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Biomedical subjects

J E Flack

Publications and source records attributed to J E Flack.

At least 37 records · Page 2Linked to original sources
PubMed1996

Critical timing of nitric oxide supplementation in cardioplegic arrest and reperfusion.

BACKGROUND: It has been shown that increased nitric oxide (NO) generation is associated with improved myocardial preservation during ischemia/reperfusion. This study sought to determine the optimal timing for NO supplementation in the setting of cardioplegic arrest, regional ischemia, and reperfusion. METHODS AND RESULTS: Isolated working rat hearts were arrested with normothermic oxygenated potassium cardioplegia for 5 minutes, followed by 60 minutes of normothermic continuous cardioplegic administration with left anterior descending coronary artery (LAD) occlusion. The hearts were divided into four groups. Hearts in group 1 were ischemic/reperfused controls without L-arginine treatment. Hearts in group 2 were perfused with 3 mmol/L L-arginine for 5 minutes before cardioplegic arrest. Hearts in group 3 were perfused with 3 mmol/L L-arginine in the cardioplegia solution. Hearts in group 4 were perfused with 3 mmol/L L-arginine for 5 minutes only during initial reperfusion. Myocardial contractile function after 30 minutes of reperfusion was significantly better in group 2 compared with the other groups and was significantly lower in group 4 than group 1. Coronary flow, although decreased from base line in all groups at 30 minutes of reperfusion, was highest in group 2. The tissue accumulation of cGMP in groups 2 and 3 increased significantly after L-arginine infusion compared with the control group (group 1). In contrast, the LAD regional cGMP after reperfusion in group 4 was comparable to group 1 and significantly lower than groups 2 and 3, whereas the circumflex region cGMP in group 4 was significantly increased over group 1, comparable to groups 2 and 3. LDH release in groups 2 and 3 was significantly lower compared with groups 1 and 4. CONCLUSIONS: As assessed by myocardial function and LDH release, L-arginine is most beneficial when given before cardioplegic arrest, effective during cardioplegic arrest, and detrimental during reperfusion. This suggests that L-arginine given during reperfusion is deleterious to optimal recovery of myocardial function in this ischemic model and that the effect of NO generation in the ischemic/reperfused myocardium may be dependent on the condition of the endothelium.

Animals↗
PubMed1996

What is the best perfusion temperature for coronary revascularization?

BACKGROUND: [corrected] A National Institutes of Health-funded clinical trial of patients undergoing coronary artery bypass randomized perfusate and myocardial preservation to cold, tepid, or warm temperatures. The goal of the trial was to evaluate neurologic function before and after operation (4 days and 1 month after operation) and to measure hematologic data for fibrinolytic potential. METHODS: The three groups comprised 116 patients who completed neurologic evaluation by means of the Mathew scale out of 130 entered into the trial (37 cold group, 50 tepid, and 43 warm). Twenty-five patients had complete hematologic studies done. All three groups were comparable before operation. The myocardial preservation protocol used blood cardioplegic solution at cold (8 degrees to 10 degrees C), tepid (32 degrees C), or warm (37 degrees C) temperature and the systemic perfusate temperature during cardiopulmonary bypass was 20 degrees (cold), 32 degrees C (tepid), or 37 degrees (warm). RESULTS: Patients in the cold group had a longer duration of intubation and postoperative hospitalization and a slightly but significantly higher peak postoperative creatine kinase MB level than patients in the warm group. There were no deaths. There was deterioration in Mathew scale findings in all three groups, and no distinction could be made between groups. However, a significantly higher number in the cold group had an abnormal postoperative neurologic examination result that prompted computed tomographic scanning (18.9% cold, 2% tepid, 9.3% warm). A cerebrovascular accident was documented by computed tomographic scanning in 8.1%, 0%, and 4.7% of patients in the cold, tepid, and warm groups, respectively (not significant). Hematologic data documented significantly increased fibrinolytic potential in the warm group. CONCLUSIONS: Perfusion temperature is a factor in recovery from cardiopulmonary bypass. Cold has more adverse neurologic sequelae that prompt computed tomographic scanning whereas warm has more activation of fibrinolytic potential. Tepid is the best temperature for optimizing recovery from cardiopulmonary bypass.

