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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Digital subtraction angiography (DSA) has been confirmed to be an accurate method for determining left ventricular function. It is a relatively non-invasive technique without inducing premature ventricular complexes. The response of left ventricular function to afterload stress was assessed using DSA for eight patients with old anterior myocardial infarction and ventricular aneurysm including that of the anterior wall (averaging 30.3 months after the acute episodes). Their ages ranged from 36 to 65 years and one patient was a woman. Prior to the investigation, we confirmed that a single DSA procedure did not alter left ventricular function in a pilot study of one patient (No. 8). After initial DSA in the basal state, methoxamine was infused intravenously (1 to 2 mg/min). When aortic systolic blood pressure increased by 30 to 50 mmHg, a second DSA was performed for each patient. Left ventricular volumes and ejection fractions were calculated by the area-length method, and regional wall motion was assessed by the visual method according to the AHA classification and the curvature radius of the apical ventricular aneurysm was calculated. Methoxamine induced neither acute heart failure nor angina pectoris in the present series. The heart rates decreased, and there were a significant increase in end-systolic volumes (p less than 0.05), end-systolic radii (p less than 0.05), and a significant decrease in ejection fractions (p less than 0.02) after methoxamine infusion. In 32 of 40 segments, regional wall motion was unchanged by methoxamine as assessed by the visual method; whereas, in the other eight, there was a deterioration.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Functional reserve of the ischemic left ventricle with ventricular aneurysm to afterload stress: digital subtraction angiographic assessments]. 391 6

Currently, considerable clinical interest exists in the vasoactivity of large coronary arteries due to the prevalence of coronary vasospasm in mediating angina pectoris and even myocardial infarction. Although arterial elastic properties have been studied extensively in acute, anesthetized animal experiments and in vitro preparations, few data are available on these properties in conscious, chronically instrumented animals, where the complicating influences of anesthesia, recent surgery, and acute manipulation of the vessel are minimized. To study vascular smooth muscle in the conscious animal we modified the transit-time dimension measurement technique by designing smaller, higher frequency (7 MHz) transducers, and introducing electronic refinements to accurately measure smaller dimensions (2 mm minimum). We applied this technique to the left circumflex coronary (LCC) artery, along with arterial pressure measurements from either chronically implantable strain-gauge manometers, or microtip catheter manometers, to study dynamic compliance and vascular control mechanisms of these arteries for periods of months in conscious, chronically instrumented animals. Infusion of an alpha-adrenergic vasoconstrictor, methoxamine (50 micrograms/kg/min), caused sustained reduction in LCC diameter (9% +/- 2%) at a time when mean arterial pressure rose by 65% +/- 5% and heart rate and mean coronary blood flow (electromagnetic flow probe) were returned to control levels. Methoxamine induced a marked leftward shift in the pressure-diameter and stress-radius relationships, reducing vascular caliber for any given stress and pressure level. Moreover, smooth-muscle activation raised the effective incremental modulus (Einc) of the coronary arterial wall when compared at similar radii, but it reduced Einc when compared at similar stress or pressure levels. Thus, for any given arterial pressure level the Einc of the LCC artery wall can be reduced considerably by the enhanced smooth-muscle activation elicited by methoxamine. Nitroglycerin (25 micrograms/kg) induced an initial decrease in LCC diameter as pressure fell and LCC blood flow rose. However, dimensions then increased, reaching a maximum 5 minutes later, when LCC blood flow was reduced, and heart rate and left ventricular dP/dt were at control levels. The calcium-channel antagonist, nifedipine, caused similar early changes, with the increase in LCC caliber persisting for 46 +/- 5 minutes while LCC blood flow returned to control in 15 +/- 3 minutes.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Measurement of arterial pressure-dimension relationships in conscious animals. 644 31