The authors investigated, in vivo, the effects of four vasodilators on venous tone in dogs. Baseline venous tone was determined from the pressure: diameter relationships in the inferior vena cava (VSIVC) and femoral vein (VSFV) as measured during several seconds of occlusion of the proximal inferior vena cava. All of the slopes were nearly linear. All vasodilators were administered in dosages sufficient to lower blood pressure by approximately 20%; these dosages also decreased systemic vascular resistance by 15% to 30%. Isosorbide dinitrate reduced VSIVC from 7.17 +/- 0.81 to 5.81 +/- 0.73 mmHg/mm and VSIVC from 59.4 +/- 13.5 to 37.2 +/- 6.6 mmHg/mm. Neither nifedipine nor nisoldipine altered VSIVC or VSFV. However, prazosin decreased VSIVC from 13.2 +/- 3.3 to 10.7 +/- 2.7 mmHg/mm and VSFV from 43.5 +/- 11.3 to 29.9 +/- 8.8 mmHg/mm. These results suggest that isosorbide dinitrate and prazosin decrease venous tone in vivo, whereas nifedipine and nisoldipine do not.
For the analysis of regional myocardial function, the measurement of regional myocardial surface area (RMA) was performed on the epicardial surface of myocardial segment lengths in a direction parallel to the superficial myocardial fibers (SLa) and at right angles to the first (SLb). In eight anesthetized dogs with opened-chests, measurements were done during a 60 s left anterior descending coronary artery occlusion and reperfusion. In the ischemic region, coronary occlusion resulted in dyskinesis in RMA, and the reduction of it during the ejection phase (ERA) decreased significantly at 10 s (p less than 0.05) and thereafter (p less than 0.01). Regional myocardial work (EWA) from the pressure-area loops during the ejection phase also decreased significantly at 10 s (p less than 0.05) and thereafter (p less than 0.01). The end-diastolic RMA (EDRMA) increased significantly at 30 s (p less than 0.01) and thereafter (p less than 0.01). In the non-ischemic region, compensatory changes were shown, namely ERA, EWA and EDRMA, increased significantly during occlusion. After reperfusion, recovery to the control level was prompt, and only EDRMA remained the increased value after 30 s (p less than 0.01). Between SLa and SLb, characteristics differed from each other, which suggested that the directional differences of SLs should be considered when regional myocardial function is assessed from unidirectional SL. The changes in RMA reflect both changes of SLa and SLb during coronary occlusion and reperfusion, and were more marked than each SL. Thus, the usefulness of RMA to assess regional myocardial function was demonstrated during coronary occlusion and reperfusion.
Unruptured asymptomatic intracranial aneurysms bleed at a rate of not less than 3% per year, with a mortality rate exceeding 50% per hemorrhage. Three-dimensional magnetic resonance angiography (3D-MRA) is able to depict the intracranial artery noninvasively and without using contrast media. The authors used 3D-MRA in 20 patients, (10 women, 10 men) with nausea, vomiting, and headache with hypertension to rule out intracranial aneurysm at same time brain computed tomography (CT) was performed. In this study, cases of subarachnoid hemorrhage (SAH) diagnosed by CT were excluded. Of 20 patients, only 1 was suspected to have intracranial aneurysm despite a normal-appearing CT, and this was confirmed by cerebral angiography. Two cases were suspected at the horizontal view of MRI; however, these were excluded by 3D-MRA. The authors began this study after finding the unruptured case, and are continuing it. The incidence thus is 5% so far. Discovering unruptured intracranial aneurysms is important for reducing the death rate from SAH, and 3D-MRA is useful for screening patients suspected of having aneurysm.
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