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Biomedical subjects

M L Marcus

Publications and source records attributed to M L Marcus.

At least 55 records · Page 3Linked to original sources
PubMed1989

Redistribution of coronary microvascular resistance produced by dipyridamole.

This study assessed the redistribution of coronary microvascular resistance during vasodilation produced by dipyridamole. Measurements of microvascular diameter and pressure in the beating left ventricle of anesthetized cats were accomplished by means of a computer-controlled system that enabled measurements in the beating heart. Resistances of coronary arteries, microvessels, and veins were calculated from the quotients of the pressure gradient across each vascular compartment and myocardial perfusion (radioactive microspheres). Administration of dipyridamole increased coronary blood flow from 1.80 +/- 0.09 to 6.42 +/- 0.31 ml.min-1. g-1 (P less than 0.05). During control conditions, 25 +/- 8% of total resistance occurred in coronary arteries (proximal to 170 microns), 68 +/- 8% of total resistance was in coronary microvessels (between arterioles less than 170 microns in diameter and venules less than 150 microns in diameter), and 7 +/- 7% of resistance resided in veins (distal to 150 microns). There was a significant redistribution (P less than 0.05) of resistance in all vessel classes after dipyridamole: coronary arteries constituted 42 +/- 6%, microvessels contained 27 +/- 5%, and veins had 31 +/- 8% of total coronary resistance. During control conditions, vascular resistance in coronary arteries and microvessels was 17 +/- 4 and 45 +/- 6 mmHg.min.g.ml-1, respectively. During vasodilation, resistance was significantly reduced (P less than 0.05) in both the arterial and microvessel segments to 6 +/- 2 and 4 +/- 2 mmHg.min.g.ml-1, respectively. Venous resistance was not significantly affected during dipyridamole-induced vasodilation. In conclusion, there was a marked reduction of coronary vascular resistance in response to dipyridamole, with the major component accounted for by dilation of microvessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Characterization of coronary vasoconstrictor site in medullary reticular formation.

The importance of sympathetic neural influences in regulating coronary blood flow has been well established. However, central nervous system pathways responsible for these effects are largely unknown. In a feline model, we have identified a site in medullary reticular formation that may play a role in neural control of the coronary circulation. Changes in heart rate (HR), mean arterial pressure (AP), Doppler coronary flow velocity (CBFV), and femoral flow velocity (FBFV) were measured in 67 anesthetized cats. Electrical stimulation in a specific region of the right medullary lateral reticular formation produced elevations in HR (12 +/- 2% from 156 beats/min), AP (41 +/- 6% from 83 mmHg), CBFV (33 +/- 7%), and femoral vascular resistance index (136 +/- 27%). After beta-adrenergic blockade (propranolol), a transient (5-15 s) stimulus-induced decrease in CBFV was observed in 67% of animals, with a 55 +/- 6% increase in coronary vascular resistance index, not the result of autoregulation. Ipsilateral stellate ganglionectomy or systemic alpha 1-adrenergic blockade abolished the CBFV decrement. Microinjection of L-glutamate into this medullary region failed to elicit either pressor or coronary vasomotor responses. It is concluded that electrical stimulation in a specific site within medullary reticular formation produces neurogenic coronary vasoconstriction as part of a more generalized activation of central sympathetic fibers. This brain stem site may play an important role in reflex or behaviorally mediated coronary responses.

Adrenergic beta-Antagonists↗
PubMed1989

Coronary dilation with standard dose dipyridamole and dipyridamole combined with handgrip.

