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Biomedical subjects

Ihn Ho Cho

Publications and source records attributed to Ihn Ho Cho.

4 recordsLinked to original sources

Direct comparison of adenosine and adenosine 5'-triphosphate as pharmacologic stress agents in conjunction with Tl-201 SPECT: Hemodynamic response, myocardial tracer uptake, and size of perfusion defects in the same subjects.

BACKGROUND: Adenosine 5'-triphosphate (ATP), a potent and inexpensive coronary vasodilator, was introduced as a pharmacologic stress agent for thallium 201 single photon emission computed tomography (SPECT). However, there has been no direct comparison of ATP and adenosine as myocardial stressors in the same subjects. METHODS AND RESULTS: Thirty-six patients underwent consecutive Tl-201 SPECT imaging with adenosine and ATP in a randomly assigned order. There were no changes in clinical status and no invasive procedures were performed between the two tests. The hemodynamic response and side effects were monitored, and myocardial tracer uptake was assessed by use of a visual grading system and quantitative analysis via a CEqual map. The hemodynamic changes and adverse effects did not differ significantly between the two groups. There were no changes in the detection of any perfusion defect on a per-subject basis, except in one. The exact agreement rate for the visual grading of the myocardial tracer uptake was 84.8%. However, the average extent of the perfusion defect and the severity score were higher with adenosine. CONCLUSION: The hemodynamic changes and the degree of myocardial uptake were similar between the adenosine and ATP infusion. However, quantitative analysis by use of a CEqual map revealed smaller perfusion defects and lower severity scores in subjects undergoing Tl-201 SPECT with ATP.

Adenosine↗

A protective role for heme oxygenase-1 in INS-1 cells and rat islets that are exposed to high glucose conditions.

Heme oxygenase-1 (HO-1) has been described as an inducible protein that is capable of cytoprotection via radical scavenging and the prevention of apoptosis. Chronic exposure to hyperglycemia can lead to cellular dysfunction that may become irreversible over time, and this process has been termed glucose toxicity. Yet little is known about the relation between glucose toxicity and HO-1 in the islets. The purposes of the present study were to determine whether prolonged exposure of pancreatic islets to a supraphysiologic glucose concentration disrupts the intracellular balance between reactive oxygen species (ROS) and HO-1, and so this causes defective insulin secretion; we also wanted to evaluate a protective role for HO-1 in pancreatic islets against high glucose levels. The intracellular peroxide levels of the pancreatic islets (INS-1 cell, rat islet) were increased in the high glucose media (30 mM glucose or 50 mM ribose). The HO-1 expression was induced in the INS-1 cells by the high glucose levels. Both the HO-1 expression and glucose stimulated insulin secretion (GSIS) was decreased simultaneously in the islets by treatment of the HO-1 antisense. The HO-1 was upregulated in the INS-1 cells by hemin, an inducer of HO-1. And, HO-1 upregulation induced by hemin reversed the GSIS in the islets at a high glucose condition. These results suggest HO-1 seems to mediate the protective response of pancreatic islets against the oxidative stress that is due to high glucose conditions.

Animals↗

Adenosine-induced long-standing postischemic left ventricular dysfunction evaluated with gated SPECT.

OBJECTIVES: This study was performed to determine the after-effects of pharmacologic stress (adenosine) on left ventricular (LV) function-end-diastolic volume (EDV), end-systolic volume (ESV), and ejection fraction (LVEF)-with Tl-201 and Tc-99m MIBI SPECT. METHODS: A total of 263 patients were grouped according to the time interval between isotope injection and imaging. Group A: within 1 hour (n = 99; men, n = 48; women, n = 51; mean age: 63.2 years), subgrouped as patients with no perfusion defect (NPD; n = 61), reversible defect (RD; n = 33), and fixed defect (FD; n = 5). Group B: 1 to 2 hours (n = 110; men, n = 66; woman, n = 44; mean age, 63 years), NPD (n = 64), RD (n = 26), and FD (n = 20). 3) Group C: 2 to 3 hours (n = 54; men, n = 30; women, n = 24; mean age, 62 years); NPD (n = 22), RD (n = 17), and FD (n = 15). All patients were in sinus rhythm during the study and had no prior history of myocardial infarction. RESULTS: In group A, in the patients with RD, poststress LVEF was significantly depressed after adenosine infusion (53.1 +/- 9.5% vs 58.3 +/- 10.2%, P < 0.001) and showed a wall motion abnormality, which was worse after stress than during rest. The mean difference in LVEF (DeltaLVEF) between rest and stress was 5.2%. The DeltaLVEF in those patients with RD was significantly higher than that in the NPD (0.9%, P < 0.01) or FD (2.1%, P < 0.05) subgroups. Twenty of the 33 patients (60.6%) with RD showed an increase in LVEF > or = 5% from poststress to rest, and the poststress ESV (43.3 +/- 19.0 mL) was significantly higher than the ESV (38.5 +/- 18.4 mL, P < 0.01) at rest, but there was no significant difference in the EDV (90.5 +/- 26.4 vs 89.7 +/- 26.2 mL). In group B, DeltaLVEF was 1.5%, 4.4%, and 1.2% in patients with NPD, RD, and FD respectively. In group C, DeltaLVEF was 2.5%, 3.2%, and 0.9% in patients with NPD, RD, and FD respectively, and there was no significant difference in DeltaLVEF among patients. In group C, 4 of 17 patients (23.5%) with RD showed an increase in LVEF > or = 5% from poststress to rest. CONCLUSION: These results showed that adenosine stress-induced postischemic LV dysfunction is well noted on early quantitative gated SPECT in patients with RD and can also be observed on delayed gated SPECT, even though the incidence of LV dysfunction is less than that in early gated SPECT.

Adenosine↗

Osteoblastoma as a cause of osteomalacia assessed by bone scan.

A 27-year-old female patient was admitted to our hospital with a history of leg pain and mass. She had a benign osteoblastoma in right tibia. Resection of the tumor without treatment by vitamin D antagonist resulted in rapid cure of the osteomalacia. Bone scintigraphy with Tc-99m MDP revealed multiple hot uptakes in initial scan, and follow up scan showed a clear resolution of the lesions.

Adult↗