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Biomedical subjects

S Rivers

Publications and source records attributed to S Rivers.

At least 19 recordsLinked to original sources

Total complement inhibition: an effective strategy to limit ischemic injury during coronary revascularization on cardiopulmonary bypass.

BACKGROUND: Activation of complement during revascularization of ischemic myocardium accentuates myocardial dysfunction. Soluble human complement receptor type 1 (sCR1) is a potent inhibitor of complement, as are heparin-bonded (HB) cardiopulmonary bypass (CPB) circuits. This study sought to determine whether total complement inhibition with the combination of sCR1 and HB-CPB limits damage during the revascularization of ischemic myocardium. METHODS AND RESULTS: In 40 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, sCR1 (10 mg/kg) was infused 5 minutes after the onset of coronary occlusion (sCR1), 10 received HB-CPB only (HB-CPB), 10 received sCR1 and HB-CPB (sCR1+HB), and 10 received neither sCR1 or HB-CPB (unmodified). Addition of sCR1 to the HB group resulted in less myocardial tissue acidosis (DeltapH = -0.72+/-0.03 for unmodified; -0.46+/-0.05 for HB; -0.18+/-0.04 for sCR1; -0.13+/-0.01 for sCR1+HB), better recovery of wall motion scores (4 = normal to -1 = dyskinesia; 1.67+/-0.17 for unmodified; 2.80+/-0.08 for HB; 3.35+/-0.10 for sCR1; 3.59+/-0.08 for sCR1+HB), less lung water accumulation (5.46+/-0.28% for unmodified; 2.39+/-0.34% for HB; 1.22+/-0.07% for sCR1; 1.24+/-0.13% for sCR1+HB), and smaller infarct size (area necrosis/area risk = 44.6+/-0.7% for unmodified; 33.2+/-1.9% for HB; 19.0+/-2.4% for sCR1; 20+/-1.0% for sCR1+HB) (P<0.05 versus unmodified; P<0.05 versus unmodified and HB groups). CONCLUSIONS: Total complement inhibition with sCR1 and sCR1+HB circuits optimizes recovery during the revascularization of ischemic myocardium.

Animals

Decreased incidence of arterial thrombosis using heparin-bonded intraaortic balloons.

BACKGROUND: This experimental study sought to determine whether heparin-bonding of intraaortic balloons (IAB) would decrease the incidence of arterial thrombosis in the absence of systemic heparinization. METHODS: In 25 adult pigs, a 9F, 40-mL IAB was inserted into the femoral artery and positioned just below the takeoff of the left subclavian artery for 9 hours. Five animals received systemic heparin, 10 animals had no heparin, and another 10 animals received no heparin but the IAB was heparin-bonded (Duraflo II). Thrombus formation was assessed using a numerical scoring system (0 = no thrombosis to 3 = thrombus >5 cm or evidence of luminal compromise). RESULTS: Animals receiving heparin and heparin-bonded IAB had no thrombus formation around the IAB (mean +/- SE; 0 +/- 0.00 heparin versus 1.55 +/- 0.29 no heparin versus 0 +/- 0.00 heparin-bonded; p < 0.005), at the insertion site (0 +/- 0.00 heparin versus 1.55 +/- 0.29 no heparin versus 0 +/- 0.0 heparin-bonded; p < 0.005), and in the distal femoral artery (0 +/- 0.00 heparin versus 2.00 +/- 0.23 no heparin versus 0 +/- 0.00 heparin-bonded; p < 0.005). CONCLUSIONS: Heparin-bonding of the IAB significantly decreases thrombus formation in the absence of systemic heparinization.

Animals

Soluble complement receptor type I limits damage during revascularization of ischemic myocardium.

