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Biomedical subjects

L C Becker

Publications and source records attributed to L C Becker.

At least 199 records · Page 11Linked to original sources

Conditions for vasodilator-induced coronary steal in experimental myocardial ischemia.

The conditions for coronary steal were determined using the two vasodilators--dipyridamole and nitroglycerin--in anesthetized dogs after ligation of the left anterior descending coronary artery (LAD). Previous studies have shown that when the non-ligated coronary arteries are normal, collateral flow increases after dipyridamole. This study utilized a model in which the distal LAD was ligated and the proximal LAD and left circumflex (LC) arteries were stenosed. Heart rate and blood pressure were kept constant. In 20 dogs, 1-1.5 mg/kg dipyridamole caused a decrease in flow to the ischemic region as measured by radioactive microspheres (0.19 to 0.14 ml/min/g, P = 0.05) while flow increased four-fold to surrounding nonischemic myocardium. The decrease in collateral flow was confined to the epicardial half of the ischemic region (0.26 to 0.14 ml/min/g, P less than 0.001) and was associated with an increase in sigmaST from 30.9 to 44.7 mV (P less than 0.01). In five dogs nitroglycerin, 5 microgram/kg/min, produced no significant changes in collateral flow or flow to other parts of the LV, and sigmaST was unchanged. Vasodilator-induced coronary steal therefore appears to require 1) an arteriolar-type dilator like dipyridamole and 2) stenoses of the arteries supplying collateral flow to the ischemic region. The steal phenomenon is probably caused by a decrease in pressure distal to the stenoses in these vessels, resulting in reduced driving pressure for collateral flow.

Animals↗

Isolated drainage of the superior vena cava into the left atrium in a 52-year-old man: a rare congenital malformation in the adult presenting with cyanosis, polycythemia, and an unsuccessful lung scan.

This report describes a 52-year-old black male with the isolated finding of an anomalous superior vena cava draining into the left atrium. The patient presented with dizziness, mild cyanosis, polycythemia and normal cardiac and pulmonary findings. The first major diagnostic clue in this confusing clinical presentation was an unsuccessful lung perfusion scan in which intravenous tracer consistently bypassed the lungs. This appears to be the first adult presenting with this rare anomaly. This condition should be suspected if cyanosis, clubbing, and a "normal" cardiac examination coexist and if the more common pulmonary and hematological causes of this triad have been excluded.

Cyanosis↗

Effects of intravenous nitroglycerin on left ventricular function and ST segment changes in acute myocardial infarction.

It has been shown previously that 30-minute infusions of intravenous nitroglycerin in patients with acute myocardial infarction are able to lower left ventricular filling pressure and improve left ventricular function while lowering mean arterial pressure by only 7 mmHg (0.9 kPa). A decrease in sigmaST in praecordial ST segment mapping studies during nitroglycerin infusion in patients with anterior infarction suggested a decrease in the extent of myocardial ischaemia. In the present study, 30 patients with acute myocardial infarction received 1- to 3-hour infusions of intravenous nitroglycerin at infusion rates sufficient to lower mean arterial pressure by an average of 22 mmHg (2.9 kPa). An improvement in ventricular function was noted in that subgroup of patients with the msot severe left ventricular dysfunction. All patients with anterior myocardial infarction underwent serial ST segment mapping and, irrespective of the presence or absence of left ventricular failure, showed a decrease in sigmaST during nitroglycerin infusion (P less than 0.005). These findings suggest that infusion of nitroglycerin improves left ventricular function and/or alters left ventricular compliance in patients with left ventricular failure complicating myocardial infarction and furthermore decreases sigmaST in all patients, irrespective of the presence or absence of left ventricular failure, suggesting that the extent of myocardial ischaemia is decreased.

Acute Disease↗

Effect of nitroglycerin and dipyridamole on regional left ventricular blood flow during coronary artery occlusion.