Intravenous dipyridamole is widely used to produce coronary vasodilation during cardiac imaging procedures. However, the routinely used dose of dipyridamole (0.56 mg/kg IV over 4 min) does not always result in maximal coronary dilation. The addition of isometric handgrip during dipyridamole coronary dilation has been reported to substantially increase coronary blood flow over dipyridamole alone. We compared the coronary vasodilation resulting from infusion of the standard dose of dipyridamole with that resulting from a maximally dilating dose of intracoronary papaverine in 12 patients with angiographically normal coronary arteries. We also assessed the effect on coronary blood flow velocity of the addition of isometric handgrip during dipyridamole coronary dilation. Changes in coronary blood flow velocity were measured with a 3F coronary Doppler catheter. The coronary flow reserve (peak/resting coronary flow velocity ratio) after dipyridamole (3.7 +/- 1.2 [mean +/- SD] was less than that seen after papaverine (4.4 +/- 0.5, p less than 0.05), and the coronary vascular resistance index during dipyridamole coronary vasodilation (0.28 +/- 0.09) was greater than during papaverine (0.22 +/- 0.03, p less than 0.05). The dipyridamole coronary flow reserve was less than 3.0 in four subjects and was 2.0 or less in two subjects. The addition of isometric handgrip to dipyridamole coronary vasodilation produced an 8% increase in mean heart rate and a 17% increase in mean arterial pressure, but coronary flow reserve was unchanged (3.8 +/- 1.1 before handgrip vs. 4.0 +/- 1.1 with handgrip). Quantitative angiography in six patients revealed no change in coronary caliber with the addition of handgrip.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiography↗
PubMed1989

Vasopressin and the mature coronary collateral circulation.

In isolated vascular rings, we have shown that mature coronary collateral vessels are highly responsive to the vasoconstrictor effects of vasopressin. The purpose of the present study was to determine the effect of concentrations of vasopressin encountered in pathophysiologic states on the collateral circulation in vivo. We studied eight open-chest anesthetized dogs with mature coronary collateral vessels 3-6 months after placement of an ameroid constrictor on the left circumflex coronary artery. The left anterior descending coronary artery was perfused at constant pressure, and peripheral coronary pressure was monitored continuously throughout each experiment. At baseline and during intracoronary infusion of vasopressin, which resulted in concentrations ranging from 8 +/- 3 to 1,340 +/- 327 microM/ml, we measured regional myocardial perfusion with radiolabeled microspheres. At baseline, regional myocardial perfusion to the collateral-dependent myocardium and to the normally perfused myocardium was similar; however, during vasopressin infusion, collateral-dependent zone flow decreased by 49 +/- 14% whereas normal zone flow decreased by only 9 +/- 9% (p less than 0.0005, normal zone perfusion vs. collateral perfusion). Vasopressin increased transcollateral resistance by 242 +/- 95% above baseline but produced a more modest increase in normal zone resistance (15 +/- 10%). The subendocardial to subepicardial perfusion ratio increased by 28 +/- 12% in the normal zone in response to vasopressin but decreased by 18 +/- 11% in the collateral-dependent zone. These data show that mature coronary collateral vessels are responsive to the vasoconstrictor effects of vasopressin at concentrations encountered in various pathophysiologic states.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

The effect of diltiazem on coronary flow reserve in humans.

Calcium channel antagonists have been shown to blunt maximal coronary flow after brief coronary occlusion and during pharmacologic coronary dilation in animals. This property, if present in humans, would result in a reduction in coronary flow reserve in the absence of intrinsic abnormalities of the coronary circulation. A reduction of maximal vasodilator capacity by calcium channel antagonists could also constitute an important anti-ischemic mechanism of action of these agents. To evaluate the effect of calcium channel antagonists on coronary flow reserve in awake humans, we measured coronary flow reserve using the coronary Doppler catheter and intracoronary papaverine at baseline and after diltiazem administered by intravenous (125 or 250 micrograms/kg bolus, 5 micrograms/kg/min infusion, n = 8) or intracoronary (150-600 micrograms bolus, n = 10) routes. Intravenous diltiazem reduced heart rate from 77 +/- 18 to 72 +/- 17 beats/min (mean +/- SD, p less than 0.005) and reduced mean arterial pressure from 96 +/- 11 to 86 +/- 15 mm Hg (p less than 0.005). Intravenous diltiazem resulted in a small decrease in coronary flow reserve (peak-to-resting flow velocity ratio) from 3.9 +/- 1.2 to 3.6 +/- 1.1 (p less than 0.01). After intracoronary diltiazem, mean arterial pressure was unchanged (control 99 +/- 12 mm Hg, diltiazem 97 +/- 13 mm Hg), and heart rate was maintained constant by atrial pacing. Coronary flow reserve was unchanged at 3.8 +/- 0.9 at baseline and after intracoronary diltiazem. Thus, treatment with diltiazem does not invalidate the measurement of coronary flow reserve for diagnostic purposes. Furthermore, these results suggest that attenuation of maximal coronary dilation by diltiazem is not a mechanism responsible for its antianginal effects.

