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M Ohyanagi

Publications and source records attributed to M Ohyanagi.

At least 19 recordsLinked to original sources

Messenger RNA for the guanine nucleotide-binding regulatory protein (G protein) is reduced in the acute ischemic myocardium.

It has been reported that the function of the guanine-binding regulatory protein (G protein), especially the alpha subunit of the stimulatory G protein (Gs alpha), in myocardium is decreased with acute ischemia. However, it is unclear whether this decrease is due to transcriptional or post-transcriptional changes. Moreover, no studies have examined the distribution of G protein mRNA in ischemic myocardium using in situ hybridization. The purpose of this study was to explore alterations in mRNA of G proteins (Gs and Gi) in ischemic hearts using in situ hybridization. We measured the levels of mRNA for Gs alpha and Gi alpha in ischemic and non-ischemic myocardium by in situ hybridization using a radioisotope imaging system. We compare these mRNA levels in ischemic and non-ischemic myocardium with Northern blot analysis and the protein levels of G proteins by Western blot analysis. The mRNA for Gs alpha and Gi alpha was distributed diffusely in normal hearts. Levels of mRNA detected by in situ hybridization were substantially reduced by acute ischemia, and these results were confirmed by Northern and Western blot analysis. These results suggest that decreased levels of mRNA and protein for G proteins may underlie the impaired function of the receptor--G protein--adenylate cyclase system in ischemic myocardium. In addition, quantitative evaluation of mRNA is possible by in situ hybridization and correlates well with Northern analysis.

Acute Disease

The effects of antianginal drugs on energy expenditure during exercise in normal subjects.

The respiratory quotient (RQ = VCO2/VO2) provides important information (ie, the ratio of carbohydrate to fat utilization) concerning energy expenditure. We studied the effects of various antianginal drugs on energy expenditure during steady-state aerobic exercise in 9 healthy adult men. The drugs used were propranolol (a non-selective beta-blocker), metoprolol (a beta-1 selective blocker), amosulalol (an alpha- and beta-blocker), nicardipine (a calcium antagonist) and isosorbide dinitrate. Each drug was administered for 2 weeks, followed by a 2-week washout period. VO2, VCO2 and RQ were measured with an expired gas analyzer during treadmill exercise tests before and during the administration of each drug. Two protocols of constant-load exercise were performed: Protocol 1 lasted for 10 min at a speed of 5.5 km/h and a grade of 0%, (at a level of about 30% peak VO2), while Protocol 2 lasted for 10 min at a speed of 7 km/h and a grade of 0%, (at a level of about 40% peak VO2). RQ during exercise was significantly increased and VO2 was decreased after propranolol, metoprolol and amosulalol (P < 0.05). Neither nicardipine nor isosorbide dinitrate produced significant changes in these values. These data suggest that propranolol, metoprolol and amosulalol increase the efficiency of energy expenditure during ordinary physical activity by increasing the utilization of carbohydrate and by decreasing the utilization of fat.

Adrenergic beta-Antagonists

Beta-adrenoceptor-G protein-adenylate cyclase complex in rat hearts with ischemic heart failure produced by coronary artery ligation.

