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C W White

Publications and source records attributed to C W White.

At least 109 records · Page 6Linked to original sources

O2 metabolite-mediated injury in perfused kidneys is reflected by consumption of DMTU and glutathione.

The contribution of toxic oxygen (O2) metabolites to ischemic renal injury is unclear because they have not been added directly to the kidney and few ways exist to effectively measure and assess the effect of these highly reactive products in biological systems. Our goal was to determine the effect of hydrogen peroxide (H2O2) or H2O2-derived products on renal function and to determine whether H2O2-mediated renal injury was reflected by consumption of dimethylthiourea (DMTU) (an exogenous O2 metabolic scavenger), depletion of renal cortical total glutathione (an endogenous O2 metabolite scavenger), and/or adenosine triphosphate (ATP). We found that addition of glucose oxidase (GO) or H2O2 to isolated perfused rat kidneys caused injury that was manifested by decreases in glomerular filtration rate, perfusion flow rate, and sodium reabsorption and that was prevented by addition of catalase (CAT) (but not inactivated CAT) or large doses of DMTU (15 mM), but not urea (15 mM). To further ascertain if the protective effect of DMTU was due to reacting with a scavenging H2O2, we conducted parallel experiments in which we measured the consumption of smaller doses of DMTU (1 mM) in kidneys perfused with GO or H2O2. We found that addition of increasing concentrations of H2O2 decreased DMTU concentration. Renal cortical total glutathione and ATP levels were also decreased by addition of GO or H2O2. In contrast to perfusion with GO or H2O2, perfusion with elastase or collagenase also caused renal injury and decreases in ATP but did not decrease DMTU concentration or tissue total glutathione. We conclude that H2O2 or H2O2-derived products are acutely toxic to the kidney and that decreases in perfusate DMTU concentration and tissue total glutathione, but not tissue ATP, may be useful for specifically assessing the presence and/or toxicity of H2O2 in renal and other biological systems.

Adenosine Triphosphate↗

Prediction of the physiologic significance of coronary arterial lesions by quantitative lesion geometry in patients with limited coronary artery disease.

Studies in animals with normal coronary arteries have shown that coronary flow reserve can be predicted by angiographic measurements of arterial stenosis. Studies in man, however, suggest that even quantitative analysis of coronary angiograms cannot predict the physiologic significance of individual coronary lesions. These studies, however, were carried out in patients with either widespread, diffuse coronary artery disease or by measurement techniques that tend to underestimate maximal coronary flow reserve. To determine the relationship between coronary arterial stenosis and coronary flow reserve (CFR) in patients with discrete limited coronary atherosclerosis, we studied 50 patients with a single discrete coronary stenosis in only one or two vessels. The minimum coronary arterial cross-sectional area (mCSA), percent area stenosis (%AS), and percent diameter stenosis in the left and right anterior oblique projections were determined by the Brown/Dodge method of quantitative coronary angiography. A No. 3F coronary Doppler catheter was placed immediately proximal to the lesion. Measurements of CFR were obtained by intracoronary administration of papaverine in doses sufficient to provide maximal arteriolar vasodilation. In 25 patients, a translesional pressure gradient was obtained with an angioplasty catheter. CFR measured in patients with coronary artery disease was compared with that in 13 patients with normal coronary vessels. In normal patients, CFR averaged 5.0 +/- 0.6 (peak/resting velocity ratio; mean +/- SEM, range 3.7 to 8.2). In patients with limited coronary artery disease, CFR was closely correlated with %AS (r = .85), mCSA (r = .79), and the translesional pressure gradient (r = .83). Additionally, the most severe percent diameter stenosis in either the left or right anterior oblique view was also highly correlated with CFR (r = .82). Importantly, all arteries with lesions producing less than 70% area stenosis and less than 50% diameter stenosis, or with greater than 2.5 mm2 mCSA had CFR of over 3.5. These results suggest that, in contrast to the poor correlation of percent area and percent diameter stenosis to CFR measured in patients with multivessel coronary artery disease, CFR measured at angiography in patients with discrete, limited coronary artery disease correlates closely with luminal stenosis determined precisely with quantitative coronary angiography. Differences in the extent of diffuse arterial narrowing may account for these discrepancies.

Blood Pressure↗

The importance of the determination of the myocardial area at risk in the evaluation of the outcome of acute myocardial infarction in patients.

