Ann Thorac Surg 1995;59:829-834
© 1995 The Society of Thoracic Surgeons
Distal Flow Determinants in Canine Myocardium Perfused Through Internal Thoracic Artery Bypass Grafts
Masaki Otaki, MD,
Robert M. Lust, PhD,
You Su Sun, MD,
Terry O. Norton, MD,
W. Randolph Chitwood, Jr, MD
Departments of Surgery and Physiology, East Carolina University School of Medicine, Greenville, North Carolina
 |
Abstract
|
|---|
The dynamic reactivity and the acute, recruitable flow capacity of an internal thoracic artery (ITA) graft remains unclear. These experiments were conducted in 20 anesthetized dogs with the left ITA grafted to the circumflex artery, off pump, using a brief local occlusion. The left main coronary artery was occluded, rendering the entire left ventricle, including anterior descending artery and circumflex regions, totally dependent on the ITA graft. When the left main coronary artery was occluded, the ITA flow immediately increased more than fivefold (93.4 +/- 9.6 mL/min; mean +/- standard deviation), representing an absolute flow value three times higher than ITA flow measured in situ on the chest wall (27.5 +/- 9.6 mL/min; p < 0.05 versus control), and the ITA graft provided total resting flow requirements (93.4 +/- 9.6 mL/min) for both left anterior descending and circumflex coronary artery perfusion territories at levels comparable with measured native flow values (y = (0.9555)x + 21.9272; r = 0.976; p < 0.05). Pharmacologic challenge with adenosine (0.2 mg • kg-1 • min-1 intravenously) significantly increased the graft flow (120.3 +/- 18.7 mL/min; p < 0.05 versus control), but also significantly decreased the mean arterial pressure (85.4 +/- 5.0 versus 74.6 +/- 6.1 mm Hg; p < 0.05). Phenylephrine (0.003 mg • kg-1 • min-1 intravenously) significantly decreased ITA graft flow (81.2 +/- 9.0 mL/min; p < 0.05 versus control) despite significantly increased perfusion pressure (84.8 +/- 6.3 versus 108.2 +/- 8.6 mm Hg; p < 0.05 versus control). Physiologic stimulation of myocardial oxygen consumption with ventricular pacing (heart rate, 150 versus 120 beats/min for control) increased ITA graft flow to 107.9 +/- 8.4 mL/min (p < 0.05 versus control), which was similar to changes observed with atrial pacing (110.3 +/- 9.7 mL/min; p < 0.05 versus control) but was not attributed to changes in perfusion pressure. After a 10-second occlusion and release of the ITA graft, the hyperemic graft flow peaked at 197.6 +/- 38.7 mL/min (p < 0.001 versus control). However, neither myocardial pacing nor short occlusion produced flow changes when assessed in the ITA in situ on the chest wall. Despite initially high flow demands, the canine ITA bypass graft is capable of very large recruitable flow and retains considerable dynamic reactivity to pharmacologically driven pressor responses and physiologically stimulated changes in myocardial oxygen demands.
|
Introduction
|
|---|
See also page 834.
In recent years, an internal thoracic artery (ITA) has been used as the conduit of choice for coronary bypass procedures because of the excellent late patency of the graft. Although superior late ITA patency is well documented, there are reports of inadequate acute flow through the ITA at the time of grafting [1–3].
The flow capacity of the ITA graft appears to be sufficient in any situation when the ITA is grafted to a single coronary artery with relatively normal distal flow requirements [4, 5]. However, ITA grafts may not provide sufficient myocardial flow if the initial native flow requirement is high. Such conditions may exist when the ITA is grafted to a coronary bed with a large distal runoff, as may occur with extensive collaterals; when the ITA graft serves multiple distal beds, as may occur with sequential grafting; or when the ITA graft serves a perfusion bed with a physiologically increased resting flow requirement, as may occur with ventricular hypertrophy [6–8]. In any of these settings, a second, supplemental vein graft often is required to provide adequate myocardial perfusion and separate the patient from extracorporeal bypass successfully. However, the use of vasopressors during weaning may produce dynamic responses from the graft directly, which significantly exacerbate the appearance of an anatomically limiting flow deficit.