We examined the role of the myocardial beta-adrenoceptor-G protein-adenylate cyclase complex in 10-week-old Wistar rats with ischemic heart failure produced by ligating the left coronary artery (l) and in sham-operated control rats (C). We determined the number of beta-adrenoceptors (Bmax), the dissociation constant (Kd) using a binding assay and adenylate cyclase activity. Levels of mRNA encoding for the alpha subunit of the stimulatory guanine nucleotide-binding protein (Gs alpha) and the alpha subunit of the inhibitory guanine nucleotide-binding protein (Gi alpha) were measured by Northern blot analysis. The amounts of Gs alpha and Gi alpha were measured by Western blot analysis. Bmax and Kd did not differ significantly between the two groups: Bmax: l, 14.7 +/- 1.3 v C, 13.4 +/- 0.9 f mol/mg protein; Kd: l, 345 +/- 31 v C, 340 +/- 28 pM (mean +/- standard error, S.E.). There were no significant differences in Gs alpha and Gi alpha concentrations between the two groups as measured by Northern blot analysis (Gs alpha: l, 91.6 +/- 4.5 v C, 96.5 +/- 2.3%; Gia; l, 95.4 +/- 3.6 v C, 90.0 +/- 3.0%) or by Western blot analysis (Gs alpha: l, 95.2 +/- 2.0 v C, 94.5 +/- 2.6%; Gi alpha: l, 91.5 +/- 3.0 v C, 95.1 +/- 2.9%). Activity of basal and MnCl2-stimulated adenylate cyclase did not differ significantly in the two groups: basal: l, 7.5 +/- 0.7 v C, 8.1 +/- 0.5 pmol cAMP/mg protein/min; MnCl2 l, 80.8 +/- 5.8 v C, 86.4 +/- 6.7 pmol cAMP/mg protein/min. Sodium fluoride and forskolin-stimulated adenylate cyclase activity were significantly lower in the hearts with ischemic failure compared with controls (sodium fluoride: l, 68.5 +/- 5.6 v C, 103 +/- 4.8 pmol cAMP/mg protein/min; forskolin: l, 84.6 +/- 6.5 v C, 117.1 +/- 5.6 pmol cAMP/mg protein/min). These data suggest the presence of myocardial Gs alpha dysfunction in ischemic heart failure. We conclude that such a dysfunction in Gs alpha may contribute to the contractile abnormalities in ischemic heart failure.

Adenylyl Cyclases

Increased levels of inhibitory G protein in myocardium with heart failure.

To identify any differences in inhibitory G protein (Gi) attributable to species or the cause of heart failure, we studied the changes in this protein in different animal models of heart failure: 1) different species; rats vs. hamsters (F1B) with cardiomyopathy induced by adriamycin (ADR) and 2) different etiologies; rats with ischemic heart failure (IHD) due to coronary artery ligation vs. rats with cardiomyopathy induced by ADR and F1B (20-week-old) hamsters with cardiomyopathy induced by ADR vs Syrian hamsters BIO 14.6 (40-week-old) with genetic cardiomyopathy, using Western blotting methods and ADP-ribosylation. We also sought to determine whether changes in the amount of Gi protein reflected the regulation of adenylate cyclase. The amount of immunodetectable Gi rose by 35% (p < 0.05) in ADR rats, 25% (p < 0.05) in ADR hamsters, 15% (p < 0.05) in IHD rats, and 28% (p < 0.05) in BIO 14.6 hamsters, as compared with control rats, F1B (20-week-old) hamsters, sham-operated control rats, and F1B (40-week-old) hamsters, respectively. Assessment of Gi by pertussis toxin-catalyzed ADP-ribosylation revealed increases in Gi of 24% (p < 0.05) in ADR rats and of 44% (p < 0.05) in BIO 14.6 hamsters, as compared with their respective controls. Gi function, as assayed by the acetylcholine-induced inhibition of adenylate cyclase, also increased. Thus, Gi protein appears to contribute to the changes in signal transduction in myocardium with heart failure.

Adenylyl Cyclases

[Quantitative evaluation of 111In-antimyosin Fab myocardial imaging in acute myocardial infarction patients].