Blood Flow Velocity↗
PubMed1989

Heterogeneous microvascular coronary alpha-adrenergic vasoconstriction.

We tested the hypothesis that humoral or neurogenic alpha-adrenergic activation in the coronary circulation would produce heterogeneous vascular reactions. To accomplish this, the epicardial coronary microcirculation was viewed through an intravital microscope using stroboscopic epi-illumination. Microvascular diameters were measured under control conditions during beta-adrenergic blockade (propranolol 1 mg/kg) and beta-adrenergic blockade with pacing; during coronary alpha-adrenergic activation in the presence of beta-adrenergic blockade with three doses of norepinephrine infusion (0.1, 0.5, and 1.0-2.0 micrograms/kg/min) or three frequencies of bilateral stellate nerve stimulation (2, 10, and 20 Hz); and during combined alpha- and beta-adrenergic blockade (phentolamine 2 mg/kg and propranolol 1 mg/kg). Diameters of both arterial and venous vessels were reduced during beta-adrenergic blockade but returned back to baseline with pacing. At the lowest level of norepinephrine infusion or frequency of bilateral stellate stimulation, microvessel constriction was not observed. At the higher doses of norepinephrine a -5.1 +/- 0.9% (1.0-2.0 micrograms/kg/min) and a -4.0 +/- 1.1% (0.5 micrograms/kg/min) decrease in diameter of arterial vessels greater than 100 microns in diameter were observed (p less than 0.05). At 10 Hz and 20 Hz of stellate stimulation, diameter decreased by -4.8 +/- 1.9% and -4.4 +/- 2.1%, respectively, in these relatively large vessels. Small coronary arterioles (less than 100 microns diameter) dilated significantly during the highest levels of nerve stimulation (9.2 +/- 2.5% increase in diameter) or infusion rate of norepinephrine (13.6 +/- 2.7% increase in diameter) (p less than 0.05). These constrictor and dilator responses were abolished following combined alpha- and beta-adrenergic blockade. Norepinephrine infusion resulted in a decrease in diameter of coronary veins and venules (7.2 +/- 1.3%) (p less than 0.05), whereas stellate stimulation did not significantly reduce venous and venular diameters. In summary, the coronary venous and venular vasculature responds to alpha-adrenergic activation from circulating norepinephrine but is not affected by stellate stimulation. In contrast, stellate stimulation and norepinephrine infusion elicit similar responses in the coronary arterial and arteriolar microvasculature. Constriction occurs in vessels greater than 100 microns in diameter, whereas dilation predominates in vessels less than 100 microns in diameter. Such heterogeneous arterial responses would undoubtedly result in a redistribution of coronary vascular resistance toward larger coronary arteries and arterioles.

Adrenergic alpha-Antagonists↗
PubMed1989

Nonuniform vasomotor responses of the coronary microcirculation to serotonin and vasopressin.

