v. bolus) combined with high-dose folinic acid (500 mg m-2 day-1 x 5.5 days by continuous i.v. infusion) and dipyridamole (75 mg p.o. every 6 h x 5.5 days) administered on a 28-day schedule in patients with stage D2 disease. A group of 13 patients have been treated. The median age was 68 years (range 48-78 years); the performance status ranged from 50% to 90%. Among 12 evaluable patients, there were no objective responders; the median time to progression was 1.9 months. Median survival after entry on this trial was 8.6 months. Treatment with FUra, high-dose folinic acid and dipyridamole was well tolerated. Only one episode each of grade 3 leukopenia, granulocytopenia, and thrombocytopenia was observed. These results suggest that, despite previous trials demonstrating activity for FUra in stage D2 prostate cancer, this disease may be relatively resistant to fluoropyrimidines and, thus, less amenable to biochemical modulation with high-dose folinic acid and dipyridamole.

Aged↗
PubMed1984

Hypoxanthine transport in mammalian cells: cell type-specific differences in sensitivity to inhibition by dipyridamole and uridine.

We have measured by rapid kinetic techniques the zero-trans influx of hypoxanthine in various cell lines and its sensitivity to inhibition by uridine, dipyridamole, nitrobenzylthioinosine and nitrobenzylthiopurine. The results and those reported earlier divided the cells into two distinct groups. In mouse P388, L1210 and L929 cells uridine and hypoxanthine had little effect on the transport of each other, supporting the view that nucleosides and hypoxanthine are transported by different carriers. In these cells, hypoxanthine transport was also uniquely resistant to inhibition by dipyridamole (IC50 (50% inhibition dose) greater than 30 microM). In Novikoff and HTC rat hepatoma, Chinese hamster ovary and Ehrlich ascites tumor cells, on the other hand, hypoxanthine and uridine inhibited the transport of each other about 50% at a concentration corresponding to the Michaelis-Menten constant of their transport, and hypoxanthine transport was strongly inhibited by dipyridamole (IC50 = 100 to 400 nM). Although these results are compatible with the view that nucleosides and hypoxanthine are transported by a common carrier in these cells, this conclusion is not supported by the finding that uridine transport is strongly inhibited in some of these cell lines, as in the first group of cells, by nitrobenzylthioinosine, whereas hypoxanthine transport is highly resistant in all cell lines tested. In contrast, the transport of both substrates is highly resistant to inhibition by nitrobenzylthiopurine. The Michaelis-Menten constants for uridine transport are about the same in all cell lines. The Michaelis-Menten constants for hypoxanthine transport are similar to those for uridine transport in some cell lines, but are much higher in others.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Effects of nitroglycerin and dipyridamole on regional myocardial blood flow.

The effects of intravenous administration of nitroglycerin or dipyridamole on distribution of myocardial blood flow in the heart after coronary underperfusion were investigated. In 18 open chest, anesthetized dogs, flow of the tubing supplying the left circumflex coronary artery (LCA) was reduced and kept constant, and then the drug was given intravenously. Before and after an administration of saline, nitroglycerin (0.04 mg/kg) and dipyridamole (0.2 mg/kg), myocardial blood flow was measured by tracer microspheres (TM). The first and second carbonized 15 mu spheres (TM1 and TM2) were injected into the left atrium and the cannulated LCA perfusion system respectively before medication. Similarly, the third and fourth spheres were given after drug. Thus, by using four different TMs (141Ce, 51Cr, 85Sr, 46Sc) regional myocardial blood flow from the LCA perfusion route (TM2 and TM4) was measured separately from that of the other normally perfused coronary route (TM1 and TM3). The effect of drugs on flow distribution of these two independent routes was measured. The LCA underperfusion produced a significant diminution of regional flow and its end/epi ratio in the LCA territory. Nitroglycerin increased end/epi ratio in the ischemic myocardium in the LCA perfusion route, but dipyridamole increased the normally perfused coronary flow but caused a shift of flow from the ischemic left ventricle to the atria and right ventricle within the LCA territory.

Animals↗
PubMed1980

Actions of aspirin and dipyridamole on lymphocyte activation.