Quantitative evaluation of 111In-antimyosin Fab myocardial (InAM) imaging was performed in 15 patients with acute myocardial infarction to evaluate which organ is the most appropriate for the control of myocardial accumulation, to compare the quantitative method with the conventional visual method, and to study which clinical indices correlate with the InAM quantitative evaluations. InAM images demonstrated the myocardium with 31 +/- 6 mean counts/pixel, lung with 14 +/- 4, upper mediastinum with 20 +/- 5, middle mediastinum with 26 +/- 5, and liver with 75 +/- 10. We considered the lung to be the most appropriate control organ for quantitative evaluations of InAM imaging, because it could be separated from the myocardium, and the measurement range was narrow. The InAM uptake index [IUI = (myocardial counts-lung counts)/lung counts] was calculated as the index of myocardial accumulation. Visual evaluations of myocardial accumulation on InAM images were classified into three grades. The IUI of grade 1 (slight) was 0.98 +/- 0.19, grade 2 (moderate) was 1.34 +/- 0.38, and grade 3 (severe) was 1.97 +/- 0.19. Visual grading was nearly in accordance with the IUI, although it was difficult to distinguish visually between grades 1 and 2. Measurement of wall motion by left ventriculography showed that reduced wall motion was associated with an IUI of 1.01 +/- 0.18 and dyskinesis with an IUI of 1.92 +/- 0.16, showing IUI can indicate regional myocardial damage. However, IUI was not correlated with indices of the overall left ventricular function, such as ejection fraction, cardiac index, and peak creatine kinase level.

Antibodies, Monoclonal

Preoperative evaluation of myocardial viability by thallium-201 imaging in patients with old myocardial infarction who underwent coronary revascularization.

The myocardial uptake and redistribution in thallium scintigraphy and the regional wall motion by echocardiography were evaluated by a semi-quantitative method in 42 patients who previously had myocardial infarction (50 target vessels) and underwent coronary revascularization. The aim of this study was to elucidate the significance of the initial image, delayed image and redistribution on thallium-201 scintigraphy for clinical diagnosis of the myocardial viability. As a semi-quantitative analysis, we used a bull's-eye display for thallium image and centerline method for echocardiographic wall motion, and compared the results before and after revascularization. As a result, the thallium grade improved postoperatively in all 17 areas which preoperative had showed redistribution, and also in 11 of the 32 areas without preoperative redistribution. The sensitivity, specificity and accuracy of preoperative thallium redistribution for predicting myocardial viability were 61%, 100% and 78%, respectively, when the postoperative improvement in the thallium grade was used as the standard. The postoperative probability of improvement in the thallium grade increased in proportion to the preoperative thallium grade (delayed image) (p less than 0.01). There was no correlation between the preoperative thallium delayed image and postoperative improvement in wall motion. Postoperative improvement in thallium image and wall motion could not be predicted from the preoperative wall motion. Thus, postoperative improvement in thallium images can be anticipated if redistribution is present on the preoperative thallium image, and the preoperative thallium delayed image is useful for predicting myocardial viability. Improvement in wall motion could not be predicted preoperatively by these methods.

Adult

Interaction between microvascular alpha 1- and alpha 2-adrenoceptors and endothelium-derived relaxing factor.

Intravital microscopy was used to study the effect of endothelium-derived relaxing factor (EDRF) on microvascular adrenoceptor sensitivity in rat cremaster skeletal muscle. NG-Monomethyl L-arginine (L-NMMA, 1-300 microM), an inhibitor of EDRF formation, produced concentration-dependent constriction of arterioles and venules. When an intermediate amount of alpha 1- versus alpha 2-adrenoceptor tone was first produced with bath-added norepinephrine (NE) in the presence of rauwolscine or prazosin, L-NMMA caused constriction with greater potency and efficacy during alpha 2 than during alpha 1 tone. During localized alpha 1 or alpha 2 constriction along an arteriole by perivascular micropipette suffusion of NE in the presence of rauwolscine or prazosin, again, bath-added L-NMMA produced constriction with greater potency during alpha 2 than during alpha 1 constriction. Like L-NMMA, disruption of EDRF release by microembolization caused baseline arteriole constriction and selectively increased alpha 2 sensitivity 75-fold. Although these findings support the hypothesis that endothelial cells possess alpha 2-adrenoceptors that promote EDRF release, a greater susceptibility of alpha 2 than alpha 1 constriction to EDRF inhibition could also account for the results. In support of this latter possibility, alpha 2 constriction was approximately 50-fold more susceptible than alpha 1 constriction to inhibition by the EDRF-like nitrodilator nitroprusside. The similarity in magnitude of this difference in sensitivity with the difference obtained in the embolization experiments does not support the hypothesis that microvascular endothelial cells in skeletal muscle possess EDRF-promoting alpha 2-adrenoceptors. However, these data do suggest that endogenous EDRF release modulates basal arteriole and venule tone and that alpha 2-adrenoceptor constriction is more sensitive than alpha 1 constriction to inhibition by EDRF.