Large-conduit coronary arteries respond to vasoactive stimuli differently than smaller coronary arterioles, but the quantitative effects of many vasoactive stimuli at various levels of the microvasculature remain unknown. To determine the site of constriction or dilation to serotonin and vasopressin in the coronary microcirculation, we studied microvascular responses in the left ventricle of anesthetized cats (n = 36). To compensate for motion due to contraction of the heart, the epicardium was visualized with stroboscopic epi-illumination controlled by a computer to flash once per cardiac cycle in mid-diastole, making the vessels appear stationary. Serotonin (16 micrograms/kg/min) or vasopressin (0.5 units/min) was infused into the left atrium while maintaining aortic pressure constant with a snare on the descending aorta or inferior vena cava. Myocardial blood flow was measured with radioactive microspheres. During infusion of serotonin, aortic pressure and heart rate did not change, but myocardial perfusion increased 90 +/- 38% (mean +/- SEM) from a control value of 159 +/- 27 ml/min.100 g. Arteries and arterioles larger than 90 microns constricted in response to serotonin (control 159 +/- 12 microns; percent change -18 +/- 3; range -41 to 10%) while arterioles less than 90 microns dilated to serotonin (control 54 +/- 7 microns; percent change 22 +/- 9; range -10 to 62%). During infusion of vasopressin, aortic pressure and heart rate did not change, and myocardial perfusion decreased 16 +/- 7% (control, 147 +/- 18 ml/min.100 g).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Coronary angiogenesis during long-term hypertension and left ventricular hypertrophy in dogs.

Many studies have documented that during the development of left ventricular hypertrophy (LVH) coronary vascular growth lags behind that of cardiac muscle. To ascertain whether significant growth of coronary resistance vessels occurs with long-standing hypertension and LVH, we studied dogs with Goldblatt (one-kidney, one-clip) hypertension seven months after surgery. Left ventricular minimal coronary vascular resistance (LV MCVR) was derived from adenosine-induced maximal flow measured with 15 microns microspheres. Morphometric data were based on perfuse-fixed hearts arrested in diastole. Hypertension and LVH were associated with a 46% increase in left ventricular weight/body weight ratio (LVH, 6.73 +/- 0.31; control, 4.62 +/- 0.30), no significant change in LV MCVR/100 g, and a reduction in total LV MCVR (LVH, 0.11 +/- 0.02 mm Hg/ml/min; control, 0.15 +/- 0.02 mm Hg/ml/min). Arterial and arteriolar wall/lumen ratios were virtually identical in the two groups. Arteriolar (lumen diameter less than 200 microns) numerical densities (arteriolar profiles/mm2) were also similar for the two groups even when analyzed according to lumen diameter size class and by ventricular location (epimyocardium, midmyocardium, and endomyocardium). Moreover, the relative frequency distribution of any arteriolar size class was similar for both groups. Because MCVR and arteriolar density were normal, this study provides new evidence that angiogenesis during long-term LVH in this model is of sufficient magnitude to enable the cross-sectional area of the coronary resistance vessels to increase in proportion to the increase in left ventricular mass.

Animals↗
PubMed1989

Comparison of the effects of increased myocardial oxygen consumption and adenosine on the coronary microvascular resistance.

The purposes of this study were to determine if coronary dilation secondary to an increase in myocardial oxygen consumption (MVO2) affects the microcirculation in a homogeneous or heterogeneous manner and to determine if comparable degrees of coronary dilation produced by increasing MVO2 or exogenous (intravenous adenosine) or endogenous (intravenous dipyridamole) adenosine have similar effects in the coronary microcirculation. The epimyocardial coronary microcirculation was observed through an intravital microscope by stroboscopic epi-illumination in anesthetized open-chest dogs. Aortic pressure and heart rate were controlled by an aortic snare and atrioventricular sequential pacing, respectively, during experimental procedures. In group 1 (n = 15), coronary arterial microvessel diameters were measured under control condition and during rapid pacing at 300 beats/min, which doubled MVO2. Increases in MVO2 caused heterogeneous vasodilation in coronary arterial microvessels (40-380 microns). There was an inverse relation between control diameter and percent increase in diameter. In group 2 (n = 15) or group 3 (n = 10), adenosine or dipyridamole was infused intravenously to increase myocardial perfusion to the same level as that obtained with rapid pacing. Adenosine and dipyridamole did not change MVO2. Adenosine and dipyridamole also caused heterogeneous vasodilation, but the effects of adenosine and dipyridamole were restricted to arterial microvessels smaller than 150 microns. From these results, we conclude that increases in MVO2 produce widespread but heterogeneous vasodilation, that is, greater dilation in smaller arterial microvessels. Comparable increases in coronary flow produced by increasing MVO2 or endogenous and exogenous adenosine do not produce identical changes in the distribution of coronary microvascular resistance.