On the basis of animal studies, we postulated that the size of the perfusion field (risk area) of an occluded coronary artery would be an important determinant of outcome in patients with acute myocardial infarction. To test this hypothesis, we measured size of the risk area in 27 patients with acute myocardial infarction by the intracoronary injection of 99mTc-macroaggregated albumin and gated nuclear imaging. After injection of the albumin spheres (5.3 +/- 1.4 hr after the onset of chest pain) streptokinase was administered and in 16 of 27 patients (59%) effective thrombolysis was achieved. Since none of the patients had evidence of a prior acute myocardial infarction, the 3 day nuclear left ventricular ejection fraction (LVEF) was considered an index of infarct size. Response to thrombolysis was analyzed according to success or failure of reperfusion and the size of the risk area (small risk area less than 25%, large risk area greater than 25% of left ventricular surface area). Standard clinical indexes correlated poorly with size of the risk area: electrocardiographic variables (r = .37), left ventricular end-diastolic pressure (r = .23), cardiac index (r = .55), and the LVEF obtained from a right anterior oblique contrast ventriculogram (r = .31). The coronary vessel responsible for the acute myocardial infarction significantly influenced size of the risk area (left anterior descending, 38 +/- 5% [mean +/- SD] vs circumflex or right coronary artery, 17 +/- 4%). However, knowledge of the site of coronary occlusion within a vessel was not helpful in predicting the size of the area at risk.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗

Methods of measurement of myocardial blood flow in patients: a critical review.

During the past decade, major progress has been made in the evolution of technology directed toward the accurate measurement of regional myocardial perfusion in patients. The deficiencies of some of the older methods (thermodilution and gas clearance) are better appreciated and improved approaches (Doppler catheters, positron-emission tomography, and digital subtraction angiography) have been developed. The new approaches should play a major role in research and for most applications the older methods will gradually be replaced. Efforts to bring these new methods to community hospitals and practicing cardiologists should be stimulated. Doppler catheters, positron-emission tomography, and digital-subtraction angiography are commercially available and Doppler catheters and digital-subtraction angiography could be easily incorporated into routine cardiac catheterization procedures. The Doppler catheter is the most inexpensive and probably the simplest to apply. In our opinion, routine measurements of coronary flow reserve will significantly improve the care of patients with coronary obstructive disease and other diseases that impair myocardial perfusion. If coronary reserve measurements are used frequently, patient selection for coronary angioplasty and bypass surgery will no longer depend entirely on visual assessment of percent diameter stenosis, a very poor criterion in many situations. Also, patients with chest pain syndromes, normal coronary vessels, and impaired coronary reserve will be identified and perhaps some effective treatment for this condition will be devised.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorptiometry, Photon↗

Does coronary artery bypass surgery restore normal maximal coronary flow reserve? The effect of diffuse atherosclerosis and focal obstructive lesions.

Aortocoronary vein bypass surgery might not restore normal maximal coronary flow reserve to bypassed coronary vessels because residual diffuse coronary atherosclerosis might limit maximal hyperemia. To investigate the effect of diffuse atherosclerosis and a focal stenosis at the graft-coronary anastomosis, we measured coronary flow reserve with an extensively validated subselective Doppler catheter in 24 patients with 35 bypass grafts perfusing angiographically normal coronary vessels. The Doppler catheter was positioned in the midportion of the graft, and coronary flow reserve was measured as the peak/resting velocity ratio after selective graft injection of a maximally vasodilating dose of papaverine. Luminal dimensions of the bypass graft, graft-coronary insertion, and bypassed coronary vessel were measured by quantitative coronary angiography (Brown/Dodge method). Measurements of coronary flow reserve and coronary dimensions of vein bypass grafts were compared with similar measurements obtained from 13 patients with normal coronary vessels and normal myocardium. Seventeen of the 35 bypass grafts perfused unobstructed coronary-vein graft anastomoses (less than 50% area stenosis) and normal myocardium. The coronary flow reserve of these 17 bypass grafts was normal (5.0 +/- 0.4, mean +/- SEM) and not significantly different from that measured in normal arteries (5.1 +/- 0.6), even though the cross-sectional area of the native coronary artery just distal to the bypass insertion was 40% smaller than in matched normal vessels. Bypass grafts perfusing hypertrophied (n = 2) or infarcted (n = 6) myocardium had significantly reduced coronary flow reserve compared with normal vessels (2.7 +/- 0.3; p less than .01), even when the infarcted wall had only minimal hypokinesis.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗

Recombinant tumor necrosis factor/cachectin and interleukin 1 pretreatment decreases lung oxidized glutathione accumulation, lung injury, and mortality in rats exposed to hyperoxia.