Animals

[Acute myocardial infarction: comparison of results of Tl-201, Tc-99m pyrophosphate and In-111 antimyosin Fab imagings].

To evaluate the extent and characteristics of infarct areas, we performed indium-111 monoclonal antimyosin Fab (InAM), thallium-201 (TL) and Tc-99m pyrophosphate (PYP) imagings in 17 patients with acute myocardial infarction, and tried to find out the mechanism that causes difference of these imagings. In each study, the extent scores as an index of the infarct area were obtained by single photon emission computed tomography (SPECT), and comparisons were made between the results obtained. The overlap between InAM and TL imagings obtained by SPECT was evaluated. Location, severity, extent and patterns of accumulation were compared between InAM and PYP with both planar image and SPECT. The extent scores of InAM correlated well with those of TL (r = 0.73, p < 0.01). However, the overlap of both methods was recognized in 8 of 17 patients, in whom wall thickness of the infarct area as obtained by echocardiography was well preserved. The left ventricular regional asynergy was mild in 6 of these 8 patients. Coronary angiography showed poor or no collateral circulation in these cases. Although there were generally close correlations of the extent scores between InAM and PYP, discrepancy was noted in 2 cases for location; 2 for severity, 5 for extent, and 3 for patterns of accumulation. These differences may be attributed to the timings of imaging, coronary reperfusion and different mechanisms of accumulation. In conclusion, the extent of acute myocardial infarction obtained by InAM correlates well with those obtained by TL and PYP, with some exceptions.

Adult

[Myocardial imaging in acute myocardial infarction using beta-methyl-p-(123I)-iodophenylpentadecanoic acid: comparison with 201Tl imaging and wall motion].

Myocardial imaging using beta-methyl-p-(123I)-iodophenylpentadecanoic acid (BMIPP) was performed in 11 patients with acute myocardial infarction. The left ventricular images were divided into 12 segments, and myocardial imagings with BMIPP were compared with coronary angiography (CAG), thallium-201 myocardial scintigraphy (TL) and wall motion obtained by two-dimensional echocardiography (WM). When the culprit lesion was at the proximal point of the left anterior descending artery (LAD), all segments showed depressed uptake. In 3 cases with single vessel disease of the LAD, inferior wall of the basis showed reduced uptake of BMIPP despite the location of the culprit lesion. In cases with discordant uptake between the two tracers, BMIPP frequently showed more severely depressed uptake than TL in the subacute phase, although the uptake of BMIPP correlated with that of TL (tau = 0.82, p less than 0.001). In such cases, the discordance was related to the improvement in WM from the acute phase to the convalescent phase. BMIPP uptake correlated with WM in the subacute phase (tau = 0.50, p less than 0.001). BMIPP showed more severely depressed uptake while WM showed mild asynergy in most cases in which discordance was found between the BMIPP and WM findings. However, there was no correlation between the change in WM from the acute to subacute phases, or the uptakes of BMIPP and TL alone. We concluded that the myocardial condition can be evaluated in detail in acute myocardial infarction by comparing the findings of BMIPP with those of TL and WM.

Aged

[The influence of findings of coronary artery on myocardial salvage in acute myocardial infarction].