Adenosine↗
PubMed1989

Biphasic effect of nitroglycerin on coronary hemodynamics in normal subjects.

Coronary blood flow responses to nitroglycerin (NTG) in patients have been reported to be extremely variable. In dogs, NTG has a striking biphasic effect on coronary hemodynamics, consisting of a brisk increase followed by a decrease in coronary flow. To determine the effect of the drug on the coronary circulation in normal humans, NTG was injected I.C. (50 and 300 mcg) in 11 normals, and its effects on coronary flow velocity were compared to those of I. C. papaverine (6, 8, 10, and 12 mg) and saline (0.5 and 3.0 ml). Coronary flow velocity was measured using a 3F coronary Doppler catheter. The effect of each drug on coronary blood flow was analyzed in terms of both magnitude and duration (s) of the transient vasodilatory response following administration. Changes in coronary flow velocity (expressed as peak/resting velocity ratio) after 6, 8, 10, and 12 mg papaverine were (mean +/- SEM) 2.7 +/- 0.1, 3.4 +/- 0.3, 3.7 +/- 0.2, and 3.9 +/- 0.2, respectively. Very mild changes were observed with saline (1.3 +/- 0.1 and 1.7 +/- 0.1 after 0.5 and 3.0 ml, respectively), while ratios of 2.4 +/- 0.2 and 3.1 +/- 0.3 were obtained after NTG 50 and 300 mcg, respectively. The effect of 300 mcg NTG was significantly greater (p less than 0.01) than that of saline, 6 mg papaverine and 50 mcg NTG, lower than that of 12 mg papaverine and not significantly different from that of 8 and 10 mg papaverine. In terms of duration, the effect of 300 mcg NTG on coronary flow velocity was more prolonged than that of saline and 50 mcg NTG, and shorter than that of 6 to 12 mg papaverine.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗
PubMed1989

Quantitative characterization and sorting of three-dimensional geometries: application to left ventricles in vivo.

A procedure for automatic sorting of three-dimensional (3-D) shapes is proposed. The procedure is applied to sort into normal and abnormal categories, human left ventricles (LV) using in vivo data from 19 subjects (ten normal and nine abnormal LV's) studied by ultrafast tomography (Cine-CT). The procedure starts by utilizing a vector in a helical coordinate system to describe the spatial geometry of each individual LV cavity. This individual vector is then anatomically aligned and normalized to eliminate effects due to size, yielding a dimensionless vector, denoted as "geometrical cardiogram" (GCG). The GCG characterizes the instantaneous 3-D geometrical information of the individual LV. For the group of healthy subjects, the Karhunen-Loeve Transform (KLT) is then applied to compress the geometric information contained in their individuals' GCG vectors, at end diastole (ED) and end systole (ES), and yield a unique set of basis vectors. The "normal shape domain" is next defined as a truncated set of the KLT basis vectors from which a normal GCG can be reconstructed with a mean squared error (MSE) smaller than a defined threshold. The calculated MSE of any individual GCG reconstructed in this domain is then used as a criterion for sorting the 3-D shapes. Hearts which yield MSE greater than the threshold are considered abnormal. When applied to the study group of 19 subjects a significant difference (p less than 0.0001) between the MSE values obtained for the normal LV's, and those obtained for the abnormal LV's was detected, thus leading to a successful sorting of all the studied LV's. Finally, the KLT is applied to yield a compact representation of the 3-D geometry of any LV (normal or abnormal).

Adolescent↗
PubMed1988

Sectional and segmental variability of left ventricular function: experimental and clinical studies using ultrafast computed tomography.

In this study, ultrafast computed tomography, a new high spatial and temporal resolution imaging system, was employed to define the range of sectional (tomographic) and segmental left ventricular function in 11 normal anesthetized dogs and 11 normal human volunteers. After intravenous infusion of contrast agent, multilevel tomographic images of the left ventricle (apex to base) were acquired at a rate of 17 frames/s. Analysis of these studies demonstrated substantial but predictable heterogeneity in left ventricular contraction from apex to base. In dogs and humans, for example, the average tomographic ejection fraction of the most basal level of the left ventricle was 40% less than that of the most apical level (p less than 0.05). In humans, circumferential segmental cavity contraction at the mid-papillary muscle level was relatively homogeneous (range 50 to 92% for 12 wedge-shaped segments around the tomographic circumference) if the reference system employed an endocardial centroid, but was less uniform if it used an epicardial centroid (range 22 to 98%). It is concluded that contraction of the normal left ventricle in dogs and humans is heterogeneous both between levels (apex to base) and within a single level (circumferential cavity contraction). However, the patterns of cavity contraction from apex to base and circumferential segmental cavity contraction within a given level as defined by ultrafast computed tomography are sufficiently narrow and predictable in normal individuals that these variables may be useful to define regional contraction abnormalities in pathologic conditions.

Adult↗
PubMed1988

The effects of cardiopulmonary bypass and cold cardioplegia on coronary flow velocity and the reactive hyperemic response in patients and dogs.

In normal coronary arteries, reactive hyperemic responses to a 20-second occlusion, an index of coronary reserve, usually demonstrate a peak-to-resting flow velocity ratio of 4:1 or more. Most intraoperative studies that have assessed reactive hyperemic responses in bypassed vessels have reported peak-to-resting flow velocity ratios of 2:1 or less following a 20-second occlusion. These decreased reactive hyperemic responses could be due to coronary vasodilatation after cardiopulmonary bypass or to an inadequate physiological result of the surgical procedure. In 14 patients with angiographically normal coronary arteries, the peak-to-resting flow velocity ratio following a 20-second coronary occlusion decreased significantly (p less than 0.05) from 4.4 +/- 0.2 (mean +/- standard error) before bypass to 3.0 +/- 0.3 after bypass. In a similar dog model, the peak-to-resting flow velocity ratio decreased by 36 to 52% during the first hour following one hour of cardiopulmonary bypass and cardioplegia. During the same period, left ventricular perfusion increased 21 to 30%, mean arterial pressure and coronary vascular resistance decreased, and myocardial oxygen consumption was unchanged. In a second group of dogs studied for the effects of duration (200 to 240 minutes) of anesthesia and thoracotomy alone, peak-to-resting flow velocity ratio was significantly lower. These clinical and experimental studies suggest that major coronary vasodilatation occurs early following cardiopulmonary bypass and cold cardioplegia, and may contribute to the blunted coronary reactive hyperemic responses reported during this time. Consequently, an intraoperative peak-to-resting flow velocity ratio of 3:1 for bypassed coronary arteries may represent an excellent physiological result.

Adolescent↗
PubMed1988

The effects of pressure-induced cardiac hypertrophy on the functional capacity of the coronary circulation.

Pressure-induced cardiac hypertrophy has many effects on the functional capacity of the coronary circulation. Many studies have been performed in both animal and humans and the major findings are as follows: 1. Most types of myocardial hypertrophy are associated with the decrement in coronary vasodilator reserve; 2. The magnitude of the decrement in coronary reserve in myocardial hypertrophy is usually much more prominent in patients with myocardial hypertrophy than in animal models; 3. Left ventricular hypertrophy secondary to systemic hypertension is associated with altered autoregulation of myocardial perfusion; 4. The perfusion abnormalities associated with hypertension and left ventricular hypertrophy are affected by various factors such as age of onset, ventricular involvement, and the stimulus for hypertrophy; 5. Left ventricular hypertrophy secondary to renal hypertension markedly augments the adverse effects of coronary occlusion. In this setting, coronary occlusion is associated with a three-fold increase in the incidence of lethal ventricular arrhythmias and a 35% increase in infarct size. Thus, pressure-induced hypertrophy profoundly alters the coronary circulation.

Angina Pectoris↗
PubMed1988

Videodensitometric analysis of coronary stenoses. In vivo geometric and physiologic validation in humans.

Assessment of the severity of coronary stenoses on arteriograms conventionally is based on subjective estimates of percent luminal diameter narrowing. However, in studies in patients with multivessel coronary artery disease, we have found a poor correlation between percent stenosis and the physiologic significance of an individual coronary obstruction. The purpose of this study was to determine whether computerized videodensitometry would allow estimation of coronary luminal area and therefore prediction of the physiologic significance of individual coronary stenoses in humans. Videodensitometry was used to define the minimal luminal area of 15 left anterior descending, 15 circumflex, and 15 right coronary artery segments in 43 patients. Computer-assisted quantitative coronary arteriography (method of Brown et al) was used to determine the minimal luminal cross-sectional area of these same segments. In each arterial segment, coronary vasodilator reserve was assessed using intraoperative (n = 18 segments) or intracoronary (n = 27 segments) Doppler measurements of coronary vasodilator reserve. Videodensitometric estimates of coronary luminal area correlated well with minimal luminal area defined using the independent geometric technique of quantitative coronary arteriography (r = 0.82, y = 0.97 X + 0.71, SEE = 1.83 mm2, n = 45) and with lesion physiologic significance as defined by studies of the peak-to-resting velocity ratio (r = 0.71, 0.92, and 0.74 for the left anterior descending, circumflex, and right coronary arteries, respectively). Thus, videodensitometry is a promising method that may supplement geometric approaches to quantitative analysis of coronary arteriograms in humans.

Absorptiometry, Photon↗
PubMed1988

Influence of risk area size and location on native collateral resistance and ischemic zone perfusion.

To examine the effect of risk area size on collateral resistance and ischemic region perfusion, we produced different sized risk areas by occluding either the left anterior descending (LAD) or the circumflex (Cx) coronary artery at different sites. The most proximal occlusion of the LAD and Cx produced risk areas of 43 +/- 5 and 36 +/- 2% of left ventricular (LV) mass, respectively, whereas distal LAD and Cx occlusions produced risk areas of 13 +/- 2 and 17 +/- 2% of LV weight, respectively. Although total collateral flow was highest to the largest risk areas, collateral flow per 100 g of ischemic myocardium was 80% higher to the small LAD risk area compared with the large LAD risk area and 43% higher to the small Cx risk area compared with the large Cx risk area. Collateral resistance, calculated from the transcollateral pressure and perfusion per 100 g of myocardium was significantly lower in the small risk areas than in the large ones. We examined the effect of risk area location on collateral perfusion and resistance. Small risk areas (6% LV mass) were created near the base and at the apex of 10 hearts. Collateral flow per 100 g was 60% higher and transcollateral resistance per 100 g 50% lower at the apex than at the base. These experiments show that collateral resistance is influenced both by ischemic region size and location. Small risk areas receive more collateral flow per mass of tissue than large risk areas, and apical risk areas receive greater quantities of collateral flow than those located at the base.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