BACKGROUND: This study was undertaken to determine whether suppression of complement activation with soluble human complement receptor type I reduces myocardial damage during the revascularization of ischemic myocardium. METHODS: In 20 pigs, the second and third diagonal coronary arteries were occluded for 90 minutes, followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 pigs, soluble human complement receptor type I (10 mg/kg) was infused over 30 minutes before the period of coronary occlusion; 10 other pigs received no soluble human complement receptor type I. Complement activation was measured by total hemolytic complement activity (expressed as a percentage of preischemic values). Ischemic damage was assessed by changes in myocardial tissue pH, wall motion scores (range, 4=normal to -1=dyskinesia), and infarct size (area of necrosis versus area at risk). RESULTS: After 180 minutes of reperfusion, hearts treated with soluble human complement receptor type I had significantly less complement activation than nontreated hearts (1.1%+/-0.09% versus 7.8%+/-0.04%, respectively; p < 0.002), less myocardial acidosis (-0.41+/-0.03 versus -0.72+/-0.03, respectively; p < 0.0001), higher wall motion scores (3.1+/-0.09 versus 1.67+/-0.16, respectively; p < 0.0001), and smaller infarct size (24.6%+/-2.0% versus 41%+/-1.3%, respectively; p < 0.0001). CONCLUSIONS: Complement inhibition with soluble human complement receptor type I significantly limits ischemic damage during the revascularization of acutely ischemic myocardium.

Acidosis

Beneficial effects of angiotensin-converting enzyme inhibitors during acute revascularization.

BACKGROUND: This experimental study was undertaken to determine whether using angiotensin-converting enzyme inhibitors during surgical revascularization of acutely ischemic myocardium would improve wall motion and limit infarct size. METHODS: Twenty pigs underwent 90 minutes of occlusion of the second and third diagonal arteries followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion. In 10 animals, the angiotensin-converting enzyme inhibitor enalaprilat (0.05 mg/kg) was infused intravenously during coronary occlusion; 10 other animals received no angiotensin-converting enzyme inhibitors. Ischemic damage was assessed by the number of cardioversions required for ventricular tachycardia or fibrillation; wall motion scores using echocardiography (4=normal to -1=dyskinesia); and infarct size using histochemical staining. Epicardial coronary artery vasomotor function was assessed using standard organ chamber methodology. RESULTS: Enalaprilat-treated hearts had the least amount of ventricular irritability (0.84+/-0.24 versus 2.77+/-0.22 cardioversions; p < 0.01), the best recovery of wall motion score (3.20+/-0.15 versus 1.52+/-0.07; p < 0.0001), and the lowest infarct size (22.6%+/-1.4% versus 37.7%+/-3.0%; p < 0.001). Endothelium-independent relaxation was preserved in all hearts; however, endothelium-dependent relaxation was impaired in both groups. CONCLUSIONS: Angiotensin-converting enzyme inhibitors reduce myocardial damage during surgical revascularization of acutely ischemic myocardium.

Angiotensin-Converting Enzyme Inhibitors

Heparin-bonded circuits decrease myocardial ischemic damage: an experimental study.

BACKGROUND: Heparin-bonded cardiopulmonary bypass circuits reduce complement activation, but their effect on myocardial function is unknown. This study was undertaken to determine whether heparin-bonded circuits reduce myocardial damage during acute surgical revascularization. METHODS: In 16 pigs, the second and third diagonal vessels were occluded with snares for 90 minutes followed by 45 minutes of cardioplegic arrest and 180 minutes of reperfusion with the snares released. During the period of coronary occlusion, all animals were placed on percutaneous bypass followed by standard cardiopulmonary bypass during the periods of cardioplegic arrest and reperfusion. In 8 pigs, heparin-bonded circuits were used, whereas 8 other pigs received nonbonded circuits. RESULTS: Animals treated with heparin-bonded circuits had the best preservation of wall motion scores (3.5 +/- 0.3 versus 2.3 +/- 0.2; 4 = normal to -1 = dyskinesis; p < 0.05), least tissue acidosis (change in pH = -0.31 +/- 0.02 versus -0.64 +/- 0.08; p < 0.05), smallest increase in lung H2O (1.7% +/- 0.7% versus 6.1% +/- .5%; p < 0.05), and the lowest area of necrosis/area of risk (20.3% +/- 2.2% versus 40.4% +/- 1.6%; p < 0.05). CONCLUSIONS: We conclude that heparin-bonded circuits significantly decrease myocardial ischemic damage during acute surgical revascularization.