201Tl stress myocardial scintigraphy was performed in convalescent patients with acute myocardial infarction, to evaluate the influence of stenosis and collateral circulation of coronary artery in acute phase, on myocardial salvage in chronic phase. In 14 cases of unsuccessful coronary revascularization (complete occlusion), a complete defect of thallium imaging in chronic phase was seen in only one case of four cases with good collateral circulation, while eight of 10 cases with poor collateral circulation. In 16 cases of poor collateral circulation, six cases showed a complete defect, although the target vessel had improved to less than 75% of stenosis. However, in cases of good collateral circulation, no case showed a complete defect when the target vessel had improved to less than 75% of stenosis. The myocardial salvage is quite possible (p less than 0.05), when the coronary angiography in acute phase showed the forward flow (99% or 90% of stenosis) before coronary revascularization and/or good collateral circulation (Rentrop 2 degrees or 3 degrees).

Adult

Occlusion of cremaster collateral circulation alters microvascular reactivity.

Surgical preparation of the rat cremaster skeletal muscle for microvascular study usually involves occlusion of the deferential artery and vein which supply a collateral circulation to the tissue. This allows removal of the testis and ductus deferens, and permits direct observation of the cremaster microvasculature. We examined with intravital microscopy the effect of this occlusion on alpha-adrenergic and nonreceptor-mediated (KCl) constriction of large arterioles (1A, 136 microns i.d.) and venules (1V, 193 microns i.d.). The acutely denervated cremaster was suspended in a tissue bath containing propranolol to block beta-adrenergic receptors. alpha 1-adrenergic (norepinephrine (NE) + rauwolscine), alpha 2-adrenergic (NE + prazosin), and KCl (+ phentolamine) concentration-response curves were obtained for bath-added agonists before vs after occlusion of the deferential circulation. Occlusion had no effect on baseline 1A diameter but increased 1V diameter slightly. Arteriolar alpha 1- and alpha 2-adrenergic sensitivities were unaffected by occlusion, but venular sensitivities were reduced by the same amount (approximately fourfold) for both receptor types. Occlusion increased arteriolar sensitivity to KCl but had no effect of venular KCl sensitivity. These data indicate that occlusion of the deferential collateral circulation can produce significant and varied effects on alpha-adrenoceptor and nonreceptor-mediated constriction of cremaster large arteriolar and venular smooth muscle, and underscore the need to avoid collateral occlusion for certain studies of the cremaster microcirculation.

Animals

Interactions between alpha-adrenoceptors and adenosine receptors on microvascular smooth muscle.

alpha 2-Adrenoceptor but not alpha 1-adrenoceptor constriction of arterioles is selectively inhibited by tissue acidosis, ischemia, and increased metabolic rate. To further examine neural-local interactions, we studied the effect of adenosine receptor stimulation on alpha 1- or alpha 2-adrenoceptor constriction. Intravital microscopy was used to study large arterioles (133 +/- 3 microns diam; mean +/- SE), small arterioles (16 +/- 1 microns), and large venules (178 +/- 3 microns) of rat cremaster skeletal muscle. Concentration-response (diameter change) curves were obtained for bath-added norepinephrine in the presence of either rauwolscine or prazosin to provide selective alpha 1- and alpha 2-constriction, respectively. The adenosine receptor agonist 5'-N-ethylcarboxamidoadenosine (2.24 x 10(-8) M) significantly attenuated both alpha 1- and alpha 2-constriction by 5- to 20-fold; alpha 1-constriction was three- to fourfold more sensitive than alpha 2-constriction. Similar inhibitory effects were obtained with adenosine (2.24 x 10(-6) M). The adenosine receptor antagonist 8-[4-[N(2-aminoethyl)carbamoylmethoxy]phenyl]-1,3-dipropylxanthine (0.7 microM) reversed the inhibitory effect of adenosine, which implicates extracellular A2 adenosine receptors. Intrinsic tone in large vessels was unaffected by adenosine receptor stimulation but was completely inhibited in small arterioles. These findings suggest that both alpha 2- and especially alpha 1-adrenoceptor constriction and intrinsic tone (of small but not large arterioles) are inhibited by physiologically relevant concentrations of adenosine.

