We have recently reported that coronary microembolization sustains myocardial ischemia with hyperemic response of coronary blood flow (CBF) induced by massive release of adenosine from the ischemic myocardium. In this study, we tested the hypothesis that this hyperemic flow caused by released adenosine improves myocardial ischemia. In eight dogs (control), microspheres (5.0 X 10(4)/ml of base-line CBF) were repetitively injected until CBF decreased toward zero, and the changes in CBF, fractional shortening, lactate extraction ratio (LER), and adenosine release were studied. In 15 other dogs, an identical procedure was done with an intracoronary infusion of prazosin (4 micrograms.kg-1.min-1, n = 8) or theophylline (0.1 mg.kg-1.min, n = 7) to elucidate the effect of adenosine, since prazosin inhibits release of adenosine from ischemic myocardium and theophylline blocks adenosine receptors. In 16 other dogs, hemodynamic and metabolic parameters were examined with and without these drugs after a single injection of microspheres (1.0 X 10(5)/ml of base-line CBF). In the control group, CBF increased to 170 +/- (SE) 14% of the base-line CBF at 16-30% of maximal embolization. In contrast, intracoronary infusion of prazosin markedly attenuated adenosine release and hyperemic response and significantly deteriorated both fractional shortening and LER. Theophylline also significantly attenuated the hyperemic response and tended to decrease both fractional shortening and LER. A salutary effect of adenosine release was further confirmed by the improvement of ischemic changes in the same dog after withdrawal of prazosin and theophylline associated with an increase in CBF. Thus we conclude that adenosine released from ischemic myocardium improves ischemia in microembolization through the hyperemic response.
The atrial filling fraction (TVIa) was reported to be restricted in patients with severe mitral stenosis more than in those with a relatively large valve area. To determine whether this relation is also the case in an individual when the valve area increased, 13 patients with mitral stenosis were examined before, 5 days and 0.5-1 year after percutaneous transvenous mitral commissurotomy (PTMC). Transmitral flow velocity profiles were examined by the continuous-wave Doppler technique. Five days after PTMC, despite the marked increase in mitral valve area [MVA; from 1.0 ± 0.3 (mean ± SD) to 2.1 ± 0.5 cm^2; p < 0.01], TVIa did not change significantly (from 7.5 ± 1.5 to 8.0 ± 1.6 cm). In the follow-up examination, MVA showed a slight decrease (1.9 ± 0.4 cm^2) while changes in the pressure half time of transmitral flow were various. TVIa did not change in 9 patients while it was augmented in 3 patients and was attenuated in 1 patient. These results indicate that the amplitude of atrial filling fraction is not related to the severity of mitral stenosis, and suggest that it may be affected by the other hemodynamic parameters, such as left atrial and ventricular characteristics of each patient.
JapaneseCiiculationSociety 474were divided into 2 grDups in which systolic LVP decreased grenter than 20t o[ that befoie ligatlon (D group} and dtd not (ND group}.Biochemical analysis of sarcoplasmtc rettculum (SR) and measurements of t ±ssue levels of ATP, lactate and pyruvate were performed togethev wtth ultrastructural observation of anyocardial cells in subendo {Endo) and subepicardial muscles (Epi}.In ischemic myocardium Ca-stimulated ATPase activity and major ATPase of SR, and tissue ATP level greatly decreased, accompanied by an increase in lactate as ±n previous reports.In non-ischemic myocardiurn of D group Ca-stimulated ATPase activity reduced significantly to 55 and 5al of those oi in Endo and Epi, respectively, and u]trastructural changes were iound to be Iittle in non-ischemic myocardial cells of D gioup.These results indtcate that metabolie changes take place in non-ischemic myocardium, especia!ly in Endo, under
The aim of the study was to investigate whether flow velocity profiles of the aorta are related to the severity of aortic valve regurgitation (AR) in patients with diseases of the aorta. Aortic root angiography, abdominal aortic flow velocity measurements by pulsed Doppler method, and regurgitant jet measurements by color Doppler echocardiography were performed in 62 patients with various etiologies of AR and 13 patients without AR. The regurgitant fraction of abdominal aortic flow velocity profiles was related to the angiographic severity of AR except for the patients with Takayasu's arteritis and those after thoracic aorta grafting who showed large regurgitant fraction regardless of AR. Color Doppler evaluation was also correlated well with angiographic findings, but it was not possible in 13 of 62 patients with AR because of the inadequate color Doppler images. Although the observation of abdominal aortic flow profiles is clinically of value in nonin vasive evaluation of AR, it could not be applied in patients with Takayasu's arteritis and those after graft surgery.
To elucidate the effects of coronary thrombolytic therapy in acute myocardial infarction, we observed serially the degree of left ventricular (LV) wall motion immediately after on day 1, and on days 7, 14, 21 and 28 after thrombolytic therapy, in 22 patients with acute anteroseptal myocardial infarction. Base-line coronary arteriography revealed significant lesions in the proximal portions of the left anterior descending artery of all the patients. The patients were categorized according to results of thrombolytic therapy as Group I-a: seven patients with spontaneous or successful recanalization within three hours of onset of chest pain; Group I-b: nine patients with successful recanalization between three and seven hours, with a mean of 4.8 hours from onset; and Group II: six patients in whom thrombolytic therapy was unsuccessful and infarct-related vessels remained totally occluded. The LV wall motion index (WMI) was defined as the sum of point scores for the degrees of regional wall motion at nine segments on serial two-dimensional echocardiograms, and used for quantitative assessments of LV function. Results were as follows: On day 1, immediately after thrombolytic therapy, the WMI of Group I-a was smaller than that of Group II. However, there was no significant difference between Groups I-a and I-b and between Groups I-b and II. These findings suggest that LV function cannot be recovered immediately after recanalization of occluded arteries unless recanalization occurs exceptionally early. Percent improvement of the WMI from days 1 to 28 in Group I-a, 65 +/- 14%, was significantly greater than that in Group I-b, 31 +/- 18%. However, Group II did not show significant improvement in the WMI. The WMI in Group I-a decreased significantly from days 1 to 7 (9.0 +/- 1.6 vs 7.1 +/- 1.8, p less than 0.05); whereas, the WMI in Group I-b showed no significant decrease until day 21. On day 1, the regional wall motion of the antero-apical wall was akinetic or dyskinetic in all patients studied. On day 28, it improved in six of seven patients in Group I-a, while it remained akinetic or dyskinetic in all patients in Groups I-b and II.(ABSTRACT TRUNCATED AT 400 WORDS)