Acid-Base Equilibrium

Salvage of ischemic myocardium with simplified and even delayed coronary sinus retroperfusion.

BACKGROUND: Despite the proven efficacy of pressure-controlled intermittent coronary sinus obstruction (PICSO) and synchronized retrograde perfusion (SRP) in salvaging ischemic myocardium, wide application of these coronary sinus (CS) retroperfusion techniques has been limited by concerns about their safety and complexity and in particular the need for repeated occlusion of the CS with a balloon. To address these concerns a simplified retroperfusion technique (SR) was developed that continuously infuses superior vena caval blood at 7 mL/min into the CS catheter without balloon occlusion. METHODS: Thirty pigs underwent 90 minutes of ischemia imposed by snaring the two largest diagonal branches of the left anterior descending artery and were randomized to one of five treatment groups: One group received no retroperfusion (control). Three groups had immediate (Im) institution of PICSO, SRP, or SR. In a final group, an initial 60 minutes of ischemia was followed by 30 minutes of delayed SR with superior vena caval blood. All animals were then placed on cardiopulmonary bypass and, after a 60-minute cardioplegic arrest, the coronary artery obstructions were removed, to simulate surgical revascularization. This was followed by 3 hours of reperfusion. The area of myocardium at risk and the area of infarction were determined by methylene blue and triphenyltetrazolium chloride staining with planimetric quantification. RESULTS: Results are reported as mean +/- standard deviation. The area of the left ventricle at risk for infarction was similar in all the treatment groups and represented 22.3% +/- 4.1% of the left ventricular mass. The area of infarction after 3 hours of reperfusion was 48.5% +/- 11.0% for the control group, 26.8% +/- 7.3% for Im-PICSO, 24.9% +/- 4.8% for Im-SRP, 22.4% +/- 6.6% for Im-SR, and 27.7% +/- 7.2% for delayed SR (p < 0.01 for each group versus control). The mean CS pressure (in mm Hg) during treatment was 6.3 +/- 1.7 for the control group, 25.7 +/- 4.5 for Im-PICSO, 22.8 +/- 3.7 for Im-SRP, 5.0 +/- 1.5 for Im-SR, and 6.3 +/- 2.1 for delayed SR (p < 0.01 for Im-PICSO and Im-SRP versus control). CONCLUSIONS: The simplified retroperfusion technique is as effective as PICSO and SRP in salvaging ischemic myocardium, but is considerably simpler. The simplified retroperfusion technique is inherently safer because of the lower CS pressures imposed by low flows and the lack of CS balloon obstruction. The efficacy of delayed SR has profound implications on possible mechanisms of ischemic myocardial salvage. Further investigation is warranted.

Animals

Conditioned stimulus determinants of conditioned response form in Pavlovian fear conditioning.

Four experiments using barpress conditioned suppression in rats found that tone evoked more freezing (immobility) than did light. Still, tone and light appeared to have similar conditioned value as assessed by suppression in Experiments 1, 2, and 3, and by blocking, second-order conditioning, and overconditioning assays in Experiments 1, 2, and 3, respectively. Experiment 4 arranged for tone to evoke less suppression than light but more freezing. Results suggest that in fear conditioning, the nature of the conditioned stimulus affects the form of conditioned responding (strong vs. weak freezing). This conclusion extends one drawn by P. C. Holland (1977) on the basis of his work in appetitive conditioning.

Animals

Combining percutaneous bypass with coronary retroperfusion limits myocardial necrosis.