Single, preexposure, parenteral injection with both recombinant tumor necrosis factor/cachectin (TNF/C) and interleukin-1 (IL-1) prolonged the survival of rats (144 +/- 9 h) in continuous hyperoxia (greater than 99% O2 at 1 atm) when compared with rats injected with boiled TNF/C and boiled IL-1 (61 +/- 2 h), TNF/C alone (61 +/- 2 h), IL-1 alone (62 +/- 2 h), or saline (64 +/- 3 h). After exposure to hyperoxia for 52 h, pleural effusion volume, pulmonary artery pressure, total pulmonary resistance, and lung morphologic damage were decreased in those rats given TNF/C and IL-1 as compared with saline-injected rats. In parallel, ratios of reduced (GSH) to oxidized (GSSG) glutathione were greater (P less than 0.05) in lungs of TNF/C + IL-1-injected rats (91 +/- 20) than of saline-injected rats (30 +/- 4) that had been exposed to hyperoxia for 52 h. No differences were found in superoxide dismutase, glutathione peroxidase, glutathione reductase, glucose-6-phosphate dehydrogenase, or catalase activities in lungs of TNF/C + IL-1- or saline-treated, hyperoxia-exposed rats. Our results indicate that pretreatment with TNF/C and IL-1 favorably altered lung glutathione redox status, decreased lung injury, and enhanced survival of rats exposed to hyperoxia.

Animals↗

Measurement of maximal coronary flow reserve: a technique for assessing the physiologic significance of coronary arterial lesions in humans.

Recent studies suggest that angiographic measurements of coronary arterial stenosis are poorly correlated with direct measurements of the capacity of the artery to conduct hyperemic blood flow. Direct measurement of coronary blood flow and the flow reserve capacity of individual coronary vessels in conscious humans, however, has been hampered by methodologic limitations. We have developed and validated a coronary Doppler catheter capable of subselectively measuring coronary blood flow velocity at the time of cardiac catheterization. Studies in seven calves demonstrated that measurements of the change in coronary blood flow velocity assessed using the Doppler catheter were highly correlated with simultaneous measurements of the change in coronary sinus blood flow (r = 0.97, slope = 1.06) and changes in blood flow velocity assessed using an epicardial Doppler probe (r = 0.95, slope = 1.04). Additional studies demonstrated that the catheter did not produce physiologically significant obstruction to coronary blood flow. Subsequent studies in 215 humans undergoing catheterization have shown that acceptable signals of phasic coronary blood flow velocity could be recorded in 176 patients. Subsequent dose response kinetic studies demonstrated that intracoronary administration of papaverine can rapidly produce maximal coronary hyperemia, equivalent in magnitude to intravenous dipyridamole, but short enough in duration to permit multiple measurements of coronary flow reserve during a single catheterization. Measurements of coronary flow reserve in patients with obstructive coronary artery disease have permitted characterization of the physiologic significance of individual obstructive coronary lesions. The development of this coronary Doppler catheter system and technique for measurement of maximal coronary flow reserve should facilitate characterization of the physiologic impact of coronary arterial lesions on coronary blood flow and studies of the coronary circulation in conscious humans.

Animals↗

Coronary obstructive lesions: assessing their physiological significance in humans.

For more than two decades cardiologists and cardiac surgeons have estimated the physiologic significance of coronary lesions by measuring percent stenosis of the obstructive vascular segment from coronary angiograms. Such measurements, when performed without computer-based analysis, are associated with substantial variability between observers, as well as within a single observer. In addition, recent intraoperative measurements of coronary reserve in individual obstructed vessels of patients with multivessel coronary disease performed with a suction Doppler probe indicate that, in the intermediate range (10% to 90% diameter stenosis), percent stenosis measurements of coronary lesions by angiography correlates poorly with coronary reserve. These studies suggest that the physiologic significance of coronary obstructions cannot be accurately assessed by visual interpretation of coronary angiograms. More sophisticated and accurate approaches are needed for assessing the physiologic significance of coronary obstructions preoperatively.