The purpose of the present study was to determine (1) the demand-stimulated, recruitable flow capacity of the canine ITA graft, (2) the reactivity of the graft in the setting of systemic vasoactive agents, and (3) the possibility that vasoactive constriction in the graft may predispose to relative ischemia and hypoperfusion syndrome.
|
Material and Methods
|
|---|
Surgical Preparation
Twenty mongrel dogs, weighing 16 to 25 kg (mean weight, 21 +/- 2.8 kg), were anesthetized with sodium pentobarbital (30 mg/kg, intravenously), intubated, and ventilated with a volume ventilator. Arterial blood pressure was monitored with a high-fidelity catheter-tipped micromanometer (Millar Instruments, Houston, TX) and the electrocardiogram was monitored continuously. A left fifth interspace thoracotomy was performed, and a left ITA graft was dissected and rotated from the chest wall as a pedicle, including the accompanying veins and adjacent muscle, from the subclavian artery proximally to the eighth intercostal interspace distally. The pericardium then was incised parallel to the phrenic nerve, its edges were sutured to the margins of the thoracotomy, and the heart was elevated in the resulting pericardial cradle. A ligature was placed on the left atrial appendage to provide retraction, exposing the atrioventricular groove, from which a 3-cm section of the proximal left circumflex coronary artery was dissected bluntly and mobilized. A short section of the left anterior descending coronary artery proximal to the first diagonal branch similarly was mobilized, enabling measurement of native resting myocardial flow in this region. Pacing wires were attached to the atrium and ventricle for use later in the measurement of demand-mediated flow responses.
The coronary anastomosis was performed using a modification of a technique described by McCarthy and Schaff [9], but without the use of a distal shunt. Once the circumflex coronary artery (CFX) had been mobilized sufficiently, snares of number 2 silk were placed around the vessels at each end of the dissected segment. Lidocaine, 1.5 mg/kg (Abbott Laboratories, North Chicago, IL), and esmolol hydrochloride, 1.0 mg/kg (Brevibloc; DuPont-Merck Pharmaceuticals, Manati, Puerto Rico), were administered intravenously. The snares then were tightened around the vessel, partially immobilizing the vessel and limiting the motion artifact associated with ventricular contraction. A coronary arteriotomy approximately 5 mm long was made, and the spatulated distal end of the ITA was anastomosed to the CFX using a continuous strand of 7-0 polypropylene suture (Davis + Geck, Inc, Danbury, CT). The time required for the anastomosis was between 8 and 13 minutes. After the completion of the anastomosis the snares occluding the CFX were released and distal perfusion was reestablished first through the native system. Under these conditions, the integrity of the anastomosis was determined, and then the ITA was released and allowed to flow in competition with the native circumflex. All hearts were reperfused approximately 30 minutes, during which time cardiac function normalized. The left main coronary artery then was occluded, rendering the entire left ventricle, including the left anterior descending artery (LAD) and the CFX regions, totally dependent on the ITA graft.
Measurements
All flow measurements were made using calibrated electromagnetic probes (Zepeda Instruments, Seattle, WA). Resting flow in the ITA in situ and in the native coronary arteries (LAD, CFX) was measured. Flow in these vessels and arterial pressure were recorded after intravenous administration of adenosine (0.20 mg • kg-1 • min-1) or phenylephrine (0.003 mg • kg-1 • min-1) and in response to ventricular or atrial pacing at a heart rate of 150 beats/min (compared with a control rate of 120 beats/min). All treatments were continuous for 10 minutes before measurements were obtained, and 20 minutes between each intervention was provided, enabling complete recovery of resting parameters.
After the ITA had been rotated and grafted to the CFX, measurement of native and ITA flow during resting competition was measured, and then the native left main coronary trunk was ligated. Pharmacologic and physiologic challenges were repeated (intravenous infusions and pacing, as before), and ITA graft flow and systemic pressure again were recorded. In addition, the reactive flow response to 10-second occlusion of the ITA graft was determined.