After an acute coronary occlusion that results in hemodynamic instability, the institution of percutaneous bypass (PB) can effectively support the failing myocardium. However, PB cannot augment coronary blood flow, and substantial regional myocardial necrosis can still occur. This experimental study was undertaken to determine whether combining PB with coronary venous retroperfusion using pressure-controlled intermittent coronary sinus occlusion (PICSO) would limit myocardial necrosis after an acute coronary occlusion. In 30 pigs, the second and third diagonal vessels were occluded with snares for 90 minutes followed by 30 minutes of cardioplegic arrest and 180 minutes of reperfusion with the snares released. During the period of coronary occlusion, 10 pigs were placed on PB, 10 pigs received PB+PICSO, and 10 pigs received no support (unmodified). Hearts treated with the combination of PB+PICSO had the highest wall motion scores (unmodified, 1.4 +/- 0.3; PB, 1.4 +/- 0.3; PB+PICSO, 2.8 +/- 0.3 [p < 0.05 versus unmodified and PB]) and the lowest area of necrosis in the area at risk (unmodified, 73% +/- 3%; PB, 43% +/- 2%; PB+PICSO, 14% +/- 2% [p < 0.05, PB and PB+PICSO versus unmodified; p < 0.05, PB+PICSO versus PB]). We conclude that combining PB with coronary venous retroperfusion significantly limits myocardial necrosis.

Animals

Limiting ischemic myocardial damage using glucose-insulin-potassium solutions.

BACKGROUND: This experimental study sought to determine whether the infusion of glucose-insulin-potassium (GIK) solutions to ischemic myocardium during revascularization would decrease myocardial damage. METHODS: In 40 pigs, the second and third diagonal vessels were occluded with snares for 90 minutes followed by 30 minutes of cardioplegic arrest and 180 minutes of reperfusion. During the periods of coronary occlusion and reperfusion, 10 pigs received GIK (glucose = 300 g/L, insulin = 50 U/L, K+ = 80 mEq/L) through the jugular vein at 1 mL.kg-1.h-1 (GIK-IV group); 10 pigs received GIK through the coronary sinus (GIK-CS group); 5 pigs received GIK through the jugular vein during reperfusion only (GIK-R group); 5 pigs received GIK through the jugular vein 2 hours prior to coronary occlusion and then during the periods of coronary occlusion and reperfusion (GIK-Pre group); and 10 pigs received no GIK (Unmodified group). Ischemic damage was assessed by wall motion scores using two-dimensional echocardiography, changes in myocardial tissue pH, and the area of necrosis in the area of risk. RESULTS: Hearts treated with GIK had significantly less tissue acidosis, higher wall motion scores, and the least tissue necrosis (14% +/- 2% GIK-Pre versus 12% +/- 2% GIK-CS versus 16% +/- 2% GIK-IV versus 25% +/- 2% GIK-R versus 73% +/- 4% Unmodified; all, p < 0.05 versus Unmodified). CONCLUSIONS: We conclude that a glucose-insulin-potassium solution reduces ischemic myocardial damage during coronary revascularization.

Animals

Role of leukocyte depletion during cardiopulmonary bypass and cardioplegic arrest.

BACKGROUND: Leukocyte depletion (LD) has been shown to be beneficial during the reperfusion of acutely ischemic myocardium; however, its role during cardiopulmonary bypass (CPB) in hearts protected with blood cardioplegia (BCP) is unknown. This experimental study sought to determine whether LD filters inserted in the CPB circuit before cardioplegic arrest and in the BCP circuit during arrest would decrease ischemic myocardial damage. METHODS: In 20 pigs, the second and third diagonal vessels were occluded for 90 minutes, followed by 45 minutes of BCP arrest and 180 minutes of reperfusion on CPB. In 5 pigs, LD filters were inserted in both the CPB and BCP circuits (LD-CPB+BCP). Five pigs had LD during BCP (LD-BCP), 5 pigs had LD during CPB (LD-CPB), and 5 pigs had no LD. Ischemic damage was assessed by wall motion scores using two-dimensional echocardiography and the area of necrosis/area of risk. RESULTS: The LD-CPB and LD-CPB+BCP groups had the highest wall motion scores and the lowest area of necrosis/area of risk. The addition of LD to BCP alone did not significantly alter wall motion scores or the area of necrosis/area of risk. CONCLUSION: Leukocyte depletion filters significantly reduce ischemic damage during acute surgical revascularization and appear to be most effective when placed in the CPB circuit before cardioplegic arrest.