Coronary Disease↗

Effects of acute atrial fibrillation on the vasodilator reserve of the canine atrium.

Acute atrial fibrillation appreciably alters atrial physiology by increasing atrial blood flow and atrial oxygen consumption. To determine the effects of atrial fibrillation on atrial vasodilator reserve atrial fibrillation was produced in dogs by electrical atrial stimulation. Reactive hyperaemic responses were measured using Doppler crystals fixed to the sinus node artery and to an adjacent right ventricular branch artery during sinus rhythm, after 20 minutes of atrial fibrillation, and after systemic administration of chromonar (a potent coronary dilator) during atrial fibrillation. During sinus rhythm the peak to resting blood flow velocity ratio after a 20 s occlusion of the sinus node artery was 3.2(1) (mean(SEM)). A 20 s occlusion of a right ventricular branch artery during sinus rhythm resulted in a significantly larger response (5.9(0.7). The repayment to debt area ratio in response to a 20 s occlusion was 1.1(0.2) for the sinus node artery but 3.9(1.0) for a right ventricular branch. During atrial fibrillation the peak to resting velocity ratio was substantially decreased in the sinus node artery (2.3(0.6)) but was not significantly changed in the right ventricular branch (4.4(0.6)). Atrial fibrillation plus chromonar abolished reactive hyperaemia in both the sinus node artery and the right ventricular branch vessel. Right atrial blood flow (microspheres) increased from 45(4) in sinus rhythm to 106(19) ml X min-1 X 100 g-1 in atrial fibrillation and to 208(22) ml X min-1 X 100 g-1 after chromonar administration during atrial fibrillation. Thus the quantitative characteristics of coronary reactive hyperaemia in the right atrium were substantially different from those in the right ventricle.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Multi-flash campimetry as an indicator of visual field loss in glaucoma.

Multi-flash campimetry is a computer-implemented technique used for the rapid assessment of temporal resolving power across the visual field. On the basis of previous reports that glaucoma patients exhibit impaired temporal sensitivity earlier than conventional perimetric field loss, the question of whether multi-flash campimetry might also be sensitive to the visual consequences of glaucoma was explored. Of the 27 patients that were tested, only one had normal temporal resolving power in both eyes, suggesting that multi-flash campimetry might be a useful aid in determining whether a patient should be diagnosed and treated as a glaucoma suspect or as a confirmed glaucoma patient.

Adult↗

Ultraviolet effects on visual acuity in pseudophakia.

Two experiments investigated visual acuity deficits in the presence of ultraviolet (UV) light after implantation of an acrylic intraocular lens (IOL). In Experiment 1, six pseudophakes exhibited a statistically significant acuity decrement of 0.5 min arc or about one line on an eye chart illuminated by light having an UV component. In Experiment 2, the vernier acuity of six pseudophakic observers decreased by 0.6 min arc, but the vernier acuity of six phakic observers, with crystalline lenses intact, was not affected significantly by UV illumination. Both experiments provide evidence that UV light decreases pseudophakic visual acuity, perhaps by chromatic aberration. These results suggest that including UV filters in IOL's could permit pseudophakic observers to use their vision more effectively.

Aged↗

Failure of pyruvate to salvage myocardium after prolonged ischemia.

Thrombolytic therapy for acute coronary occlusion may be more effective if combined with substrate-enhanced reperfusion. In this study, we examined the utility of pyruvic acid, an important metabolic substrate, in salvaging ischemic myocardium. Twenty-six anesthetized dogs underwent 3 h of circumflex coronary occlusion followed by 90 min of reperfusion with administration of intracoronary pyruvate or vehicle. To test the sensitivity of the model in detecting differences in infarct size, eight additional dogs underwent coronary occlusion of shorter duration (45 min), an intervention that is known to reduce infarct size. Collateral perfusion to the ischemic zone during coronary occlusion was similar in experimental and control groups. Whereas a shorter duration of occlusion (45 min) decreased the infarct-to-risk area ratio by 54% compared with a longer duration of occlusion (90 min), neither early (15 min prior to occlusion) nor late (3 h after occlusion) onset of intracoronary infusion of pyruvate shifted the infarct-risk relationship (control: y = 74x - 8.7, r = 0.99; early infusion: y = 0.76x - 9.5, r = 0.85; late infusion: y = 0.58x - 5.5, r = 0.79). The failure of intracoronary administration of pyruvate to limit infarct size raises questions as to its potential clinical utility in the setting of acute myocardial ischemia.