Adult↗
PubMed1995

Drug-induced heat-shock preconditioning improves postischemic ventricular recovery after cardiopulmonary bypass.

BACKGROUND: Heat-stress preconditioning of mammalian heart has been found to confer protection against ischemic reperfusion injury. Heat shock is generally provided by warming the animal by mechanical means, which is often impractical in a clinical setting. Amphetamine, a sympathomimetic drug, can elevate the body temperature as a result of enhanced endogenous lipolysis. In this study, we examined the effects of heat shock induced by amphetamine on postischemic myocardial recovery in a setting of coronary revascularization for acute myocardial infarction. METHODS AND RESULTS: Adult Yorkshire swine were injected with amphetamine (3 mg/kg IM) (n = 12), and body temperature was continuously monitored. For control studies, the pigs were injected with saline (n = 12). Five swine in each group were killed after 3 hours to obtain biopsies of vital organs to measure heat-shock protein (HSP) mRNAs. After 40 hours, the remaining 7 pigs in each group were placed on cardiopulmonary bypass, and the isolated, in situ heart preparations were subjected to 1 hour of occlusion of the left anterior descending coronary artery followed by 1 hour of global hypothermic cardioplegic arrest and 1 hour of reperfusion. Postischemic myocardial performance was monitored by measuring left ventricular (LV) pressure, its dP/dt, myocardial segment shortening, and coronary blood flow. Cellular injury was examined by measurement of creatine kinase release. The antioxidant enzymes superoxide dismutase and catalase were also assayed. Amphetamine treatment was associated with the induction of mRNAs for HSP 27, HSP 70, and HSP 89 in all the vital organs, including heart, lung, liver, kidney, and brain. Amphetamine also enhanced superoxide dismutase and catalase activities in the heart. Significantly greater recovery of LV contractile functions was noticed, as demonstrated by improved recovery of LV developed pressure (61% versus 52%), LV dP/dtmax (52% versus 44%), and segment shortening (46.2% versus 10%) and reduced creatine kinase release in the amphetamine group. CONCLUSIONS: The results demonstrate that amphetamine can induce whole-body heat shock that can precondition the heart, enhancing cellular tolerance to ischemia-reperfusion injury. Amphetamine is a sympathomimetic drug that may be used for preconditioning.

Amphetamine↗
PubMed1995

Improved 4- and 6-hour myocardial preservation by hypoxic preconditioning.

BACKGROUND: A brief hypoxic episode can precondition myocardium against a subsequent ischemic-reperfusion injury. The present study sought to determine whether intracellular ionic alterations, induced expression of heat-shock proteins (hsps), and/or catalase are involved in the cellular mechanisms by which hypoxic preconditioning can preserve postischemic function in a model of prolonged hypothermic storage. METHODS AND RESULTS: Two groups of isolated working rat hearts were studied: control (CON) and hypoxically preconditioned (HP) hearts. Hearts were arrested at 4 degrees C with St Thomas' cardioplegic solution and immersion-stored for either a 4- or 6-hour period. Myocardial function (ie, heart rate, aortic flow, coronary flow, developed pressure, and its first derivative dP/dtmax) was determined at baseline, after preconditioning, and during reperfusion. At similar time points, myocardial [Na+]i, [K+]i, [Mg2+]i, and [Ca2+]i were measured using an atomic absorption spectrophotometer, and the induction of hsp 70 and catalase mRNAs was assayed using Northern blot analysis. After 4 and 6 hours of hypothermic storage, aortic flow, dP/dtmax, and [K+]i were increased, whereas [Na+]i and [Ca2+]i were decreased significantly in the HP group compared with the CON group. Steady state mRNA levels of catalase and hsp 70 were increased from baseline levels only in the HP group, with a peak (2.8- and 2.4-fold versus baseline) after 4 hours of storage. CONCLUSIONS: Our results indicate that intracellular ionic alterations and upregulation of catalase and hsp 70 gene expression may contribute to the mechanisms underlying hypoxic preconditioning, leading to improved postischemic function during prolonged hypothermic storage of hearts.

Animals↗
PubMed1995

Hypoxic preconditioning enhances functional recovery after prolonged cardioplegic arrest.

The purpose of this study was to assess the ability of hypoxic preconditioning to improve myocardial salvage after prolonged hypothermic cardioplegic arrest. Isolated working rat hearts were arrested at 4 degrees C with St. Thomas' Hospital cardioplegic solution and immersion stored for 4 or 6 hours. Two groups were studied, control and hypoxically preconditioned (HP) hearts. After 4 hours' preservation, aortic flow, coronary flow, and the first derivative of aortic pressure were 8.7 +/- 1.6 mL/min, 17.8 +/- 1.6 mL/min, and 2,064 +/- 123 mm Hg/s, respectively, in control hearts (n = 11) and 25.7 +/- 2.5 mL/min, 27.1 +/- 2.5 mL/min, and 2,655 +/- 93 mm Hg/s, respectively, in HP hearts (n = 11) (p < 0.05). After 6 hours' preservation, aortic flow, coronary flow, and the first derivative of aortic pressure were 3.5 +/- 1.2 mL/min, 18.8 +/- 0.4 mL/min, and 1,622 +/- 226 mm Hg/s, respectively, in control hearts (n = 6) and 21.5 +/- 3.2 mL/min, 25.5 +/- 2.3 mL/min, and 2,439 +/- 239 mm Hg/s, respectively, in HP hearts (n = 6) (p < 0.05). After 6 hours' preservation, adenine nucleotides and creatine phosphate levels were not significantly different between the two groups, but lactate dehydrogenase release was significantly increased (p < 0.05) in control versus HP hearts (4.66 +/- 0.58 IU/L versus 1.98 +/- 0.28 IU/L). We conclude that hypoxic preconditioning reduces cellular necrosis and preserves myocardial function after prolonged hypothermic cardioplegic arrest.

Adenine Nucleotides↗
PubMed1995

Tranexamic acid significantly reduces blood loss associated with coronary revascularization.

Four hundred fifteen patients undergoing coronary revascularization over a 12-month period were divided into two groups: 209 controls in the first 6 months received no tranexamic acid (TA) before cardiopulmonary bypass and 206 patients in the second 6 months received TA as a hemostatic agent. The demographics and the surgical techniques used were similar in the two groups. With TA there was a significant decrease in blood loss postoperatively, from 1,114.1 mL in the controls to 803.7 mL in those given TA (p < 0.001); in red blood cell use, from 1.7 units/patient in the controls to 0.69 units/patient in those given TA (p < 0.001); in fresh frozen plasma requirements, from 0.23 units/patient in the controls to 0.024 units/patient in those given TA (p < 0.01); and in platelet transfusion, from 1.06 units/patient in the controls to 0.30 units/patients in those given TA (p < 0.01). The percentages of patients not receiving any blood products were 65% in those given TA versus 49% in the controls (p < 0.01). There was no significant difference between the two groups in the incidence of perioperative myocardial infarction, cerebrovascular accidents, pulmonary embolism, or venous thrombosis to clearly suggest hypercoagulability. In this study, TA profoundly affected the coagulopathy associated with bypass in patients undergoing coronary revascularization. It significantly reduced blood loss and blood product transfusions. Any potential increased thrombotic complications could not be clearly demonstrated in this study, but should not be ignored.

Aged↗
PubMed1995

Influence of steroids on complement and cytokine generation after cardiopulmonary bypass.

BACKGROUND: It is recognized that the inflammatory mediators complement and cytokines are generated during cardiopulmonary bypass as an endogenous response to extracorporeal circulation. METHODS: Nineteen randomized patients (10 steroid/9 nonsteroid) entered an institutional review board-approved protocol to measure complement and interleukin level generation before and after elective coronary revascularization. The steroid regimen involved 1 g of methylprednisolone sodium succinate intravenously before bypass and 4 mg of dexamethasone every 6 hours for four doses during the first 24 hours of recovery. Complement and interleukin levels were measured before bypass, immediately after bypass, and at 24, 48 and 72 hours of recovery. RESULTS: In the nonsteroid group, there was a significant elevation in all inflammatory mediators relative to the steroid group. The predominant changes occurred at 24 hours after operation. CONCLUSIONS: Steroids produced a dramatic reduction in complement and interleukin levels. The number of patients was clearly too small to document a clinical consequence of steroid administration.

Aged↗
PubMed1995

L-arginine reduces endothelial inflammation and myocardial stunning during ischemia/reperfusion.

BACKGROUND: This study evaluated whether the nitric oxide precursor L-arginine could reduce ischemia/reperfusion injury by preventing leukocyte-endothelial interactions. METHODS: Normothermic regional ischemia was induced in the open-chest working pig heart for 30 minutes followed by 90 minutes of reperfusion. A preischemic 10-minute intravenous infusion of 4 mg.kg-1.min-1 of L-arginine (n = 12) was compared with 12 control pigs. Nitric oxide release was measured from the coronary sinus using an amperometric probe. Left ventricular function, malonaldehyde, creatine kinase, myocardial oxygen extraction, and the soluble adhesion molecules (intracellular adhesion molecule-1, endothelial leukocyte adhesion molecule-1, and vascular cell adhesion molecule-1) were measured. RESULTS: Nitric oxide release was significantly reduced from baseline throughout ischemia/reperfusion only in the control group. Systolic and diastolic function, and myocardial oxygen extraction were also significantly decreased during early reperfusion in the control compared with the L-arginine group. Peak creatine kinase release was not significantly different between groups. The incidence of ventricular fibrillation, malonaldehyde release, and soluble intracellular adhesion molecule-1, endothelial leukocyte adhesion molecule-1, and vascular cell adhesion molecule-1 were each significantly decreased during reperfusion in the L-arginine group. CONCLUSIONS: L-Arginine reduced lipid peroxidation, plasma levels of soluble adhesion molecules, myocardial stunning, and arrhythmias. These results support an excessive endothelial injury/inflammatory response after regional ischemia/reperfusion that can be ameliorated through augmented nitric oxide.

Animals↗
PubMed1995

Does interruption of normothermic cardioplegia have adverse effects on myocardium? A retrospective and prospective clinical evaluation.

A total of 154 patients who underwent isolated coronary revascularization (coronary artery bypass grafting) using retrograde, near-continuous, warm cardioplegia for myocardial protection, were arbitrarily divided into three groups according to the cumulative cardioplegic interruption (i.e. the sum total of all the short cardioplegic interruption periods, expressed as a percentage of the cardiac arrest period). Group 1 (39 patients) had < 20% interruption (mean(s.e.m.) 12.5(0.01)%), group 2 (82 patients) had 20-39% interruption (mean(s.e.m.) 30.1(0.01)%) and group 3 (33 patients) had > 40% interruption (mean(s.e.m.) 45.4(0.01%). The three groups were comparable except for longer clamp time in group 3 and a lower cardiac index in group 1. The mean number and duration of cardioplegic interruptions and reperfusions and multiple clinical outcomes were recorded. Clinical outcomes (Q) wave perioperative infraction, use of an intra-aortic balloon pump, mortality, and length of stay in the intensive care unit and hospital) were the same in all groups despite significant differences in percent, number and duration of interruption and reperfusion as well as cardiac arrest. The only significant differences found were in the level of creatine kinase-MB (CK-MB) and use of inotropes after surgery, both being higher in group 1 than in groups 2 and 3 (which is the opposite of what would be expected). Intraoperative hemodynamic (cardiac index and left ventricular ejection fraction) and metabolic evaluations (CK-MB, lactate production and oxygen extraction) in 22 additional patients who underwent coronary artery bypass grafting showed no significant differences between two groups having < 30% versus > 30% cumulative cardioplegic interruption. It is concluded that warm cardioplegic interruption as used clinically has no adverse effects on the myocardium in patients undergoing coronary revascularization. Warm retrograde near-continuous blood cardioplegia is an effective method of myocardial protection.

Aged↗
PubMed1995

Constitutive nitric oxide release is impaired after ischemia and reperfusion.

Myocardial ischemia and reperfusion may result in endothelial dysfunction and reduced release of nitric oxide. With the use of an amperometric sensor, the first direct measurements of constitutive nitric oxide release from a beating heart were measured from the coronary effluent of isolated working rat hearts subjected to ischemia and reperfusion. Rats, six to eight per group, were randomly studied as follows: control (no pretreatment) and pretreatment with the nitric oxide donor L-arginine (3 mmol/L), its enantiomer D-arginine (3 mmol/L), nitric oxide inhibitor N omega-nitro-L-arginine methyl ester (100 mumol/L), and combined N omega-nitro-L-arginine methyl ester/L-arginine. Isolated hearts were pretreated for 10 minutes before 30 minutes of global ischemia and 30 minutes of reperfusion. A nonischemic control group (n = 4) was continuously perfused with oxygenated unsupplemented buffer. After ischemia/reperfusion, hearts supplemented with L-arginine recovered significantly (p < 0.05) increased developed pressure, first derivative of the aortic pressure (dP/dtmax), and aortic flow compared with all other hearts that underwent ischemia/reperfusion. In addition, nitric oxide release was significantly (p < 0.05) increased during reperfusion in the L-arginine group. During reperfusion, the recovery of aortic flow correlated with nitric oxide release (r = 0.81, p < 0.0001). We conclude that after ischemia/reperfusion, endothelial dysfunction results in decreased nitric oxide release, which can be ameliorated with L-arginine pretreatment. The direct cytoprotective properties of nitric oxide may contribute to improved functional recovery in hearts pretreated with L-arginine. Augmentation of the L-arginine/nitric oxide pathway may provide a new approach for improved recovery after cardiovascular operations.

Animals↗
PubMed1995

Does cardiopulmonary bypass temperature correlate with postoperative central nervous system dysfunction?

A National Institutes of Health-funded trial of perfusate temperature and neurological function was begun in the Baystate Medical Center in February 1994. It randomizes patients having coronary revascularization to three temperatures--warm (37 degrees C), tepid (32 degrees C), and cold (20 degrees C)--for systemic perfusate and blood cardioplegia temperature at 37 degrees C warm, 32 degrees C tepid, and 6 degrees C to 10 degrees C cold. The goal is to have a quantitated neurological examination performed prior to operation, prior to discharge at day 3 or 4, and at a 1-month follow-up interval. The initial 51 patients completing a 1-month follow-up broke down to 14 cold, 22 tepid, and 15 warm. The neurological examination quantitated their performance on the Mathew Scale, an ordinal measure from 1 to 100, with 100 being normal. There was a significant (p < 0.05) decrease across the entire study from preoperative to postoperative that was no longer present at late follow-up. Although the lowest mean scores (94.8) occurred in the warm group, they were not statistically different from the other groups', and there was no discernible influence of temperature on neurological function. Additional patients will be entered to validate a difference if such exists.

Aged↗
PubMed1994

Fast-track recovery of the coronary bypass patient.

A new approach termed "fast-track recovery" ws undertaken at both the Baystate Medical Center and Hartford Hospital. The fast-track protocol involves the following principles: (1) preoperative education; (2) early extubation; (3) methylprednisolone sodium succinate before bypass followed by dexamethasone for 24 hours postoperatively; (4) prophylactic digitalization, metoclopramide HCl, docusate sodium, and ranitidine HCl; (5) accelerated rehabilitation; (6) early discharge; (7) a dedicated fast-track coordinator to perform both daily telephone contact and a 1-week postoperative examination; and (8) a routine 1-month postoperative visit with a PA or MD. To evaluate the effects of this approach on patient care, a retrospective 1-year analysis was undertaken in both institutions with all coronary artery bypass grafting patients compared in a consecutive manner before the origin of the fast-track protocol and subsequent to its beginning. There were 280 patients in the fast-track and 282 in the non-fast-track group. The two groups were not significantly different except inexplicably there was a lower ejection fraction in the fast-track group and a longer cross-clamp time. Postoperatively, the mean time to extubation decreased from 22.1 to 15.4 hours, and peak weight gain decreased from 2.8 to 1.6 kg from the non-fast-track to the fast-track group (p < 0.01). This was accompanied by significant (p < 0.001) decreases in intensive care unit duration from 2.4 to 1.9 days and in postoperative length of stay from 8.3 to 6.8 days from the non-fast-track to the fast-track group. There was no increase in morbidity or mortality associated with the fast-track protocol either early or late. Thirty-day hospital readmission was not significantly different between the two groups. Fast-track methodology is effective, and we routinely employ this approach for all patients undergoing cardiopulmonary bypass.

Aged↗
PubMed1994

Emergency cardiopulmonary bypass in the cardiac surgical unit can be a lifesaving measure in postoperative cardiac arrest.

BACKGROUND: Postoperative cardiac arrest that is not responsive to conventional resuscitation is uniformly fatal. Sixteen patients who experienced postoperative ventricular fibrillation (VF) and arrest over a 6-year period and did not respond to open chest resuscitation were placed on an emergency basis on cardiopulmonary bypass (CPB) in the cardiac surgical intensive care unit (CSICU). METHODS AND RESULTS: Data were reviewed by retrospective analysis. Nine of the 16 patients (56.3%) survived, and they spent a mean of 9 +/- 2.8 days in the CSICU and a mean of 17 +/- 4.6 days in the hospital. They all are alive 1 month to 5 1/2 years later. The mean interval between VF/arrest and CPB in the CSICU was 50 +/- 6.7 minutes (range, 25 to 83 minutes) for survivors and 51 +/- 6.1 minutes (35 to 83 minutes) for nonsurvivors (P = .98). The duration of CPB in the CSICU was 111 +/- 16.0 minutes (range, 55 to 189 minutes) for survivors and 167 +/- 20.7 minutes (range, 80 to 232 minutes) for nonsurvivors (P = .05). There were no apparent differences between survivors and nonsurvivors in age, history of arrhythmias, use of antiarrhythmics, congestive heart failure, recent myocardial infarction, ejection fraction, preoperative intra-aortic balloon pump, urgency, or type of operation. Surgical variables and postoperative medications and electrolytes (after the primary procedure) were similar. The use of cardioplegic arrest during CPB in the CSICU was higher among survivors (3 of 9) compared with 0 of 7 for nonsurvivors (P = .21). There was no mediastinitis and only two minor soft tissue infections among survivors. CONCLUSIONS: The use of CPB in the CSICU can achieve significant survival in patients who have otherwise irreversible cardiac arrest and/or VF after surgery; the incidence of infection in patients undergoing CPB in the CSICU is very low; and the use of warm cardioplegic arrest may enhance the changes of survival in this type of patient.

Aged↗
PubMed1994

Normothermic cardioplegia prevents intracellular calcium accumulation during cardioplegic arrest and reperfusion.

BACKGROUND: Development of intracellular calcium overloading is to be a primary factor in cellular injury during myocardial reperfusion. We studied the effects of different temperatures during continuously perfused cardioplegic arrest on the changes of intracellular calcium concentration ([Ca2+]i) level in isolated rat hearts. METHODS AND RESULTS: Rat hearts were perfused by the Langendorff technique with Krebs-Henseleit bicarbonate (KHB) buffer. The [Ca2+]i was monitored by loading the heart with fura-2 acetoxymethyl ester and by using a [Ca2+]i analyzer. [Ca2+]i was calculated by determining the maximal and minimal fluorescent intensity for each heart. The hearts (n = 6 in each group) were subjected to cardioplegic arrest by continuous perfusion of oxygenated crystalloid K+ (15 mEq/L) cardioplegic solution (CPS) at different temperatures (4 degrees C, 20 degrees C, 28 degrees C, 37 degrees C) for 120 minutes, followed by 30 minutes of normothermic KHB buffer reperfusion. A fifth group received continuous perfusion as a control with 37 degrees C KHB buffer. The baseline values of [Ca2+]i were comparable in all experimental groups. In hearts perfused with 4 degrees C CPS, [Ca2+]i increased significantly during reperfusion (from 221 +/- 24 nmol/L [mean +/- SEM] at baseline to 341 +/- 19 at the end of reperfusion, P < .05). CPS perfusion at 20 degrees C also induced significant Ca2+ overloading during reperfusion, but not as much as in the 4 degrees C group. No significant [Ca2+]i increase occurred at 28 degrees C or 37 degrees C. CONCLUSIONS: Continuous cardioplegic perfusion at lower temperatures (ie, 4 degrees C or 20 degrees C) induces Ca2+ overloading during reperfusion, which is detrimental to the optimal recovery of ventricular performance, while normothermic cardioplegic perfusion prevents the development of Ca2+ accumulation. These results provide experimental evidence for a detrimental effect of prolonged hypothermic continuous cardioplegia.

Animals↗
PubMed1993

Postischemic deterioration of sarcoplasmic reticulum: warm versus cold blood cardioplegia.

Impaired cardiac sarcoplasmic reticulum (SR) function, as evidenced by reduced SR Ca2+ uptake rate and decreased SR Ca(2+)-adenosine triphosphatase activity, has been found in postischemic "stunned" myocardium and in hearts subjected to hypothermic arrest. In this study, we compared the effects of retrograde continuous coronary sinus warm blood cardioplegia (WBC) and retrograde intermittent cold blood cardioplegia (CBC) on cardiac SR function and postischemic ventricular functional recovery in pig hearts. Twelve in situ isolated pig hearts supported by cardiopulmonary bypass were subjected to 120 minutes of cardioplegic arrest with either WBC (37 degrees C) or CBC (6 degrees to 10 degrees C), followed by 60 minutes of 37 degrees C reperfusion. Left ventricular global contractile function and coronary blood flow were measured before arrest and during reperfusion. Cardiac SR was isolated from left ventricular biopsy specimens, and 45Ca2+ uptake by SR and SR Ca(2+)-adenosine triphosphatase activity were determined. The recovery of left ventricular global contractile function as indicated by the maximum of the first derivative of left ventricular pressure was significantly improved in the WBC group compared with that of the CBC group (70% versus 46%; p < 0.05). The SR Ca(2+)-adenosine triphosphatase activity was better preserved after 60 minutes reperfusion in WBC compared with CBC (0.31 +/- 0.02 versus 0.20 +/- 0.03 microM Pi/min/mg protein, p < 0.05), and the recovery of SR Ca2+ uptake was significantly improved by WBC compared with CBC (1.15 +/- 0.12 versus 0.83 +/- 0.04 microM Ca2+/min/mg protein; p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