The actions of aspirin and dipyridamole on lymphocyte activation in vitro have been studied. Aspirin inhibits lymphocyte activation when measured by protein synthesis or by 3H-thymidine incorporation at therapeutic concentration. Dipyridamole also strongly inhibits 3H-thymidine incorporation, but is a less potent inhibitor of protein synthesis at therapeutic concentrations. Aspirin/dipyridamole combinations did not show synergism as inhibitors of lymphocyte activation. It is concluded that these drugs has dissimilar actions on the lymphocyte and that dipyridamole will not serve as an aspirin-sparing drug in anti-inflammatory therapy.

Animals↗
PubMed1992

Reaction of dipyridamole with the hydroxyl radical.

Dipyridamole [2,6-bis-diethanolamino-4,8-dipiperidinopyrimido-(5,4-d)pyri midine], a well known platelet aggregation inhibitor, shows powerful hydroxyl radical scavenging activity by inhibiting OH.-dependent salicylate and deoxyribose degradation. Steady-state competition kinetics experiments with deoxyribose were carried out to evaluate the second-order rate constant for the reaction between hydroxyl radical and dipyridamole. OH. radicals were generated either by a Fenton-type reaction or by X-ray irradiation of water solutions. A second-order rate constant k(Dipyridamole + OH.) of 1.72 +/- 0.11 X 10(10) M-1 s-1 and of 1.54 +/- 0.15 X 10(10) M-1 s-1 was measured by Fenton chemistry and by radiation chemistry, respectively. Mannitol was used as an internal standard for hydroxyl radicals in steady-state competition experiments with deoxyribose. A rate constant K(Mannitol + OH.) of 1.58 +/- 0.13 X 10(9) M-1 s-1 and 1.88 +/- 0.14 X 10(9) M-1 s-1 was measured in the Fenton model and in the water radiolysis system, respectively. Both these rate constants are in good agreement with the published data obtained by the "deoxyribose assay" and by pulse radiolysis.

Deoxyribose↗
PubMedDate not supplied

Myocardial technetium 99m-labeled teboroxime clearance derived from canine scans differentiates severity of stenosis after dipyridamole.

BACKGROUND: The purposes of this study were to determine (1) whether perfusion defects and differential teboroxime clearance observed on serial postdipyridamole planar gamma camera images have utility in differentiating severity of coronary stenosis in canine myocardium and (2) whether single-zone (99mTc activity in one zone over time) or dual-zone (99mTc activity ratio in two zones over time) quantitative analysis provides the most useful characterization of teboroxime clearance kinetics. METHODS AND RESULTS: Accordingly, eight dogs received a mild coronary stenosis (microsphere-determined, post-dipyridamole flow > or = 0.4 ml/min/gm) and 10 dogs received a severe coronary stenosis (flow < or = 0.3 ml/min/gm). In three control dogs there was no coronary stenosis. Teboroxime (5 mCi) was injected after dipyridamole (0.8 mg/kg/min), and gamma camera imaging was begun immediately and continued for 60 minutes. Quantitative analysis of single-zone clearance curves indicated that teboroxime retention for both zones of stenosis (mild = 66.3% +/- 2.8%, SEM; severe = 69.5% +/- 3.7%) was significantly greater than control zone retention (54.5% +/- 3.0%; p < 0.05) at 10 minutes. Retention in mild (37.2% +/- 1.9%, SEM) and severe (42.3% +/- 1.5%) zones of stenosis was significantly different from each other at 60 minutes (p < 0.05). There was a significant direct, linear correlation of flow with teboroxime clearance at 20 minutes (r = +0.74, normal and ischemic zones). Quantitative analysis with dual-zone count ratios (stenosed/normal) demonstrated significant differences among control (0.93 +/- 0.04, SEM), mild stenoses (0.54 +/- 0.04), and severe stenoses (0.39 +/- 0.03) as early as 2 minutes after administration of 99mTc-labeled teboroxime. The correlation coefficient for flow ratio versus dual-zone counts/pixel ratio at 20 minutes was r = +0.74. CONCLUSION: Thus in this canine stenosis model with dipyridamole, gamma camera imaging could distinguish mild from severe coronary stenoses by either single- or dual-zone analysis.

Animals↗