Animals↗

Alterations in ventricular excitability in conscious dogs during development of chronic heart failure.

Arrhythmias in patients with heart failure may result from altered electrophysiological properties of the myocardium. To examine changes in ventricular excitability during cardiac failure and to relate these changes to ventricular structural and neurochemical abnormalities, right ventricular failure was produced in dogs by pulmonary artery banding and by creating tricuspid regurgitation. Right and left ventricular excitability thresholds were tested biweekly in heart failure (HF) and sham-operated conscious dogs by means of strength-duration curves (1-40 ms) at basic cycle lengths (BCL) of 300-500 ms until time of death (21-188 days). Marked increases in the excitability threshold of the right ventricle occurred in HF (mean maximum % increase, 205 +/- 42 at BCL 500 ms). Smaller, though significant increases in the left ventricular excitability threshold in HF were also seen (mean maximum % increase 103 +/- 36 at BCL 500 ms). Increases in the excitability threshold of the left as well as the right ventricles occurred, even though ventricular dilation (2-D Echo) was confined to the right ventricle. The time course of changes in the excitability threshold was variable (maximum occurrence at 21 +/- 3 days right ventricle, 23 +/- 11 days left ventricle). Tyrosine hydroxylase activity and norepinephrine content of the right ventricle were markedly depleted at death, when the excitability threshold was high. Similar though nonsignificant trends in reductions of these sympathetic neurochemicals were seen in the left ventricle. Levels of choline acetyltransferase and QNB binding in both ventricles were unaffected.

Animals↗

Dimethylthiourea decreases acute lung edema in phorbol myristate acetate-treated rabbits.

Treatment with dimethylthiourea (DMTU), a potent O2 metabolite scavenger, prevented neutrophil-mediated acute edema in lungs of rabbits given phorbol myristate acetate (PMA) and in isolated rabbit lungs perfused with neutrophils and PMA. DMTU-treated rabbits given PMA did not increase their lung weight-to-total body weight ratios (5.0 +/- 0.3) or lung lavage albumin concentrations (14 +/- 4.6 mg/dl) in comparison to untreated rabbits given PMA (6.6 +/- 0.5 and 60 +/- 10 mg/dl, respectively). Similarly, DMTU-treated isolated rabbit lungs perfused with neutrophils and PMA did not gain weight (0 g) or increase their lavage albumin concentrations (82 +/- 17 mg/dl) in comparison to untreated lungs perfused with neutrophils and PMA (71 +/- 3.1 g and 1,299 +/- 47 mg/dl, respectively). DMTU did not appear to decrease edema by preventing increases in pulmonary arterial pressures (PAP). First, treatment with DMTU did not decrease initial PAP increases in rabbits given PMA. Second, even though addition of DMTU attenuated PAP increases in isolated lungs perfused with neutrophils and PMA, DMTU-treated isolated lungs did not develop acute edema when subjected to mechanical increases in venous outflow pressures. The mechanism by which DMTU decreases lung edema is unclear but may involve scavenging of toxic O2 metabolites, since DMTU also decreased hydrogen peroxide (H2O2) and hydroxyl radical (OH) concentrations in in vitro mixtures containing neutrophils and PMA.

Acute Disease↗

O2 metabolites and neutrophil elastase synergistically cause edematous injury in isolated rat lungs.