Coronary vasodilators have been variously reported to increase, decrease, or have no effect upon blood flow to ischemic myocardium. Consequently, the effects of two different types of dilators, nitroglycerin (TNG) and dipyridamole, were studied with radioactive microspheres in open-chested dogs after coronary artery ligation. Given as a bolus i.v. injection 0.4 mg TNG resulted in an increase in blood flow to nonischemic areas of myocardium and a preservation of flow to ischemic regions, despite a fall in blood pressure. 5 min later blood pressure and nonischemic flow were back to base line, and a small selective increase in flow to ischemic myocardium was found (0.15-0.18 ml/min per g, P less than 0.05). During an 0.2 mg/min infusion of TNG, and also after 1 mg/kg i.v. dipyridamole, ischemic flow was maintained in the face of a 20-30% reduction in blood pressure. In this setting, nonischemic flow was unchanged during TNG and doubled after dipyridamole. With the addition of methoxamine in both dilator groups, blood pressure returned to base line while flow to ischemic areas increased above base-line values (TNG, 0.16-0.20 ml/min per g, P less than 0.01; dipyridamole, 0.18-0.31 ml/min per g, P less than 0.05). Epicardial ST segment elevations increased during TNG infusion and were unchanged after dipyridamole, but with addition of methoxamine, ST segments became less elevated in both drug groups, concomitant with the observed increase in collateral blood flow. These data indicate that both types of coronary vasodilators, when used in conjunction with methoxamine to support blood pressure, reduce collateral resistance, increase collateral flow, and reduce epicardial ST-segment elevations.

Animals↗

Dipyridamole echocardiography in the detection of vulnerable myocardium in the early postinfarction period.

To evaluate the effect of dipyridamole on regional wall motion after myocardial infarction two-dimensional echocardiograms were obtained on 21 postinfarction patients immediately before and 7 to 10 minutes after the intravenous infusion of ddipyridamole (0.60 mg/kg). All patients underwent coronary angiography, and 20 patients underwent scintigraphy with dipyridamole thallium immediately subsequent to dipyridamole echocardiography. Dipyridamole augmented noninfarct zone regional wall motion in 20 of 31 regions supplied by nonstenotic coronary arteries. In contrast, only one of eight regions of noninfarct zone myocardium supplied by coronary arteries with greater than a 70% luminal diameter narrowing (vulnerable myocardium) was able to augment the regional wall motion subsequent to dipyridamole administration (p = 0.05). Dipyridamole echocardiography appears to be a safe and sensitive technique that may be useful in the detection of vulnerable myocardium in the early postinfarction period.

Adult↗

Granulocyte accumulation in ischemic/reperfused myocardium: assessment with a technetium-99m-labeled antigranulocyte monoclonal antibody in the dog.

This study tested the usefulness of technetium-99m-labeled antigranulocyte monoclonal antibody BW250/183 (AGMAb) for identifying granulocyte accumulation in ischemic/reperfused canine myocardium. In dogs with 90 minutes coronary artery occlusion and 180 minutes reperfusion (n = 8), ischemic/reperfused myocardial samples demonstrated 8.5 +/- 2.4 times more Tc-99m-AGMAb accumulation than nonischemic samples. Dogs given Tc-99m-labeled nonspecific human immunoglobulin instead of Tc-99m-AGMAb (n = 3) had about half as much accumulation (4.5 +/- 1.6, P < .05). Ex vivo myocardial imaging of Tc-99m-AGMAb demonstrated marked uptake in infarcted regions identified by absent triphenyl tetrazolium chloride staining. The amount of uptake was inversely related to the severity of ischemia (determined by radioactive microspheres) and directly correlated with tissue myeloperoxidase activity, a specific marker of granulocyte accumulation. No increase in Tc-99m-AGMAb uptake occurred in dogs with 90 minutes ischemia and no reperfusion (n = 3) or 15 minutes ischemia and 180 minutes reperfusion (n = 2). In conclusion, Tc-99m-AGMAb is taken up in reperfused infarcted myocardium by both nonspecific and specific mechanisms. Because the amount of uptake reflects myocardial granulocyte accumulation, Tc-99m-AGMAb combined with nuclear imaging techniques may be useful for studying inflammatory processes in the heart in experimental animal models and human beings.

Animals↗