Effects of cardioplegic solutions on conductive coronary arteries (original) (raw)
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Journal of Thoracic and Cardiovascular Surgery, 1996
University of Wisconsin solution has provided excellent myocardial pres. ervation. However, the high potassium content of the currently available University of Wisconsin solution has been implicated in coronary artery endothelial damage. We placed 16 neonatal (age 1 to 3 days) Duroc piglet hearts on an isolated nonworking perfusion circuit. Endothelium-dependent and endothelium-independent vasodilation were tested by measuring coronary blood flow after intracoronary infusion of bradykinin (10 -6 mol/L) and nitroprusside (10 -6 mol/L), respectively. In addition, nitric oxide levels were measured after bradykinin infusion. The hearts were then arrested blindly with either a modified University of Wisconsin solution (group 1; n = 8, K + = 25 mEq/L) or standard University of Wisconsin solution (group 2; n = 8, K + = 129 mEq/L) by infusion of cardioplegic solution every 20 minutes for a total of 2 hours. After bradykinin infusion, the mean coronary blood flow increased by 237.1% -14.0% of baseline valves before arrest and by 232.8% +-16.0% after arrest in group 1 (p = not significant). As in the first group, the mean coronary blood flow in group 2 increased by 231.1% +_ 13.7% before arrest; however, the increase in mean coronary blood flow after arrest was significantly attenuated (163.3% +-12.8%, p < 0.01). The loss of endothelium-dependent coronary blood flow response in group 2 correlated with a decreased capacity to release nitric oxide after arrest (prearrest 8.25 +-2.30 nmol/min per gram versus postarrest -2.46 -2.29 nmol/min per gram, p < 0.01). Endotheliumindependent vasodilatory response revealed no significant difference between groups before and after arrest. These results suggest that the low-potassium University of Wisconsin solution provides superior p r o t e c l tion of the endothelium by preserving the endothelium-dependent vasodilatory response to nitric oxide release. (J Thorac Cardiovasc Surg 1996;112: 103-10) T he University of Wisconsin solution (UWS), developed by Wahlberg, Southard, and Belzer I in 1986, has been used successfully to preserve the pancreas, 2 kidney, 3 and liver 4 in both laboratory and clinical settings. Numerous studies have demonstrated that UWS also provides excellent myocardial preservation in a variety of animal models. 5-s Fur-From the Division
Development of cardioplegic solution without potassium: experimental study in rat
Revista Brasileira de Cirurgia Cardiovascular, 2013
Introduction: Myocardial preservation during open heart surgeries and harvesting for transplant are of great importance. The heart at the end of procedure has to resume its functions as soon as possible. All cardioplegic solutions are based on potassium for induction of cardioplegic arrest. Objective: To assess a cardioplegic solution with no potassium addition to the formula with two other commercially available cardioplegic solutions. The comparative assessment was based on cytotoxicity, adenosine triphosphate myocardial preservation, and caspase 3 activity. The tested solution (LIRM) uses low doses of sodium channel blocker (lidocaine), potassium channel opener (cromakalin), and actin/myosin cross bridge inhibitor (2,3-butanedione monoxime). Methods: Wistar rats underwent thoracotomy under mechanical ventilation and three different solutions were used for "in situ" perfusion for cardioplegic arrest induction: Custodiol (HTK), Braile (G/A), and LIRM solutions. After cardiac arrest, the hearts were excised and kept in cold storage for 4 hours. After this period, the hearts were assessed with optical light microscopy, myocardial ATP content and caspase 3 activity. All three solutions were evaluated for direct cytotoxicity with L929 and WEHI-164 cells. Results: The ATP content was higher in the Custodiol group compared to two other solutions (P<0.05). The caspase activity was lower in the HTK group compared to LIRM and G/A solutions (P<0.01). The LIRM solution showed lower caspase activity compared to Braile solution (P<0.01). All solutions showed no cytotoxicity effect after 24 hours of cells exposure to cardioplegic solutions. Conclusion: Cardioplegia solutions without potassium are promised and aminoacid addition might be an interesting strategy. More evaluation is necessary for an optimal cardioplegic solution development.
Role of potassium concentration in cardioplegic solutions in mediating endothelial damage
The Annals of Thoracic Surgery, 1991
We studied the effect of potassium concentration in cardioplegic solutions on endothelial function by examining its influence on 5-hydroxytryptamine-(5-HT) and nitroglycerin-induced vasodilation in the isolated rat heart. Forty-eight rat hearts were perfused on a modified Langendorff preparation. After a baseline record of increase in coronary flow induced by M 5-HT and 10 pg/mL nitroglycerin, the hearts were perfused for 30 or 60 minutes with either St. Thomas' solution or Bretschneider solution containing 20 mmol/L of potassium or for 30 minutes with either solution containing 30 mmol/L of potassium (n = 8 in each). Initially, 5-HT and
The Journal of Thoracic and Cardiovascular Surgery, 1989
Physical and mechanical effects of cardioplegic injection on flow distribution and myocardial damage in hearts with normal coronary arteries The physical and mechanical effects of injecting crystaDoid cardioplegic solution under various pressures and flows was studied (in canine hearts) to establish a safe method for administering it in the presence of normal coronary arteries. A constant pressure system (300 mm Hg = 15 psi) was maintained in the solution reservoir, and flows and pressures were varied with the use of cannulas of different inner diameters: 0.8, 1.35, 1.6, 2.3, 2.58, and 2.80 mm. Cardioplegia distribution was measured by 15~m radioactive microspheres. Peak flow rate, total flow, and mean flow rate per infusion were measured by an inIineelectromagnetic flowmeter probe. Direct aortic root pressure, time to standstiU, and myocardial temperatures were recorded by continuous monitoring. Cardiac isoenzymes were measured in the coronary sinus, peripheral blood, and directly in the myocardial tissue. Histologic changes 'in the left ventricle were examined by light microscopy. The results showed that the higher the flow and pressure, the shorter the prearrest period, the better the flow distribution, and the faster the myocardial temperature drop. Mean aortic root pressures higher than 110 mm Hg and peak flow rates greater than 1500 mljmin caused a higher incidence of mechanical-physical trauma to the vascular endothelium and the endocardium, but ceDuiar protection was good. Low pressure (less than 30 mm Hg) and peak flows (less than 125 mljmin) showed a higher incidence of cellular (myocardial) ischemia, focal necrosis, and uneven flow distribution. An aortic root pressure of 61 ± 5 mm Hg, a mean peakflow rate of 622 ± 52 mljmin, and a total flow of 600 mI for the first injection seem to offer the best cellular protection with minimal physical injury to the endothelium and endocardium for a mean canine heart weight of 236 gm.
Comparison of distribution beyond coronary stenoses of blood and asanguineous cardioplegic solutions
The Journal of Thoracic and Cardiovascular Surgery, 1983
Comparison of distribution beyond coronary stenoses of blood and asanguineous cardioplegic solutions In seven dogs on cardiopulmonary bypass, a critical stenosis (75% to 90 %) of the left anterior descending coronary artery (LAD) was produced. Alternate 250 mlfmin infusions of asanguineous and blood cardioplegic (4 0 C) solutions were made for 3 to 5 minutes. Poststenotic flow (jlowmeter), intramyocardial temperature, and aortic pressure were measured. During cardioplegic infusions of 250 mlfmin, aortic pressure was 34 ± 4 mm Hg higher with blood cardioplegia than with asanguineous cardioplegia (82 ± 7 versus 48 ± 8 mm Hg*). Poststenotic cardioplegic flow was 39% ± 9% * higher (29 ± 5 versus 18 ± 5 ml/min*) with blood cardioplegia. Consequently, blood cardioplegia resulted in more rapid arrest (20 ± 2 versus 45 ± 5 seconds*) and lower myocardial temperature (6 0 ± 1 0 C*) in the region of LAD blood supply; posterior ventricular myocardial cooling was similar (unobstructed vessels) with both solutions. These data show that the reduced viscosity of asanguineous cardioplegia compared to blood cardioplegia results in lower aortic pressure. Consequently, the higher aortic pressure with blood cardioplegia results in superior cardioplegic delivery beyond obstructed coronaries and better myocardial cooling. We conclude that the decreased viscosity of 4 0 C asanguineous cardioplegia causes diversion of cardioplegic solution from the obstructed to the normal coronary bed.
Perfusion with Non-Oxygenated Tyrode Solution Causes Maximal Coronary Vasodilation in Canine Hearts
Clinical and Experimental Pharmacology and Physiology, 1987
1. Coronary vasodilator effects of non-ischaemic hypoxia (perfusion with nonoxygenated Tyrode solution) and ischaemic. hypoxia (coronary occlusion) were compared. 2. The left anterior descending coronary artery (LAD) of six in situ canine hearts was perfused selectively at controlled pressure with normal arterial blood or with non-oxygenated Tyrode solution. LAD flow was measured continuously with an electromagnetic flowmeter. Reactive hyperaemic blood flow responses following 3 rnin Tyrode perfusion were compared with responses following 3 min complete coronary occlusion. 3. Control LAD blood flow was 26.9 f 4.6 ml/min. A 3 rnin period of Tyrode perfusion caused a peak reactive hyperaemic blood flow of 15 1 ? 3 1 ml/min, which was not significantly different from that caused by 3 rnin occlusion, 123 k 17 ml/min. The duration and total volume of reactive hyperaemia flow following Tyrode perfusion were smaller than values following occlusion. 4. The present findings demonstrate that myocardial hypoxia per se is a sufficient vasodilatory stimulus to account for the peak reactive hyperaemic flow following 3 rnin occlusion, but that the prolonged reactive hyperaemic response depends on vasodilator metabolites which accumulate in ischaemic myocardium.
The Annals of Thoracic Surgery, 1993
University of Wisconsin (UW) solution has been reported to enhance myocardial preservation in heart transplantation. To evaluate the effects of UW solution on coronary artery endothelial function, we designed experiments to compare UW solution with a standard crystalloid hyperkalemic cardioplegic solution (CHCS). Isolated rat hearts were studied in a modified Langendorff apparatus for coronary endothelial function. Groups 1 and 2 were perfused with 4 degrees C CHCS (24 mmol/L of KCl) and UW solution, respectively, for 10 minutes at a pressure of 80 cm H2O, whereas group 3 underwent warm ischemia for 10 minutes. Groups 4 and 5 were perfused with and stored for 4 hours in cold (4 degrees C) CHCS and UW solution, respectively. Group 6 underwent 4 hours of topical cooling (4 degrees C) without any cardioplegic perfusion. All groups had 6 hearts each. Endothelium-dependent relaxation and endothelium-independent relaxation of the coronary arteries were tested by infusing 5-hydroxytryptamine (5HT) (10(-6) mol/L) and sodium nitroprusside (10(-5) mol/L), respectively, before and after perfusion with and storage in one of the two cardioplegic solutions. The coronary vasodilatation induced by 5HT and sodium nitroprusside was not altered in hearts perfused with (group 1) or perfused with and stored in CHCS (group 4). Coronary flow increase after 5HT infusion was significantly decreased in hearts perfused with (group 2) (before, 35% +/- 10%; after, 13% +/- 10%; p < 0.01) or perfused with and stored in UW solution (group 5) (before, 34% +/- 5%; after, -5% +/- 12%), indicating severe endothelial dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)
European Journal of Cardio-Thoracic Surgery, 1996
Objective. Hearts or parts of hearts are often ischemic prior to infusion of the cardioplegic solution and have a more or less dilated coronary bed. We made an investigation whether coronary dilation just prior to induction of cardiac arrest by aortic clamping and infusion of crystalloid cardioplegic solution would influence cardioprotection. Methods. Isolated buffer-perfused rat hearts (100 cm H20 pressure (=73.5 mmHg), 37°C) were used. After a stabilization period the perfusion of 8 rats (group 1) was stopped and the hearts arrested with 5 ml CS (100 cm H20, 12°C). Equal amounts of cardioplegic solution were then delivered every 20 minutes for the entire 3~ hour hypothermic ischemic period. Following ischemia the hearts were reperfused for 60 minutes. In group 2 (n=8) 1 ml 10-2 mmol Papaverine was given into the aortic root just prior to the first cardioplegic solution infusion in order to induce coronary vasodilation. The procedure was identical in the two groups during ischemia and reperfusion. Results. During the ischemic period coronary resistance increased in group 2. During reperfusion group 2 had lower coronary flow (P=0.001), left ventricle developed pressure (P=0.002) and a higher creatine kinase release (P=0.003) than group 1 hearts. Group 2 also had a lower adenosine-triphosphate (6.51+0.40 gmol-g-1 and 14.03_+0.59 gmol.g-1, respectively, P=0.011), creatine phosphate (24.70_+1.02 ~tmol.g-1 and 36.50+__1.31 gmol-g-1, respectively, P-0.020) and a larger fall in dry/wet-weight ratio (1.7_+0.4 and 0.8_+0.5, respectively, P=0.043). Conclusions. Vasodilation (i.e. ischemia) just prior to infusion of crystalloid cardioplegic solution may impair myocardial protection even when the cardioplegic solution is delivered at a relatively low and presumably safe pressure.