Addition of glucose oxidase (GO) increased H2O2 concentrations and decreased antielastolytic activities of beta-D-glucose containing perfusates of isolated rat lungs. Pretreatment with GO also caused acute edematous injury (increased lung weight gains, increased recovery of Ficoll in lung lavages, and increased pulmonary arterial pressures) in isolated lungs perfused with purified human neutrophil elastase (NE). Acute edematous injury in isolated lungs pretreated with GO and then NE exceeded levels found in lungs following addition of GO or NE alone or NE before GO. Simultaneous addition of catalase (an H2O2 scavenger) or methoxy-succinyl-L-alanyl-L-alanyl-prolyl-L-valine-chloromethyl ketone (an NE inhibitor, but not aminotriazole-inactivated catalase, N-tosyl-L-phenyl-alanine chloromethyl ketone (a chymotrypsin inhibitor) or N-alpha-p-tosyl-L-lysine chloromethyl ketone (a trypsin inhibitor), prevented acute edematous injury in isolated lungs perfused with both GO and NE. This observation indicated that injury was dependent on both H2O2 and NE, especially since the relative inactivating specificities of the inhibitors for H2O2 or NE, respectively, were confirmed under similar conditions in vitro. The synergistic nature of the interaction between H2O2 and NE-mediated injury was further clarified when GO- and NE-induced lung injury was prevented by addition of an oxidant-resistant NE inhibitor (Eglin-C), but not an oxidant-sensitive NE inhibitor (human alpha 1-protease inhibitor, alpha 1PI). Moreover, treatment with H2O2 also decreased the ability of alpha 1PI but not Eglin-C to decrease NE activity in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Quantitative angiographic morphology of coronary stenoses leading to myocardial infarction or unstable angina.

Identification of a characteristic morphology of a coronary stenosis likely to result in myocardial infarction would facilitate the prospective evaluation of infarct prevention strategies and identification of high-risk patients. We postulated that coronary lesions associated with recent myocardial infarction or unstable angina would have an angiographic morphology suggesting disruption of an atherosclerotic plaque and would appear morphologically different from lesions associated with chronic stable angina. To test this hypothesis, quantitative coronary angiography (Brown-Dodge method) was performed in 15 patients 4 to 30 days after myocardial infarction, in 10 patients with the abrupt onset of unstable angina and single-vessel coronary disease, and in 15 patients with chronic stable angina without prior myocardial infarction. Serial arterial diameters (20 to 40) within each lesion were determined and the degree of luminal irregularity was quantitated by calculation of an "ulceration" index. The majority of all lesions analyzed resulted in severe luminal stenosis (mean 78% area stenosis, all groups). Despite small differences in mean lesion severity among groups, overlap in the degree of luminal compromise prevented precise classification of lesions associated with myocardial infarction or unstable angina based on percent stenosis or minimum luminal cross-sectional area. The mean ulceration index of lesions in patients with unstable angina and in the infarct-related vessel in those with acute myocardial infarction was 0.62 +/- 0.05 (+/- SEM) and 0.61 +/- 0.03, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Angina, Unstable↗

Intracoronary papaverine: an ideal coronary vasodilator for studies of the coronary circulation in conscious humans.

An ideal coronary vasodilator for studying coronary flow reserve in humans would rapidly produce maximal coronary vasodilation, be short acting to permit repeated measurements, and not alter systemic hemodynamics. The two commonly used vasodilators (dipyridamole and meglumine diatrizoate) do not satisfy these criteria; meglumine diatrizoate does not produce maximal hyperemia and dipyridamole has a long duration of effect (greater than 30 min). In this study we used a subselective coronary Doppler catheter to measure the dose-response kinetics of a shorter acting vasodilator, intracoronary papaverine. In 10 patients with normal coronary vessels, the maximal vasodilator response to papaverine was compared with that to intravenous dipyridamole (0.56 mg/kg infused over 4 min) and intracoronary meglumine diatrizoate. The increase in coronary blood flow velocity after the maximal dose of papaverine (4.8 +/- 0.4 peak/resting velocity ratio, mean +/- SEM) was nearly identical to that seen after infusion of dipyridamole (4.8 +/- 0.6) and was significantly greater than that after meglumine diatrizoate (3.1 +/- 0.2, p less than .01). At maximal hyperemia, mean arterial blood pressure fell 9 +/- 2% (mean +/- SEM) after intracoronary papaverine, 8 +/- 4% after dipyridamole, and 3 +/- 3% after meglumine diatrizoate. The dose-response kinetics of intracoronary papaverine were studied in 13 patients with normal coronary arteries. In the left coronary artery, maximal vasodilation (5.4 +/- 0.6) was achieved with 8 mg in six of eight patients and with 12 mg in all patients. In the right coronary artery, maximal vasodilation (4.8 +/- 0.7) was achieved with 6 mg in four or five patients and with 8 mg in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