Animals

Enhanced recovery of ischemic myocardium by combining percutaneous bypass with intraaortic balloon pump support.

Although percutaneous bypass (PB) can support the failing myocardium, regional ischemic damage may still occur beyond a coronary occlusion. This study sought to determine whether the addition of intraaortic balloon pump (IABP) support to PB would result in more optimal salvage of ischemic myocardium. In 30 pigs, the second and third diagonal vessels were occluded with snares for 90 minutes followed by 30 minutes of cardioplegic arrest and 3 hours of reperfusion with the snares released. During the period of coronary artery occlusion, 10 pigs were placed on PB, 10 pigs received PB plus IABP support, and 10 pigs received no support (the unmodified group). The hearts treated with the combination of PB and IABP support exhibited the highest wall motion scores (3.3 +/- 0.20 for the PB plus IABP group [p < 0.05 from the unmodified group and from the PB group]; versus 1.40 +/- 0.30 for the PB group versus 1.37 +/- 0.33 for the unmodified group), the least tissue acidosis (change in pH, -0.30 +/- 0.2 for the PB plus IABP group [p < 0.05 from the PB group] versus -0.60 +/- 0.10 for the PB group versus -0.41 +/- 0.13 for the unmodified group), and the least area of necrosis (25% +/- 5% for the PB plus IABP group [p < 0.05 from the unmodified group and from the PB group]; versus 43% +/- 2% for the PB group [p < 0.05 from the unmodified group] versus 73% +/- 3% for the unmodified group).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis

Reduction of myocardial necrosis by positioning the intra-aortic balloon pump in the ascending aorta.

The presence of severe peripheral vascular disease may necessitate inserting an intra-aortic balloon pump (IABP) directly into the ascending aorta. As positioning an IABP into the descending aorta may be hazardous and difficult through the ascending aorta, this experimental study sought to determine the effects of positioning an IABP in the ascending aorta on myocardial recovery during urgent surgical revascularization. The second and third diagonal coronary arteries in 30 pigs were occluded with snares for 90 min followed by 30 min of cardioplegic arrest and 180 min of reperfusion with the snares released. During the period of coronary occlusion, ten pigs received an IABP in the descending aorta, ten had an ascending aorta IABP and ten received no IABP support. The best recovery of wall motion, least tissue acidosis and lowest area of necrosis occurred when an IABP was positioned in the ascending aorta. It is concluded that myocardial recovery is enhanced when an IABP is positioned in the ascending aorta during urgent surgical revascularization.

Acidosis

Detrimental effects of interrupting warm blood cardioplegia during coronary revascularization.

Warm blood cardioplegia has emerged as a substitute for cold blood cardioplegia as a method of myocardial protection. However, the continuous infusion of blood in this technique may obscure the operative field and necessitate interruption of warm blood cardioplegia. This experimental study was therefore undertaken to determine whether interrupting warm blood cardioplegia during coronary revascularization would increase myocardial damage. In 30 adult pigs, the second and third diagonal vessels were occluded with snares for 90 minutes. All animals underwent cardiopulmonary bypass and 45 minutes of cardioplegic arrest. During the period of cardioplegic arrest, 10 pigs received intermittent antegrade/retrograde infusion of cold blood cardioplegic solution (4 degrees C) 10 pigs received continuous retrograde infusion of warm blood cardioplegic solution (37 degrees C) at 100 ml/min, and 10 pigs received retrograde infusion of warm blood cardioplegic solution that was interrupted for three 7-minute periods. After aortic unclamping, the coronary snares were released and all hearts were reperfused for 180 minutes. Interrupting retrograde warm blood cardioplegia resulted in more tissue acidosis during cardioplegic arrest (6.20 +/- 0.16 interrupted retrograde warm blood cardioplegia and 6.45 +/- 0.12 continuous retrograde warm blood cardioplegia, both p < 0.05 compared with 6.98 +/- 0.17 intermittent antegrade and retrograde cold blood cardioplegia), decreased echocardiographic wall-motion scores (4 [normal] to -1 [dyskinesis]; 2.06 +/- 0.30 interrupted retrograde warm blood cardioplegia, p < 0.05 compared with 3.30 +/- 0.40 intermittent antegrade and retrograde cold blood cardioplegia, 2.80 +/- 0.40 continuous retrograde warm blood cardioplegia), and increased tissue necrosis as measured by the area of necrosis/area at risk (38% +/- 5% interrupted retrograde warm blood cardioplegia, p < 0.05 compared with 21% +/- 2% intermittent antegrade and retrograde cold blood cardioplegia; 25% +/- 2% continuous retrograde warm blood cardioplegia). We concluded that interrupting warm blood cardioplegia during coronary revascularization diminishes the effectiveness of warm blood cardioplegia and results in increased ischemic damage.