Adenosine

Differential activation of alpha 1- and alpha 2-adrenoceptors on microvascular smooth muscle during sympathetic nerve stimulation.

The relative contribution of postjunctional alpha 1- and alpha 2-adrenoceptors to constriction of microvessels was examined during sympathetic nerve stimulation and sympathetic escape (difference between peak and steady-state constriction). Large arterioles (120 +/- 4 microns control diameter) and venules (174 +/- 6 microns) and small arterioles (13 +/- 4 microns) were examined in rat cremaster skeletal muscle during stimulation of the cremaster efferent innervation (decentralized lumbar sympathetic chain, 0.5-16 Hz, 2-minute train). The muscle was suspended in a tissue bath, and diameter was measured with intravital microscopy. Frequency-response curves were obtained after vehicle (prazosin or rauwolscine) was added to the bath. In large arterioles, prazosin (10(-7) M) significantly attenuated constriction by 60-80%; a fivefold higher concentration had no additional effect. In contrast, rauwolscine (1 to 5 x 10(-7) M) had no effect. Venules evidenced minimal response to nerve stimulation. In small arterioles, rauwolscine (5 x 10(-7) M) significantly attenuated constriction by 50-60%, while prazosin (10(-7) M) had no effect. These data suggest that for large arterioles, which are known to possess both receptors, alpha 1-adrenoceptors are preferentially stimulated by nerve-released norepinephrine. In contrast, sympathetic constriction of small arterioles is mediated by alpha 2-adrenoceptors. Compared with large arterioles, small arterioles exhibited greater peak and steady-state constriction at all frequencies, with maximal responses achieved over the 0.5-4 Hz range. Large arterioles exhibit graded constriction over the entire frequency range. Sympathetic escape exhibited a small, negatively correlated frequency dependence for large arterioles, tended to be greater for small arterioles, and was more evident in large arterioles during alpha 2-adrenoceptor constriction at low-frequency stimulation. This distinct neural control of large resistance vessels by alpha 1-adrenoceptors and small terminal arterioles by alpha 2-adrenoceptors may allow neurogenic regulation of these vessel segments to be differentially susceptible to modulation by other extrinsic and intrinsic vasoactive controls that preferentially interact with alpha 1- and alpha 2-adrenergic contractile mechanisms.

Animals

[Quantitative evaluation of acute myocardial infarction by In-111 antimyosin Fab myocardial imaging].

For quantitative evaluation of acute myocardial infarction, In-111 antimyosin Fab myocardial imaging (InAM) was performed in 17 patients with myocardial infarction who underwent Tl-201 (TL) and Tc-99m pyrophosphate (PYP) myocardial imaging in acute phase. For calculating the infarct size, voxel counter method was used for analysis in PYP and InAM, and extent and severity score were used on bull's-eye polar map in TL. The most appropriate cut-off level ranged from 65 to 80% by the fundamental experiment using cardiac phantom. The cut-off level of 0.70 (InAM) and 0.65 (PYP) were used for clinical application of voxel counter analysis. The infarct size calculated by InAM and PYP was compared with wall motion abnormality index by echocardiography (WMAI), TL extent score, TL severity score, peak CK and sigma CK. Infarct size by InAM showed the following correlations with other indices. PYP: r = 0.26 (ns), TL extent score: r = 0.72 (p less than 0.01), TL severity score: r = 0.65 (p less than 0.05), WMAI: r = 0.69 (p less than 0.05). The infarct size by PYP did not show any correlations with these indices. Therefore, the infarct size by InAM showed better correlations with TL and WMAI than that of PYP. So InAM was considered superior to PYP for quantitative evaluation of acute myocardial infarction.

Aged

[Coronary revascularization evaluated by thallium-201 myocardial scintigraphy: a follow-up study].

To elucidate changes with time in T1-201 scintigraphy after coronary revascularization, T1-201 stress myocardial scintigraphy was performed at least twice during the follow-up period (from one to 12 months) in 58 patients with ischemic heart disease (12 with angina, and 46 with myocardial infarction) who had undergone PTCA or A-C bypass surgery. The perfusion defects were classified in 4 grades, and scintigraphic changes over grade 1 were judged significant. We evaluated; 1) time of scintigraphic improvement after revascularization, 2) presence of reverse redistribution, and 3) assessment of coronary restenosis. Scintigraphic improvement was observed in 21 of 58 patients during a 3- to 12- month follow-up period, 7 of whom improved within one month. Reverse redistribution after coronary revascularization was observed in 8 of the 58 patients (14%), including 6 who showed scintigraphic improvement in 3 to 12 months (2 were not examined). Among 29 patients whose coronary angiogram and Tl-201 scintigram were compared, 11 had angiographic evidence of restenosis and 4 of them showed deterioration of scintigraphic findings (sensitivity 57%, specificity 68%, and accuracy 66%). In conclusion, scintigraphic improvement was observed over various periods (immediately after and up to 12 months) after coronary revascularization. Reverse redistribution appears to be a predictor of good prognosis. Coronary restenosis cannot always be reliably assessed by Tl-201 scintigraphy.

Adult

[Diagnostic utility of 111In-antimyosin Fab scintigraphy in acute myocardial infarction: comparison with 201Tl and 99mTc-pyrophosphate myocardial scintigraphy].

To assess the diagnostic accuracy, extent, and characteristics of 111In-antimyosin Fab scintigraphy (In-AM) in acute myocardial infarction (AMI), we studied In-AM in 17 patients with AMI and compared with In-AM, 99mTc-PYP and 201Tl scintigraphy. Intensity of In-AM uptake was classified into 3 grades. Fourteen of 17 patients (82%) showed positive uptake of In-AM. The locations of infarct area diagnosed by In-AM were in accordance with those by electrocardiography. There was a good correlation between the extent score of In-AM planar and that of SPECT (r = 0.72), In-AM SPECT and Tl SPECT (r = 0.79), In-AM planar and PYP planar (r = 0.92), In-AM SPECT and PYP SPECT (r = 0.76), respectively (p less than 0.01). Thus, In-AM is a useful method for diagnosis of AMI.

Adult

[Exercise tolerance in patients after successful percutaneous transluminal coronary angioplasty].

In 32 patients with successful percutaneous transluminal coronary angioplasty (PTCA), we performed treadmill exercise tests (TMET) before and about one month after PTCA to assess the correlation between the improvement in coronary artery lesions and exercise tolerance. Either the Bruce protocol (B: n = 12) or the modified Bruce protocol (MB: n = 20) was used; with the latter being applied to patients whose cardiac function seemed depressed. In 15 patients, oxygen consumption (VO2) was measured by analyzing the expired gases, 13 patients underwent exercise thallium-201 myocardial perfusion scintigraphy before and after PTCA, whose results were compared with those of TMET. In both B and MB protocols, the treadmill walking time was significantly prolonged after PTCA, compared to that before PTCA (B: 7.4 +/- 1.3 vs 9.5 +/- 1.9, MB: 11.4 +/- 3.5 vs 12.7 +/- 3.5 min). Heart rates (HR) and rate pressure products (RPP) were significantly increased after PTCA in both protocols (HR B: 139 +/- 18 vs 154 +/- 17, MB: 121 +/- 20 vs 137 +/- 19 bpm, RPP B: 26,500 +/- 5,600 vs 30,300 +/- 6,700, MB: 19,400 +/- 6,200 vs 22,700 +/- 6,600 mmHg.bpm), however, systolic blood pressure did not change significantly after PTCA in either protocol. While there was a significant improvement in VO2 after PTCA (21.6 +/- 6.3 vs 25.7 +/- 4.2 ml/kg/min), the O2-pulse remained unchanged. Thallium-201 myocardial scintigraphy revealed improvement of myocardial perfusion in 8 of the 13 cases examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult