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Biomedical subjects

S Levitsky

Publications and source records attributed to S Levitsky.

At least 91 records · Page 5Linked to original sources
PubMed1991

Myocardial oxygen consumption after fibrillation in the nonhypertrophied porcine ventricle.

Prior studies of nonischemic ventricular fibrillation have identified variable bioenergetic defects that depend on the prevailing frequency of electrical activation, coronary perfusion pressure, and left ventricular wall tension. In hearts in the adequately perfused, vented, and nondistended state the myocardial oxygen consumption of ventricular fibrillation may not be significantly different than that of the empty, beating heart. Thus, the present study investigated both global normothermic ischemic and nonischemic prolonged ventricular fibrillation effects on cardiac energetics when quantitated in the same heart under constant and defined nonworking conditions. At constant heart rate and perfusion pressure, preload recruitable stroke work was preserved in the nonischemic group but depressed to 41% of control postischemically (p = 0.018). Under control conditions, no significant differences in myocardial oxygen consumption between the various nonworking cardiac states were detected. However, postischemic empty, beating hearts and empty, fibrillating hearts both extracted (31%) and consumed (26%) less oxygen (p less than 0.03 each) without concomitant coronary hyperemia. Prolonged nonischemic ventricular fibrillation increased coronary blood flow 158% (p less than 0.03) without augmenting myocardial oxygen consumption. These data contrast with the previously reported increased oxygen demand of ventricular fibrillation and suggest that postischemic fibrillation is not bioenergetically deleterious in the nonhypertrophied heart under controlled working conditions.

Animals↗
PubMed1990

Ventriculoarterial coupling influences regional contractility.

The purpose of this study was to adjudicate whether concomitant manipulation of inotropic state and arterial elastance influences linear indices of regional contractility. Fifteen autonomically denervated open-chest porcine hearts were instrumented with midmyocardial ultrasonic crystals and aortic and left ventricular chamber microamanometers. Linear left anterior descending coronary artery regional stroke work vs preload relationships (RSW) were generated by 10-sec vena caval occlusion at control and altered contractile states (either dopamine, 5 micrograms/kg/min, or propranolol, 0.2 mg/kg) and following arterial elastance variation (phenylephrine or nitroprusside), effecting an average 30% change in mean arterial pressure (MAP). Global contractility (dP/dt) was doubled (227% of control) by dopamine and halved (35% of control) by propranolol at constant preload (end-diastolic volume, end-diastolic pressure) and afterload (MAP). Regional contractility (RSW slope) was increased from 135 +/- 11 to 211 +/- 28, P less than 0.01, by dopamine, but unchanged with propranolol (106 +/- 10 vs 118 +/- 14, NS). Bidirectional changes in aortic elastance depressed the dopamine-augmented RSW slope (115 +/- 17, nitroprusside; 132 +/- 14, phenylephrine; P less than 0.01 vs dopamine). These differences were attenuated by propranolol infusion (98 +/- 7, nitroprusside; 132 +/- 9, phenylephrine; NS vs propranolol). Thus, optimizing ventriculoarterial coupling should supersede simple afterload manipulation in perioperative cardiac support.

Animals↗
PubMed1990

Effects of low extracellular calcium on cytosolic calcium and ischemic contracture.

We have shown that myocardial cytosolic calcium [Cai] rises during ischemia. Simultaneously membrane bound stores are depleted. The [Cai] rise precedes the onset of irreversible ischemic contracture. We found that a low extracellular calcium [Cao] (100 microM) perfusate decreased peak contracture pressure and delayed the time to onset and to peak of ischemic contracture in the isolated retroperfused rabbit heart subjected to 37 degrees C ischemia. [Cai] was measured with the intracellular [Cai] fluorescent indicator Fura-2 AM (10 microM) in a separate group. In the group exposed to 2.45 mM Ca2+ there was a significant rise (P less than 0.05) in [Cai] to above 50% of preischemic value after 30 min of ischemia. The [Cai] in the low [Cao] perfused group at 30 min of ischemia was 30% below the preischemic value. The peak of the [Cai] rise in the low [Cao] perfusate group was markedly attenuated and delayed to 40 min. Taken together it appears that low calcium perfusate (100 microM) prior to ischemia attenuates the ischemia-induced [Cai] rise, delays the onset, and decreases the force of contracture with irreversible ischemic injury.

Adenosine Triphosphate↗
PubMed1990

Reduced atrial contribution to left ventricular filling in patients with severe tricuspid regurgitation after tricuspid valvulectomy: a Doppler echocardiographic study.

Patients undergoing valvulectomy for isolated tricuspid valve endocarditis offer the unique opportunity to study the effects of acquired right ventricular volume overload on left ventricular filling in persons free of pulmonary hypertension and preexisting left heart disease. Eleven patients who had undergone total or partial removal of the tricuspid valve were compared with 11 age-matched control subjects; Doppler echocardiographic techniques were used to quantify changes in left ventricular filling and to relate them to changes in left ventricular and left atrial geometry caused by right ventricular and right atrial distension. The late diastolic fractional transmitral flow velocity integral, a measure of the left atrial contribution to left ventricular filling, was significantly decreased in patients undergoing tricuspid valvulectomy compared with control subjects (0.22 +/- 0.11 versus 0.32 +/- 0.09; p less than 0.04). Severe tricuspid regurgitation in these patients resulted in marked right atrial distension, reversal of the normal interatrial septal curvature and compression of the left atrium such that left atrial area was significantly smaller than in control subjects (5.9 +/- 2.2 versus 8.6 +/- 1.2 cm2/m2; p less than 0.005). Acting as a receiving chamber, the left ventricle was maximally compressed by the volume-overloaded right ventricle in late diastole, coincident with the timing of atrial systole, resulting in a significant increase in the left ventricular eccentricity index compared with that in control subjects (1.35 +/- 0.14 versus 1.03 +/- 0.1; p less than 0.001). Thus, right ventricular volume overload due to severe tricuspid regurgitation results in left heart geometric alterations that decrease left atrial preload, impair left ventricular receiving chamber characteristics and reduce the atrial contribution to total left ventricular filling.

Adult↗
PubMed1990

Labetalol for the control of elevated blood pressure following coronary artery bypass grafting.

In a multicenter study, the efficacy and safety of intravenous (IV) labetalol for the control of elevated blood pressure were studied in the intensive care unit (ICU) in 65 patients within 4 hours following coronary artery bypass grafting (CABG). Patients with pre-existing ventricular dysfunction, bradycardia, bronchospastic disease, or postoperative complications were excluded. All patients were monitored with a thermodilution pulmonary artery catheter. Entry criteria were a systolic blood pressure (SBP) greater than 140 mm Hg or diastolic blood pressure (DBP) greater than 90 mm Hg for at least five minutes. Intravenous labetalol was loaded incrementally (5, 10, 20, and 40 mg at 10-minute intervals) to a maximum cumulative dose of 75 mg, until either SBP decreased 10% or DBP decreased 10% and was less than 90 mm Hg. Responders were entered into a 6-hour maintenance period, and received 5 to 40 mg of IV labetalol every 10 minutes as needed for blood pressure control. Hemodynamic data and temperature were recorded at baseline, just before each dose of labetalol during the loading period, and at the end of the maintenance period. Alternative therapy was given in the case of nonresponse or adverse events. Intravenous labetalol successfully controlled post-CABG hypertension in 55 of 65 patients (85%); of these, 46 responded to 35 mg or less. Although 28 patients required no further labetalol in the maintenance period, in the others dosage varied from 5 to 400 mg. Reductions in SBP and DBP were associated with moderate reductions in pulse pressure (SBP-DBP) and heart rate (HR). Cardiac index decreased by 18.5%, with a 12.5% decrease in stroke index and 8.1% decrease in HR. Systemic vascular resistance did not increase significantly. Four patients (6%) developed hypotension related to IV labetalol. There was one death due to perioperative myocardial infarction, which was unrelated to labetalol use. The mechanism of action of IV labetalol in controlling hypertension after CABG surgery seems to be moderate negative inotropy and chronotropy. Its alpha-blocking effects seem to be important in preventing reflex vasoconstriction. This is directly opposite to the primary vasodilator effect found when IV labetalol is used to control nonsurgical hypertension. Because of these actions, labetalol should be avoided or used with caution in patients with preoperative and postoperative cardiac dysfunction. In patients with normal left ventricular function, IV labetalol appears to be a safe, effective agent in controlling post-CABG hypertension, with the added potential benefit of enhanced myocardial oxygen balance.

Analysis of Variance↗
PubMed1990

The effect of cardiac hypertrophy on changes in cytosolic free calcium concentration during ischemia.

Chronic ventricular hypertrophy caused by pressure overload is a common associated risk factor in congenital cardiac surgery. Because calcium controls contractile protein interaction, we postulated that inducing ventricular hypertrophy from birth alters the way myocytes are able to regulate free cytosolic calcium (Cai) during ischemia. In this study we measured Cai with a recently developed intracellular fluorescent probe trapped inside myocytes by deesterification. The probe shifts its fluorescence spectra (from 380 to 340 nm; fluorescence measured at 510 nm) when it binds to calcium in direct relation to Cai. We studied the effects of ischemia at 37 degrees C (up to 50 minutes) on Cai in newborn (3 to 5 days), adult control (2 to 4 months old), and hypertrophied (2 months old; aortic banding done at 10 days) isolated retroperfused rabbit hearts loaded with Fura-2. In a separate group of hearts (n = 6 per group) we measured isovolumic peak developed pressure with an intracavity balloon in hearts subjected to 30 minutes of ischemia at 37 degrees C and 30 minutes of reperfusion. The recovery of peak developed pressure (percent of preischemic control) was 101% +/- 6% in control, 85% +/- 4% (p less than 0.05 vs control) in newborn, and 67% +/- 7% (p less than 0.05 vs control) in hypertrophied hearts. Cai-dependent fluorescence rose to 160% +/- 30% of preischemic baseline levels by 30 minutes of ischemia in control versus a decline to 55% +/- 7% (p less than 0.05 vs control) in newborn and 51% +/- 2% (p less than 0.05 vs control) in hypertrophied hearts by 30 minutes of ischemia. We conclude that hypertrophied and newborn hearts have a lower Cai during ischemia compared with adult hearts, and this is associated with a worse recovery of cardiac function. The lower Cai may be the result of irreversible binding of calcium to contractile proteins.

Animals↗
PubMed1990

Deferoxamine fails to improve postischemic cardiac function in hypertrophied hearts.

Myocardial hypertrophy is a well-recognized risk factor in congenital cardiac surgery. Hypertrophied hearts have been demonstrated to have an increased vulnerability to ischemia/reperfusion injury. We studied the effects of the iron chelator and hydroxyl radical scavenger deferoxamine given during early reperfusion in a model of isolated retroperfused rabbit hearts made hypertrophic by aortic banding early in life (1 week of age). The rabbits were studied at 6-8 weeks of age, and the hearts were subjected to 30 minutes of 37 degrees C ischemia followed by 30 minutes of reperfusion. Postischemic recovery of isovolumic developed pressure was measured by using an intracavitary balloon in both the untreated (n = 6) and the deferoxamine-treated (n = 6) groups and compared with normal age-matched controls. Deferoxamine (50 mumol/kg) was given to one group with the hypertrophied hearts during the first 10 minutes of reperfusion. The left ventricular weight/body weight ratio in the hypertrophied hearts was 2.9 +/- 0.4 x 10(-3) (n = 14) versus 2.0 +/- 0.1 x 10(-3) in the age-matched controls (p less than 0.05). Postischemic peak developed pressure recovered to 102 +/- 6% of the preischemic value in the normal hearts after 30 minutes of reperfusion compared with 75 +/- 5% for the untreated and 71 +/- 4% for the deferoxamine-treated hearts (p less than 0.05 vs. control). We conclude that chronic hypertrophy from early in life leads to increased susceptibility to ischemia and that the iron chelator deferoxamine is not effective in preventing the injury of reperfusion in hypertrophied hearts.

Animals↗
PubMed1990

Splenic septic emboli in endocarditis.

The significance of septic emboli to the spleen is inferred by the frequency of septic emboli in general seen in patients with left-sided infective endocarditis who are referred for valve replacement. To determine the proper management of splenic infarcts and abscess due to septic emboli, we retrospectively reviewed the records of 108 patients with left-sided endocarditis who underwent valvular surgery at the University of Illinois Hospital from 1980 through 1988. Intravenous drug abuse was the etiology in 68% (n = 73). The incidence of splenic infarcts and abscess was 19% (n = 20), but an incidental finding of splenic infarcts was found in 38% (n = 11) of 29 asymptomatic patients who had computed tomograms. Streptococci and staphylococci were the causative organisms in 85% (n = 17). Localized findings were absent in 90% of splenic infarcts and abscesses. Abdominal computed tomograms were diagnostic of the sequelae of splenic septic emboli in 100%. No patient had intra-abdominal bleeding complications associated with cardiopulmonary bypass. Splenectomy was performed in 50% (n = 10) of patients 3-24 days (mean, 11.2 days) after valve replacement. Indications for splenectomy included persistent sepsis in 60% (n = 6), large (greater than 2 cm) and peripheral lesions in 30% (n = 3), and splenic rupture in 10% (n = 1). Perioperative mortality of patients who underwent splenectomy was 30% (n = 3). The following conclusions can be drawn: 1) Splenic septic embolus is common in endocarditis. 2) Abdominal computed tomography should be performed for all patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Abscess↗
PubMed1989

Maturational difference in functional/metabolic sequelae of free radical formation on reperfusion.

To detect maturational differences with ischemia/reperfusion injury on cardiac metabolism and function, isolated nonworking rabbit hearts were subjected to 30 min of 37 degrees C ischemic arrest and reperfusion. Pre- and postischemic high energy phosphate contents (ATP, ADP, AMP), conjugated diene (products of free radical mediated lipid peroxidation) production, and peak isovolumic developed pressure (PDP) were measured in newborn (3-5 days, n = 8), 2- to 3-week-old (n = 8), and adult (2-4 months, n = 8) rabbits. ATP content decreased significantly during ischemia in all three age groups but recovered significantly toward preischemic levels in the newborn and 2-week-old groups but not in adult animals. AMP was much better preserved in the two younger groups with significantly higher levels at end-ischemia. Conjugated dienes were present in newborn and adult heart in small amounts at preischemia and rose slightly by end-ischemia. Newborn hearts accumulated large amounts of dienes by 10 min of reperfusion, which were significantly greater than those adult hearts. PDP returned to 85 and 91% of control in newborn and 2-week-old hearts, respectively, and to only 66% of control in adult hearts (P less than 0.05). These data suggest that the postischemic immature heart recovers energy stores and ventricular function faster than the adult heart which can be attributed to preservation of the total adenine nucleotide pool during ischemia. This improved recovery occurs despite a greater amount of free radical-mediated lipid peroxidation with reperfusion in newborn hearts.

Adenine Nucleotides↗
PubMed1989

Upgrading acellular to sanguineous cardioplegic efficacy.

To determine which biochemical entity of the red cell is responsible for preventing augmented postischemic myocardial oxygen consumption (MVO2), 28 canine hearts instrumented with ultrasonic dimension crystals underwent simultaneous determination of stroke work (SW) and MVO2 during incremental volume loading on right heart bypass before and 30 min after 2 hr of 10 degrees C cardioplegic arrest with unmodified oxygenated crystalloid cardioplegia (OC), OC with histidine of equal buffering capacity as 18% hematocrit blood (OC + H), or OC with 200 units/ml of superoxide dismutase and catalase (OC + SOD/C). In all groups, the slope of the linear SW vs end-diastolic volume relationship, Mw, and the slope of the linear SW vs MVO2 relationship, Me, were unchanged after cardioplegic arrest. The intercept of the SW vs MVO2 relationship, Eo, was augmented an average of 22.2% in the OC group, but both OC + H and OC + SOD/C prevented this subtle expression of ischemic injury. The characteristic of the red cell most likely responsible for the myoprotective efficacy of blood cardioplegia is buffering capacity; however, since the effects of tissue acidosis are partially mediated by free radicals, the use of free radical scavengers can also ameliorate ischemic damage incurred during cardioplegic arrest.

Animals↗
PubMed1989

Quantitative assessment of aortic regurgitation by colour flow Doppler in an open chest canine model.

Colour flow Doppler maps the extent of the flow velocity disturbance of aortic regurgitation onto the two dimensional echocardiographic image of the left ventricular cavity. The spatial extent of this flow velocity disturbance expressed as a percentage of end diastolic left ventricular cavity area (CD%) was compared to regurgitant fraction (RF), measured volumetrically, in nine open chest dogs with varying degrees of surgically created aortic regurgitation (RF 0-85%). Right heart bypass controlled venous return to the left atrium and hence net left ventricular output, while total left ventricular output was measured with an aortic electromagnetic flow probe under various loading conditions, achieving mean diastolic transvalvular pressure gradients of 23-114 mm Hg, net left ventricular outputs of 750-3000 ml.min-1 and diastolic filling periods of 162-320 ms. A linear correlation between CD% and RF (r = 0.89) was demonstrated over this wide range of loading conditions. At a given transvalvular diastolic pressure gradient [68(SD9) mm Hg] CD% was linearly proportional to regurgitant aortic orifice area (r = 0.87). Thus CD% is proportional to the volumetric severity of aortic regurgitation under a wide range of haemodynamic conditions and varies appropriately with regurgitant aortic orifice area when diastolic transvalvular pressure gradient is held constant. The application of these principles to the non-invasive quantitation of valvular regurgitation by colour Doppler appears feasible.

Animals↗
PubMed1989

Randomized clinical trial of fibrin sealant in patients undergoing resternotomy or reoperation after cardiac operations. A multicenter study.

A multicenter study was conducted to test the efficacy and safety of fibrin sealant as a topical hemostatic agent in patients undergoing either reoperative cardiac surgery (redo) or emergency resternotomy. A total of 333 patients from 11 centers in the United States were included in the study. Patients were randomly assigned to initially receive the fibrin sealant or a conventional topical hemostatic agent when such was required during an operation. The end point used to evaluate the agent's efficacy was local hemostasis, the number of bleeding episodes controlled within 5 minutes. The fibrin sealant group from the prospective study was compared with historical matched control subjects for postoperative blood loss, need for resternotomy, blood products received, and hospital stay. It was also compared with historical nonmatched control subjects for the incidence of resternotomy and mortality. The results showed a 92.6% success rate for fibrin sealant in controlling bleeding within 5 minutes of application, compared with only a 12.4% success rate with conventional topical agents (p less than 0.001). Fibrin sealant also rapidly controlled 82.0% of those bleeding episodes not initially controlled by conventional agents. High-volume postoperative blood loss was significantly less (p less than 0.05) in the fibrin sealant group than in the matched controls. Additionally, resternotomy rates after redo operations were significantly lower in the fibrin sealant group (5.6%) than in the nonmatched historical control group (10%) (p less than 0.0089). There were no significant differences in hospital stay or blood products received between the fibrin sealant group and matched historical controls and no difference in mortality between the fibrin sealant group and nonmatched historical controls. There were no documented instances of adverse reactions, transmission of viral infection (hepatitis B, non-A/non-B hepatitis), or human immunodeficiency virus seroconversion. This study shows that fibrin sealant is safe and highly effective in controlling localized bleeding in cardiac operations. Fibrin sealant reduces postoperative blood loss and decreases the incidence of emergency resternotomy. These findings make fibrin sealant a valuable hemostatic agent in cardiac surgery.

Aprotinin↗
PubMed1989

Effects of exogenous vasoconstrictors on coronary vascular resistance and prostacyclin production of the quiescent heart: the inhibitory effect of aspirin.

The in situ heart is exposed to blood-borne vasoconstrictor agents (e.g., vasopressin) which, if unopposed, may cause radically increased coronary vascular resistance (CVR). Release of endogenous vasodilator, such as prostacyclin (PGI2), is a possible mitigating mechanism. We investigated the ability of the heart to maintain CVR within a narrow range when exposed to exogenous vasoconstrictors. The isolated rat heart was perfused at constant flow rate (5-6 ml/min) with oxygenated Krebs-Ringer bicarbonate solution (37 degrees C, pH 7.4), and was rendered quiescent by a local injection of lidocaine to the atrio-ventricular node. Changes of perfusion pressure, indicating changes of CVR, were monitored and the cardiac effluent was collected for analysis of 6-keto PGF1 alpha and thromboxane B2 (stable metabolites of PGI2 and thromboxane A2, respectively) by radioimmunoassay. Hearts were infused with four different vasoconstrictors (i.e., serotonin, vasopressin, angiotensin II and the thromboxane A2/PGH2 mimetic, U46619). There was a linear relationship between the dose-dependent increase in CVR and PGI2 production in serotonin, U46619 and vasopressin-infused quiescent heart. Vasoconstriction induced by angiotensin II was not dose-dependent and was unrelated to PGI2 production. Thus, PGI2 is produced in response to coronary vessel constriction, presumably to mitigate the constriction. No detectable thromboxane B2 was released by any of these vasoconstrictors. Partial inhibition (approximately 50%) of PGI2 production by aspirin (5.6 microM) treatment resulted in a paradoxically decreased vasoconstriction except at the lowest level of serotonin and vasopressin. Aspirin (1 mM) greatly reduced PGI2 production (approximately 90%) but the fall in CVR persisted.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1989

Review of invasive treatments of coronary artery disease.

Coronary artery disease is a difficult clinical entity to manage, and all forms of current therapy are palliative in nature. Results from the large randomized studies have clearly demonstrated the superiority of surgical versus medical therapy in subsets of patients previously described herein. As patients with severely compromised ventricles are demonstrated to fare better with bypass procedures, the number of patients that should be operated upon continues to grow. With refinements in operative and perioperative care and increased use of the internal mammary artery as the bypass conduit, it is inevitable that more subgroups will be determined to be best managed by surgical revascularization. For the present time, medical treatment is preferred for the vast majority of patients who were shown by randomized trials not to benefit significantly from surgical intervention. However, caution must be used in excluding patients based on trial results that used surgical techniques and conduits that are ten years old. The role of angioplasty in the invasive treatment of ischemic cardiac disease is still in evolution. Although not yet proved by vigorous trials, it is a procedure that most likely will continue to be used in many clinical applications. The high rate of restenosis after angioplasty, which is a formidable problem, may be a factor that will limit the application of angioplasty to patients with acute myocardial infarction or to those who do not desire surgical intervention. The answers to these and other complex problems of patient management must await well-designed prospective trials comparing angioplastic with surgical revascularization. Clinical use of some of the experimental procedures mentioned is certain; the efficacy and role of these procedures in the treatment of ischemic cardiac disease must also be defined with future studies.

Angioplasty, Balloon↗
PubMed1989

The efficacy of blood cardioplegia is not due to oxygen delivery.

Twenty-seven canine hearts instrumented with ultrasonic dimension crystals underwent simultaneous determination of stroke work and myocardial oxygen consumption during incremental volume loading on right heart bypass before and 30 minutes after 2 hours of cardioplegic arrest at 10 degrees C. Three cardioplegic solutions were used: Hematocrit values were 17.0% (group I), 8.2% (group II), and 0% (group III). In all groups the slope of the linear stroke work versus end-diastolic volume relationship, a measure of contractility, was unchanged after ischemic arrest. However, the myocardial oxygen consumption for basal metabolism was increased an average of 25.5% after arrest with plasma (group III). Since the plasma concentration in all three groups was identical, and the oxygen available to the hearts during ischemia was the same in groups II and III, the efficacy of blood-based cardioplegic solutions cannot be attributed to a plasma component or to the greater oxygen-carrying capacity of the red blood cell. Future studies should attempt to identify the salutory entity of the red cell responsible for preservation of myocardial oxygen consumption efficiency.

Animals↗
PubMed1989

Compartmentalizing chemomechanical transduction in the ejecting heart.

The efficiency of transferring the total energy generated by ventricular contraction (pressure-volume area, PVA) to external work (EW) and internal work (IW) and the myocardial oxygen consumption (MVO2) at zero PVA were determined during volume loading on right heart bypass before and after a 50% augmentation (CaCl2, 0.03 mEq/kg/min, n = 7) or depression (20 minutes of 37 degrees C ischemia with 30 minutes of reperfusion, n = 7) of the contractile state. An increased EW efficiency (64% +/- 7% vs. 81% +/- 6%, p less than 0.01) with reciprocally decreased IW efficiency (36% +/- 7% vs. 19% +/- 6%, p less than 0.01) occurs with calcium chloride-augmented contractility. A reversible ischemia and reperfusion insult has the converse effect on these relative efficiencies (EW, 73% +/- 4% vs. 49% +/- 4%; IW, 27% +/- 4% vs. 51% +/- 4%; each p less than 0.01). Calcium chloride increases the oxygen requirements of both basal metabolism (28 +/- 2 vs. 67 +/- 9 ml O2/beat/100 gm LV, p less than 0.01) and fiber shortening (11 +/- 5 vs. 62 +/- 11 ml O2/beat/100 gm LV, p less than 0.01). The postischemic heart has a decreased oxygen need for shortening (20 +/- 2 vs. 3 +/- 4 ml O2/beat/100 gm LV, p less than 0.01), paralleling the depressed inotropic state. This new model of compartmentalized chemomechanical transduction may allow specific modulation of the energetic derangements attendant to the surgically treated heart.

Animals↗