Animals

Warm versus cold blood cardioplegia--is there a difference?

This experimental study sought to compare the effectiveness of warm blood cardioplegia versus cold blood cardioplegia in protecting areas of ischemic myocardium during urgent coronary revascularization. In 40 adult pigs, the second and third diagonal vessels were occluded with snares for 90 minutes. All animals were then placed on cardiopulmonary bypass and underwent 45 minutes of cardioplegic arrest followed by 3 hours of reperfusion during which time the coronary snares were released. During the period of cardioplegic arrest, 10 pigs received antegrade continuous warm blood cardioplegic solution (37 degrees C) at 100 ml/min; 10 animals received retrograde warm blood cardioplegic solution at 100 ml/min; 10 received intermittent, antegrade cold blood cardioplegic solution (4 degrees C), and 10 animals received intermittent, antegrade/retrograde cold blood cardioplegic solution. Hearts protected with antegrade warm blood cardioplegic solution had the lowest pH values in the area at risk (6.59 +/- 0.10 antegrade warm blood cardioplegia versus 6.80 +/- 0.10 retrograde warm blood cardioplegia versus 6.72 +/- 0.18 antegrade cold blood cardioplegia versus 6.85 +/- 0.15 antegrade/retrograde cold blood cardioplegia and the highest area of necrosis (42% +/- 3% antegrade warm blood cardioplegia versus 26% +/- 2% [p < 0.05 from antegrade warm blood cardioplegia] retrograde warm blood cardioplegia versus 31% +/- 2% [p < 0.05 from antegrade warm blood cardioplegia] antegrade cold blood cardioplegia versus 21% +/- 2% [p < 0.05 from antegrade warm blood cardioplegia] antegrade/retrograde cold blood cardioplegia). We conclude that in the presence of an acute coronary occlusion with ischemic myocardium, warm blood cardioplegic solution should be given in a continuous retrograde fashion and does not result in myocardial protection superior to the protection that can be achieved with antegrade/retrograde cold blood cardioplegic solution.

Animals

Reduction of infarct size with coronary venous retroperfusion.

BACKGROUND: The purpose of this study was to determine whether coronary venous retroperfusion with pressure-controlled intermittent coronary sinus occlusion (PICSO) alone and in combination with coronary venous substrate enhancement using L-glutamate would decrease ischemic damage after surgical revascularization for an acute coronary occlusion. METHODS AND RESULTS: In 40 pigs, the second and third diagonal vessels were occluded with snares for 90 minutes followed by 30 minutes of cardioplegic arrest and 180 minutes of reperfusion with the coronary snares released. During the period of coronary occlusion, 10 pigs received PICSO using a balloon-tipped triple-lumen catheter in the coronary sinus; 10 pigs received PICSO plus oxygenated blood transfused retrograde via the PICSO catheter (7 ml/min), 10 pigs received PICSO plus an oxygenated blood L-glutamate (13 mM) solution, and 10 pigs received neither PICSO, blood, nor L-glutamate through the coronary sinus (unmodified). Hearts treated with PICSO had higher wall motion scores (1.27 +/- 0.33 for unmodified, 2.40 +/- 0.40* for PICSO, 2.45 +/- 0.20* for PICSO plus blood, 2.85 +/- 0.30* for PICSO plus L-glutamate; *p < 0.05 from unmodified where 4 is normal to -1 is dyskinesia), lower area of necrosis-to-area of risk ratio using histochemical staining techniques (73 +/- 4% for unmodified, 27 +/- 4 for PICSO; 18 +/- 2* for PICSO plus blood, 12 +/- 1* PICSO plus L-glutamate; *p < 0.05 from unmodified), significantly less tissue acidosis (pH) compared with the unmodified group (pH, -0.41 +/- 0.13 for unmodified, -0.16 +/- 0.03* for PICSO, -0.19 +/- 0.02* for PICSO plus blood, -0.20 +/- 0.08* for PICSO plus L-glutamate; *p < 0.05 from unmodified). CONCLUSIONS: Coronary venous retroperfusion with PICSO alone and in combination with coronary venous substrate enhancement using L-glutamate significantly decreases ischemic damage during urgent surgical revascularization.