In conducting the experiment we adhered strictly to the guiding principles for the Care and Use of Laboratory Animals of the American Physiological Society. All data are expressed as the mean +/- the standard deviation. Differences between a resting value and a treatment flow/pressure response was assessed using Student's t test for paired differences, and corresponding probability values less than 0.05 were considered statistically significant.
|
Results
|
|---|
Flow in the ITA in situ on the chest wall was 27.5 +/- 9.6 mL/min, and arterial pressure was 85.4 +/- 5.0 mm Hg. Flow was unchanged in response to pharmacologic challenge using adenosine, (28.2 +/- 8.4 mL/min) or phenylephrine (26.1 +/- 8.9 mL/min), despite significant changes in systemic perfusion pressure (75.3 +/- 6.1 and 107.6 +/- 8.1 mm Hg, respectively; both p < 0.05), suggesting active dilation of the ITA in response to adenosine and active constriction of the ITA in response to phenylephrine. Increasing myocardial oxygen demands did not change systemic perfusion pressure and did not have a significant impact on ITA flow in situ (ventricular pacing, 28.1 +/- 10.2 mL/min; atrial pacing, 28.5 +/- 9.8 mL/min).
The flow in the LAD and CFX perfusion territories before and after grafting, with and without occlusion of the left main coronary trunk, is summarized in Table 1
. Neither grafting nor occlusion of the left main artery caused a significant change in distal perfusion, suggesting both technical adequacy of the anastomosis and sufficient flow capacity in the ITA graft. When the left main coronary artery was open, the ITA graft flowed in competition in the CFX distribution, provided slightly less than half (17.1 +/- 4.1 mL/min) of the total distal CFX flow (43.1 +/- 9.8 mL/min), but did not influence or contribute to LAD perfusion (35.5 +/- 6.0 mL/min). The relative contribution of the graft to each regional perfusion was demonstrated by occluding the graft while the native circulation remained intact. Ligating the graft did not change LAD flow but did cause an increase in proximal circumflex flow to maintain distal perfusion. When the left main artery was occluded, the ITA flow increased to 93.4 +/- 9.6 mL/min, a value more than five times higher than observed in competition, and more than three times higher than intact flow measured in situ on the chest wall.
The distribution of the ITA graft flow in the setting of left main occlusion is provided in Figure 1. The LAD and CFX distal flows were maintained (see Table 1
), and the presumed values for septal flow were estimated by subtracting the combined distal flow from the total graft flow. Estimated differently, linear regression was performed on the relationship between measured ITA graft flow and combined measured distal flow. The relationship was fit by a line with a slope close to unity (0.9555) and a high degree of correlation (0.976). The y-intercept offset (21.9) reasonably approximates the unmeasured flow previously assigned by subtraction to perfusion territory between the two coronary flow probes (Fig 2).
View larger version (14K):
[in this window]
[in a new window]
|
Fig 1. . Distribution of the total graft flow (ITA), after ligation of the left main coronary, to anterior (LAD) and posterolateral (CFX) regions. Unmeasured flow to proximal areas between the LAD and CFX probes was determined by subtracting (LAD + CFX) from ITA, and is designated Septals.
|
|
View larger version (17K):
[in this window]
[in a new window]
|
Fig 2. . Scatter plot and linear regression of the relationship between measured, combined distal flow before grafting and internal thoracic artery (ITA) graft flow after occlusion of the left main coronary artery. All values were obtained during resting conditions. There was very good correlation (r = 0.976) between the graft flow and the distal flow, suggesting adequate flow support from the graft within ranges observed with the intact, native circulation.
|
|
Adenosine had a more profound effect on ITA flow as a graft than as a native vessel. Adenosine again significantly decreased ITA resistance, but in this case graft flow actually was increased (120.3 +/- 18.7 mL/min; p < 0.05 versus control), rather than simply maintained (Fig 3), despite a comparable but significant decrease in mean arterial pressure (85.4 +/- 5.0 versus 74.6 +/- 6.1 mm Hg; p < 0.05). The increased flow response may reflect a more pronounced effect on the distal coronary arterioles compared with similar vessels subserved by the ITA in the chest wall.
View larger version (18K):
[in this window]
[in a new window]
|
Fig 3. . Flow in the ITA graft measured under resting conditions (basal), with systemic infusion of adenosine (ADO) or phenylephrine (PE), and in response to atrial (A-Pace) or ventricular (V-Pace) myocardial pacing. All of the flows (mean +/- standard deviation) were significantly different from basal (p < 0.05), even though differences in perfusion pressure were evident only with ADO and PE. Changes in flow with ADO and PE were opposite from predicted changes based on systemic perfusion pressure, suggesting active vasodilation and constriction, respectively, whereas flow changes with pacing were independent of perfusion pressure and proportional to the increased heart rate, suggesting active hyperemia in support of increased oxygen utilization.
|
|
Similarly, but conversely, phenylephrine significantly increased ITA graft resistance, but in this case graft flow was decreased (81.2 +/- 9.0 mL/min; p < 0.05 versus control), rather than simply maintained (see Fig 3), despite significantly increased perfusion pressure (84.8 +/- 6.3 versus 108.2 +/- 8.6; p < 0.05). Again, the quantitative differences in flow response to comparable pharmacologic and hemodynamic challenge between the ITA as a graft and as a native vessel probably are related to the differential sensitivity of the respective distal perfusion beds. Nonetheless, the qualitative responsiveness of the vessel, ie, dilatation with adenosine and constriction with phenylephrine, were comparable in both positions.
Physiologic augmentation of oxygen consumption with pacing increased the graft flow, a finding not observed in the in situ ITA, suggesting that the graft response was demand specific, rather than coincidentally related to the pacing parameters. When heart rate was increased 25% from 120 to 150 beats/min, a comparable increase in flow was observed, which did not differ with the site of pacing (ventricular, 107.9 +/- 8.4 mL/min; atrial, 110.3 +/- 9.7 mL/min; both p < 0.05 versus control) (see Fig 3).
Even though the initial flow load created by ligating the left main coronary trunk was quite high, the ITA graft still had additional recruitable flow capacity. After a 10-second occlusion of the graft, reactive hyperemic flows peaked at levels approximately twice basal (197.6 +/- 38.7 mL/min; p < 0.05).
|
Comment
|
|---|
The excellent long-term patency rates and the much lower incidence of postoperative atherosclerosis in ITA bypass grafts relative to saphenous vein grafts are well documented [1–3]. However, some concerns still exist regarding the dynamic reactivity and absolute flow capacity of the ITA graft, at least acutely. Several reports have suggested that coronary flow reserve with ITA grafting may not be adequate, and that saphenous vein grafts support larger flow reserves and are thus better able to meet demands imposed by large perfusion beds [6–8]. However, the attenuated flow reserve of the ITA graft may be temporal, if it exists at all. The angiographic diameter of the ITA has been noted to increase after operation [4, 10–12] suggesting dilatation and perhaps anatomic remodeling and enlargement of the ITA in response to chronically elevated distal perfusion requirements. Several studies also have compared flow reserve in saphenous vein grafts and ITA grafts during catheterization several days after operation and found no differences in coronary flow reserves between the grafts [10–12]. Animal experiments have not demonstrated a difference in flow reserve between ITA and vein grafts [13, 14]. Although a comparison with saphenous vein grafts was not performed in the present study, these data clearly indicate the existence of a significant flow reserve in the ITA graft, demonstrated with the increase in flow when the left main artery was ligated, again when myocardial oxygen consumption was stimulated by pacing, and finally when reactive hyperemia was induced after reperfusion of a brief occlusion.
Reactive hyperemia is a well-documented phenomenon describing the rebound overshoot in reperfusion flow after a brief occlusion. The peak flow observed during hyperemia may be several times higher than basal levels, and represent on oxygen delivery two or threefold the oxygen debt incurred [15]. Reactive hyperemia has been used as an indicator of both flow reserve of anatomically intact systems and the critical extent of a stenosis in a flow-limited environment. Hodgson and associates [5] measured the coronary flow reserve to contrast-induced hyperemia and could not demonstrate a difference between saphenous vein grafts and ITA grafts. However, the response to contrast is inconsistent, and the comparison of vein grafts and ITA grafts serving different perfusion beds with different resting flow requirements renders some of the comparisons problematic. Nonetheless, the fundamental tenet of Hodgson and associates' study, that the ITA graft will support the capacity for a significant, dynamic, recruitable flow, also is supported by the findings of this study.
Evaluating the effects of vasoactive agents on coronary graft reactivity in vivo is difficult because of the concomitant changes in peripheral resistance, heart rate, and direct and indirect responses of the dependent coronary beds that also may occur [14, 16]. The present study is limited by the same considerations, but interpretation is strengthened by comparing the graft-dependent flow response with the native flow response under the same systemic influences. In this way, although systemic parameters may change, differences in distal perfusion may be more directly attributable to graft specific responses not evident in the native flow response. Thus, although the graft-dependent and native flow responses to adenosine were comparable, the responses to phenylephrine were opposite, suggesting a graft-specific limitation.
Adenosine is a well-known mediator of coronary vasomotion, producing vasodilatation at least in part through direct actions on coronary vascular smooth muscle, but also through interaction with vascular endothelium and associated release of endothelium-derived relaxation factors [17–19]. The relative sensitivity of the coronary system to adenosine was demonstrated by comparing the flow responses in the ITA serving intercostal and sternal arterioles, and in the ITA graft serving myocardial vessels. Phenylephrine is an 
-adrenergic receptor agonist and may decrease graft flow, not only through an effect on the graft directly, but also through constriction of the large, dependent coronary vessels to which the ITA is anastomosed [16]. The direct effects of phenylephrine on ITA graft resistance is unclear. Two older studies have reported that phenylephrine increased flow in ITA grafts [20, 21], whereas a more recent study indicated that phenylephrine decreased flow in both ITA and saphenous vein grafts [16].
Any of the results could be explained by varying combinations of effects on systemic perfusion pressure, changes in myocardial oxygen consumption with changes in afterload, and direct effects on the dependent coronary vessels. The graft-dependent increase in distal flow with systemic adenosine is comparable with the native flow response. In striking contrast, the response to phenylephrine was quite different between graft-dependent and native conditions. The potential for relative ischemia with intravenous phenylephrine and ITA graft-dependent perfusion is demonstrated in Figure 4. Systemically, phenylephrine increased peripheral resistance, which increased both coronary perfusion pressure and myocardial afterload. A slightly increased heart rate was also observed. Under these conditions, whereas total distal perfusion increased 23% when supplied by native coronary arteries (115.4 +/- 9.3 mL/min; p < 0.05 versus basal), graft-dependent total distal perfusion decreased 13% compared with basal flow and more than 30% compared with the expected native flow response (81.2 +/- 8.0 mL/min). In a setting known to produce increased native flow requirements, decreased flow was measured when perfusion was graft-dependent, suggesting a graft-limiting perfusion defect and a relative ischemia. However, the response to reactive hyperemia clearly demonstrates that the perfusion defect is not the result of an anatomic flow limit, but the specific response of the ITA graft to a systemic vasoconstrictor. The results from the present study clearly establish the specific vasoconstricting effect of phenylephrine directly at the level of the ITA graft, at doses commonly used systemically in the perioperative management of hypotension. The difference between the native response and the graft-dependent response in total distal perfusion suggests a flow deficit capable of generating a relative ischemia, resulting directly from the action of the drug on the graft, and not due to any anatomic limitations of the conduit.
View larger version (16K):
[in this window]
[in a new window]
|
Fig 4. . Comparison of the total distal flow under resting conditions (basal) and in response to phenylephrine when supported by the native circulation (PE-Native) and when supported by the internal thoracic artery graft (PE-Graft). Note that although flow was augmented in the native circulation, it was decreased under the same systemic parameters in the graft-dependent condition. Both PE values are significantly different from basal (mean +/- standard deviation; p < 0.05).
|
|
The canine ITA is relatively large in relation to the size of the coronary vessels. In addition, canine myocardium is collateralized more extensively. The advantage of the existing collaterals in this setting is that small residual perfusion is continued during the period of occlusion while the coronary artery--ITA anastomosis is constructed, obviating the need for extracorporeal circulation. Very few experimental studies of coronary grafts have been conducted simply because many mammalian species tolerate extracorporeal circulation more poorly than humans. Therefore, although collateral circulation complicates interpretation of regional ischemia studies in canines, the presence of collaterals is a key feature in enabling this study of global ischemia to be completed. Spontaneous coronary artery disease also is not found in canines, and the presence of other lesions in ungrafted vessels in humans undergoing coronary artery bypass grafting is a factor difficult to model experimentally. As such, flow studies involving ITA--coronary artery grafts should be extrapolated to clinical settings only with great caution. However, these caveats notwithstanding, the present animal studies do offer some observations not readily obtained in clinical settings. For example, the relative capacity of the ITA as a graft is best compared with the native flow requirements, which are virtually impossible to determine in the chronically ischemic, acutely revascularized myocardium. To evaluate systematically the response of the ITA before rotation from the chest wall, and again under the same conditions after grafting, is a time-consuming process not easily accomplished in the operating room, yet provides useful information in evaluating how much of a graft-dependent response is the graft and how much is the dependent bed. Also, by rendering the entire ventricle dependent on a single graft, two things were accomplished. First, the resting flow demands were increased, partially negating the larger known flow capacity of the canine ITA graft compared with human. Second, the potential for competition, steal, or collateral-dependent changes between multiply grafted vessels to the same heart was eliminated. Although the data should be extrapolated with caution, these results do suggest that if hypoperfusion is evident in an ITA graft-dependent region, vasopressors with -agonistic properties probably should be avoided if possible.
|
Acknowledgments
|
|---|
We recognize the assistance of Kathy Dennis in the technical conduct of these experiments, and Laurie Rouse in preparing the manuscript. Suture was provided generously by Davis + Geck, Inc, Danbury, CT.
|
Footnotes
|
|---|
Presented at the Fortieth Annual Meeting of the Southern Thoracic Surgical Association, Panama City Beach, FL, Nov 4--6, 1993.
Address reprint requests to Dr Lust, Cardiothoracic Research Laboratories, East Carolina University School of Medicine, Greenville, NC 27858-4354.
|
References
|
|---|
- Jones EL, Lattouf OM, Weintraub WS. Catastrophic consequences of internal mammary artery hypoperfusion. J Thorac Cardiovasc Surg 1989;98:902–7.[Abstract]
- Barner HB. Blood flow in the internal mammary artery. Am Heart J 1973;86:570–1.[Medline]
- Flemma RJ, Singh HM, Tector AJ, Lepley D, Frazier BL. Comparative hemodynamic properties of vein and mammary artery in coronary bypass operations. Ann Thorac Surg 1975;20:619–27.[Abstract]
- Schmidt DH, Blau F, Hellman C, Grzelak L, Johnson WD. Isoproterenol-induced flow responses in mammary and vein bypass grafts. J Thorac Cardiovasc Surg 1980;80:319–26.[Medline]
- Hodgson JM, Singh AK, Drew TM, Riley RS, Williams DO. Coronary flow reverse provided by sequential internal mammary artery grafts. J Am Coll Cardiol 1986;7:32–7.[Abstract]
- Hamby RI, Aintablian A, Wisoff BG, Hartstein ML. Comparative study of the postoperative flow in the saphenous vein and internal mammary artery bypass grafts. Am Heart J 1977;93:306–15.[Medline]
- McBride LR, Barner HB. The left internal mammary artery as a sequential graft to the left anterior descending system. J Thorac Cardiovasc Surg 1983;86:703–5.[Abstract]
- Wakabayashi A, Beron E, Lou MA, Mino JY, daCosta IA, Connolly JE. Physiological basis for systemic-to-coronary artery bypass graft: inadequacy of the internal mammary artery for this purpose and appraisal of the ascending aorta as its proximal site. Arch Surg 1970;100:17–9.[Abstract/Free Full Text]
- McCarthy PM, Schaff HV. A cost effective technique for experimental coronary artery bypass. J Thorac Cardiovasc Surg 1988;96:30–2.[Abstract]
- Björk VO, Ivert T, Landou C. Angiographic changes in internal mammary artery and saphenous vein grafts two weeks, one year and five years after coronary bypass surgery. Scand J Thorac Cardiovasc Surg 1981;15:23–30.[Medline]
- Vogel JHK, McFadden RB, Spence R, Jahnke CR Jr, Love JW. Quantitative assessment of myocardial performance and graft patency following coronary bypass with the internal mammary artery. J Thorac Cardiovasc Surg 1978;75:487–98.[Medline]
- Ivert T, Huttunen K, Landou C, Björk VO. Angiographic studies of internal mammary artery bypass grafting. J Thorac Cardiovasc Surg 1988;96:1–12.[Abstract]
- Barner HB, Kaiser GC, Jellinek M, et al. Aorto-coronary vein graft and internal mammary--coronary anastomosis. Arch Surg 1972;105:908–11.[Abstract/Free Full Text]
- Myojin K, Weiss G, Mee R, et al. Functional comparison of coronary bypass grafts of the saphenous vein and internal mammary artery. J Thorac Cardiovasc Surg 1980;79:713–7.[Abstract]
- Guyton AC. The coronary circulation and ischemic heart disease. In: Guyton AC, ed. Medical physiology. Philadelphia: Saunders, 1981:298--308.
- Jett GK, Arcidi JM Jr, Dorsey LMA, Hatcher CR Jr, Guyton RA. Vasoactive drug effects on blood flow in internal mammary artery and saphenous vein grafts. J Thorac Cardiovasc Surg 1987;94:2–11.[Abstract]
- Hashimoto K, Kurosawa H, Horikoshi S, Miyamoto H, Suzuki K. Perfusion pressure control by adenosine triphosphate given during cardiopulmonary bypass. Ann Thorac Surg 1993;55:123–6.[Abstract]
- Berne R. The role of adenosine in the regulation of coronary blood flow. Circ Res 1980;47:907–13.
- Hoffman WE, Satinover I, Miletich DJ, Albrecht RF, Gans BJ. Cardiovascular changes during sodium nitroprusside or adenosine triphosphate infusion in the rat. Anesth Analg 1982;61:99–103.[Abstract/Free Full Text]
- McCormick JR, Kaneko M, Baue AE, Geha AS. Blood flow and vasoactive drug effects in internal mammary and venous bypass grafts. Circulation 1975;51(Suppl 1):73–80.
- Geha AS, Krone RJ, McCormick JR, Baue AE. Selection of coronary bypass anatomic, physiological, and angiographic considerations of vein and mammary artery grafts. J Thorac Cardiovasc Surg 1975;70:414–31.[Abstract]
Related Article
-
DISCUSSION
Ann. Thorac. Surg. 1995 59: 834.
[Extract]
[Full Text]
This article has been cited by other articles:
|
|
|
|
 
Y. Louagie, M. Buche, P. Eucher, and J.-C. Schoevaerdts
Intraoperative flow measurements in gastroepiploic grafts using pulsed Doppler
Eur. J. Cardiothorac. Surg.,
March 1, 1999;
15(3):
240 - 246.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. Gurevitch, H. I. Miller, I. Shapira, A. Kramer, Y. Paz, M. Matsa, R. Mohr, and V. Yakirevich
High-Dose Isosorbide Dinitrate for Myocardial Revascularization With Composite Arterial Grafts
Ann. Thorac. Surg.,
February 1, 1997;
63(2):
382 - 387.
[Abstract]
[Full Text]
|
|
|
Top
Abstract
Introduction