Angioplasty, Balloon, Coronary

Superiority of retrograde cardioplegia after acute coronary occlusion.

Because antegrade cardioplegia may limit the distribution of cardioplegia beyond a coronary occlusion, this study was undertaken to determine whether retrograde coronary sinus cardioplegia provides superior myocardial protection during revascularization of an acute coronary occlusion. In 20 adult pigs, the second and third diagonal branches were occluded with a snare for 1 1/2 hours. Animals were then placed on cardiopulmonary bypass and underwent 30 minutes of ischemic arrest with multidose, potassium, crystalloid cardioplegia. In 10 animals, the cardioplegia was given antegrade through the aortic root, whereas in 10 others, it was given retrograde through the coronary sinus. After the arrest period, the coronary snares were released and all hearts were reperfused for 3 hours. Postischemic damage in the myocardium beyond the occlusions was assessed by wall motion scores using two-dimensional echocardiography (4 = normal to -1 = dyskinesia), the change in myocardial pH from preischemia, and the area of necrosis/area of risk (histochemical staining). Hearts protected with retrograde coronary sinus cardioplegia had less tissue acidosis (change in pH = 0.08 +/- 0.03 versus 0.41 +/- 0.13; p less than 0.05), higher wall motion scores (2.0 +/- 0.6 versus 1.3 +/- 0.3; not significant), and less myocardial necrosis (43.4% +/- 3.6% versus 73.3% +/- 3.5%; p less than 0.0001). We conclude that retrograde coronary sinus cardioplegia provides more optimal myocardial protection than is possible with antegrade cardioplegia after revascularization of an acute coronary occlusion.

Acid-Base Equilibrium

Continuous versus intermittent cardioplegia in the presence of a coronary occlusion.

Coronary artery occlusions can alter the distribution of cardioplegia and result in ischemic damage. This study was undertaken to determine whether continuous antegrade cardioplegia delivery would result in colder temperatures and provide better washout of acid metabolites than is possible with intermittent antegrade cardioplegia when coronary occlusions are present. Twenty pigs were placed on cardiopulmonary bypass and underwent 2 hours of ischemic arrest with occlusion of the middle left anterior descending coronary artery followed by 1 hour of reperfusion without occlusion of that artery. Ten pigs received intermittent (every 20 minutes) antegrade potassium crystalloid cardioplegia (4 degrees C), and 10 others had the same solution given continuously (30 mL/min). Cardioplegia distribution was assessed by continuous monitoring of myocardial pH (Khuri pH probe) and temperature in the region beyond the occlusion of the left anterior descending coronary artery. Both cardioplegic techniques resulted in tissue acidosis (continuous group, 6.69 +/- 0.08, versus intermittent group, 6.73 +/- 0.07; not significant). Average temperature in the left anterior descending coronary artery during arrest was also similar in both groups (continuous group, 18.3 degrees +/- 0.5 degrees C, versus intermittent group, 18.2 degrees +/- 0.5 degrees C). Because of these metabolic changes, both cardioplegic techniques resulted in abnormal wall motion in the anteroseptal region using two-dimensional echocardiography, but the scores were not significantly different (continuous group, 1.5 +/- 0.3, versus intermittent group, 1.6 +/- 0.4; 4 = normal to 0 = dyskinesia).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals