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Biomedical subjects

G A Geffin

Publications and source records attributed to G A Geffin.

At least 37 records · Page 2Linked to original sources

Microsphere reference flow samples during systemic flow adjustment.

Regional myocardial blood flow measurements in the right heart bypass preparation can be particularly valuable, since this preparation provides control of the main hemodynamic determinants of coronary blood flow. We examined the validity of aortic reference flow samples in relation to coronary samples during continuous systemic flow adjustment for aortic pressure control in six dogs on right heart bypass, anesthetized with chloralose and urethan. Microsphere concentrations were compared in paired reference flow samples drawn from the aortic arch and from a coronary artery for 119 left atrial microsphere injections. During left subclavian artery infusion and during femoral artery infusion at rates above 2,000 ml/min, there were high percentage errors in microsphere concentration between paired samples, consistent with aortic sample dilution by systemically infused blood. In 52 injections during withdrawal or femoral infusion below 2,000 ml/min, at cardiac outputs of 390-4,800 ml/min, the percentage error was 0.001 +/- 1.18% (SE); the absolute value of this error was below 20% in 96%, and below 10% in 77% of these injections. Linear regression related these coronary to aortic microsphere concentrations by the equation Y = 1.005X - 1.64, r = 0.997, Sy.x = 13.2 (5.9%). (Sy.x represents the standard deviation from regression.) These data indicate that valid aortic reference flow samples can be obtained within specific hemodynamic conditions during systemic flow adjustment in the right heart bypass preparation.

Animals↗

Oxygenation of cardioplegic solutions. Potential for the calcium paradox.

Oxygenation of crystalloid cardioplegic solutions is beneficial, yet bicarbonate-containing solutions equilibrated with 100% oxygen become highly alkaline as carbon dioxide is released. In the isolated perfused rat heart fitted with an intraventricular balloon, we recently observed a sustained contraction related to infusion of cardioplegic solution. In the same model, to record these contractions, we studied myocardial preservation by multidose bicarbonate-containing cardioplegic solutions in which first the calcium content and then the pH was varied. An acalcemic cardioplegic solution (Group 1) and the same solution with calcium provided by adding calcium chloride (Group 2) or blood (Group 3) were equilibrated with 100% oxygen. Ionized calcium concentrations were 0, 0.10 +/- 0.06, and 0.11 +/- 0.07 mmol/L and pH values were 8.74 +/- 0.07, 8.54 +/- 0.08, and 8.40 +/- 0.07, all highly alkaline. Hearts were arrested for 2 hours at 8 degrees +/- 2.5 degrees C and reperfused for 1 hour at 37 degrees C. At end-arrest, myocardial adenosine triphosphate was depleted in all three groups, significantly in Groups 2 and 3. In Group 1 the calcium paradox developed upon reperfusion, with contracture (left ventricular end-diastolic pressure = 60 +/- 7 mm Hg), creatine kinase release up to 620 +/- 134 U/L, a profound further decrease in adenosine triphosphate to 1.9 +/- 1.7 nmol/mg dry weight, and either greatly impaired or no functional recovery (17% +/- 10% of prearrest developed pressure). Three hearts in this group released creatine kinase during arrest and did not resume beating during reperfusion. In Groups 2 and 3, the calcium paradox did not occur; functional recovery was 61% +/- 4% and 71% +/- 9% at 5 minutes of reperfusion. In two additional groups (4 and 5), the pH of the acalcemic cardioplegic solution was decreased by equilibration with 2% and 5% carbon dioxide in oxygen to 7.53 +/- 0.03 and 7.11 +/- 0.02. Contractions during arrest were smaller than in Groups 1, 2, and 3; adenosine triphosphate was maintained during arrest; functional recovery was 101% +/- 3% and 96% +/- 4% at 5 minutes of reperfusion. We conclude that acalcemic solutions with carbon dioxide are superior to highly alkaline calcium-containing solutions. If oxygenation of cardioplegic solutions, of proved value, causes severe alkalinity, then calcium paradox may result even with hypothermia. This hazard is prevented by adding calcium or blood to the solution or carbon dioxide to the oxygen used for equilibration.

Adenine Nucleotides↗

Optimal myocardial preservation with an acalcemic crystalloid cardioplegic solution.

The effect of the calcium and oxygen contents of a hyperkalemic glucose-containing cardioplegic solution on myocardial preservation was examined in the isolated working rat heart. The cardioplegic solution was delivered at 4 degrees C every 15 minutes during 2 hours of arrest, maintaining a myocardial temperature of 8 degrees +/- 2 degrees C. Hearts were reperfused in the Langendorff mode for 15 minutes and then resumed the working mode for a further 30 minutes. Groups of hearts were given the oxygenated cardioplegic solution containing an ionized calcium concentration of 0, 0.25, 0.75, or 1.25 mmol/L or the same solution nitrogenated to reduce the oxygen content and containing 0 or 0.75 mmol ionized calcium per liter. The myocardial adenosine triphosphate concentrations at the end of arrest in these six groups of hearts were 15.6 +/- 1.2, 9.5 +/- 0.5, 8.2 +/- 1.1, 4.9 +/- 1.8, 10.1 +/- 2.0, and 1.6 +/- 0.4 nmol/mg dry weight, respectively. At 5 minutes of working reperfusion, the percentages of prearrest aortic flow were 80 +/- 2, 62 +/- 4, 33 +/- 6, 37 +/- 5, 48 +/- 7 and 46 +/- 8, respectively. The differences among the groups in adenosine triphosphate concentrations and in functional recovery diminished during reperfusion. In hearts given the hypoxic calcium-containing solution, there was a marked increase in coronary vascular resistance during the administration of successive doses of cardioplegic solution, which was rapidly reversible upon reperfusion. These data indicate that hearts given the acalcemic oxygenated solution had better adenosine triphosphate preservation during arrest and better functional recovery than hearts in any other group. Addition of calcium to the oxygenated cardioplegic solution decreased adenosine triphosphate preservation and functional recovery. Oxygenation of the acalcemic solution increased adenosine triphosphate preservation and functional recovery. The lowest adenosine triphosphate levels at end arrest were observed in hearts given the hypoxic calcium-containing solution. In the setting of hypothermia and multidose administration, the addition of calcium to a cardioplegic solution resulted in increased energy depletion during arrest and depressed recovery.

Animals↗

Calcium-induced ventricular contraction during cardioplegic arrest.

Cardiac arrest induced by hyperkalemic perfusion is generally considered to represent a state of complete electromechanical arrest. However, high-energy phosphate concentrations and ventricular function decrease with increasing cardioplegic calcium concentrations, possibly because of elevated resting muscle tone produced by calcium influx. We examined isolated rat hearts containing an isovolumic intraventricular balloon for the presence of contractile activity during the administration at 10 degrees C of a cardioplegic solution containing potassium, 20 mEq/L. Significant left ventricular pressure was developed (35.6% +/- 4.3% of prearrest systolic pressure) during administration of a solution containing a calcium concentration of 1.0 mmol/L and far less (9.7% +/- 1.6% of prearrest systolic pressure) with a calcium-free cardioplegic solution. The muscle contraction diminished with repeated doses, was increased by increasing cardioplegic calcium content, and was inhibited by magnesium. Adenosine triphosphate and creatine phosphate concentrations were 9.0 +/- 1.4 and 7.0 +/- 0.9 nmol/mg dry weight immediately after infusion of 15 ml of a hypoxic cardioplegic solution containing calcium, versus 13.3 +/- 1.3 (p less than 0.02) and 31.9 +/- 3.5 nmol/mg dry weight (p less than 0.0001) after a hypoxic acalcemic solution was given. When repeated doses of a hypoxic cardioplegic solution containing calcium in a concentration of 1.0 mmol/L were given at 15 minute intervals at 10 degrees C, ischemic contracture (a sustained development of ventricular pressure, mean 51% +/- 4% of prearrest systolic pressure) resulted within 1 hour. Coronary vascular resistance was increased during the muscle contractions induced by calcium-containing solutions, markedly so during contracture. Calcium-related mechanical activity was also observed during hypothermic cardioplegic arrest in five of six isolated isovolumic canine hearts. We conclude that hearts remain potentially active mechanically during cold hyperkalemic arrest and undergo energetically wasteful contraction when stimulated with calcium-containing hyperkalemic cardioplegic solutions.

Adenine Nucleotides↗

Effect of preload on ischaemic and non-ischaemic left ventricular regional function.

The response to preload of ischaemic and non-ischaemic regions of the left ventricle was studied in 14 dogs undergoing right heart bypass with mean aortic pressure and heart rate held constant. Regional function was measured by sonomicrometry before and after coronary artery occlusion. In the ischaemic region, as expected, there was paradoxical systolic lengthening (that is, systolic shortening was negative) but as stroke volume was progressively increased end diastolic length increased, whereas end systolic length changed little; thus systolic lengthening decreased (systolic shortening increased). Ischaemic regions that were dyskinetic at low stroke volumes were virtually akinetic at high stroke volumes. Additional studies showed that this response was not attributable to increased regional blood flow at high preloads and occurred over a wide range of heart rates and mean aortic pressures. Plots of systolic shortening against end diastolic length, expressing the regional Frank-Starling relation, were well described by linear regression in both ischaemic and non-ischaemic regions, although a few of these relations were better described by higher order polynomials. The slopes of these relations in the ischaemic region were 0.86(0.05) before and 0.83(0.06) after ligation, reflecting a small effect of preload on end systolic length. The data suggest that when contractility and afterload are constant preload determines the magnitude and in certain instances the sign of systolic shortening. In any ischaemic regions incapable of developing force the positive slope of the Frank-Starling relation is attributable to myocardial passive elastic properties. Paradoxical lengthening does not, however, necessarily indicate the absence of active force development; positive and negative values of systolic shortening describe a continuous spectrum of regional contractility. Thus the effects of preload and contractility on systolic shortening in ischaemic as well as non-ischaemic myocardium require differentiation.

Animals↗

Improved myocardial preservation with oxygenated cardioplegic solutions as reflected by on-line monitoring of intramyocardial pH during arrest.

To examine the relationship between intramyocardial pH during global ischemic arrest and subsequent functional and biochemical recovery, 40 canine hearts were subjected to 4 hours of arrest at 10 degrees C. Four groups, each containing 10 hearts, were differentiated by the oxygen concentration of a hyperkalemic crystalloid cardioplegic solution (CCS), which was infused every 20 minutes. In group 1 the CCS was equilibrated at 4 degrees C with nitrogen to remove oxygen. In group 2 the CCS was aerated at 4 degrees C. In group 3 the CCS was treated to achieve an oxygen tension (PO2) similar to group 2 but with a reduced nitrogen content to prevent bubble formation, which is theoretically possible during reperfusion ("myocardial bends"). In group 4 the CCS was fully oxygenated at 4 degrees C. The resulting PO2 of CCS measured at 10 degrees C was less than 20, 170, 170, and 750 mm Hg in groups 1, 2, 3, and 4, respectively. Left ventricular function (LVF) was assessed from function curves at constant mean aortic pressure and heart rate. Functional recovery, expressed as a percentage of prearrest LVF, was 38.1% +/- 10.7% in group 1 and 84.0% +/- 8.1% in group 4 (p less than 0.008). Functional recovery was 64.9% +/- 5.5% and 69.1% +/- 7.0% in groups 2 and 3, which had similar PO2. Differences in recovery between groups 2 and 3 and group 1 approached statistical significance (p less than 0.05, NS). The mean-integrated intramyocardial pH during arrest was higher (p less than 0.003) in group 4 (7.14 +/- 0.05) than in group 1 (6.84 +/- 0.06) or group 2 (6.86 +/- 0.07). The minimum intramyocardial pH during arrest was higher in group 4 than in any other group (p less than 0.002). Myocardial adenosine triphosphate concentration at the end of arrest, expressed as a percentage of its prearrest value, was highest in group 4 (75.9% +/- 8.1%) and lowest in group 1 (54.3% +/- 5.7%), a difference approaching statistical significance (p less than 0.05, NS). These data suggest that the measurement of intramyocardial pH is a useful on-line indicator of the adequacy of preservation during hypothermic arrest and that excess nitrogen in aerated CCS had little or no effect on recovery. The data confirm the hypothesis that oxygenation of CCS is associated with good myocardial preservation, which may be attributed to the provision of oxygen for the support of aerobic metabolism during arrest.

Animals↗

Myocardial oxygen consumption with isoproterenol versus calcium chloride in hypocalcemic ventricular failure in dogs.

In 30 dogs on right heart bypass we compared the effects of isoproterenol with those of calcium chloride on myocardial oxygen consumption and on left ventricular function in the setting of ventricular depression produced by ionized hypocalcemia. In 22 dogs (Groups A and B) either isoproterenol or calcium chloride was infused, left ventricular function curves were generated, and end-diastolic pressure vs segment length plots were obtained. In 8 dogs (Group C), with initial hypocalcemia, both isoproterenol and calcium chloride were infused separately in random order to produce an equal decrease in left ventricular end-diastolic pressure at constant mean aortic pressure, heart rate, and cardiac output. Myocardial oxygen consumption and indices of left ventricular function were obtained. In Groups A and B, both drugs, when administered to the ventricle depressed by hypocalcemia, displaced left ventricular function curves upward and to the left. Left ventricular stroke work at constant left ventricular end-diastolic pressure increased (from 13.0 +/- 1.3 to 31.2 +/- 2.3 g X m for isoproterenol; from 13.9 +/- 2.5 to 32.5 +/- 2.5 g X m for calcium chloride). In Group C, there were no significant differences between left ventricular end-diastolic pressure, end-diastolic internal diameter, myocardial oxygen consumption, or peak left ventricular dP/dt in the hypocalcemic periods preceding isoproterenol and calcium chloride infusion. When the two drugs caused matched decreases in left ventricular end-diastolic pressure (-7.4 +/- 0.5 cm H2O for isoproterenol; -7.3 +/- 0.8 cm H2O for calcium chloride) there were similar decreases in end-diastolic internal diameter. However, isoproterenol was associated with a significantly greater (P less than 0.001) myocardial oxygen consumption (13.7 +/- 0.4 ml X 100 g-1 X min-1) than calcium chloride infusion (11.9 +/- 0.4 ml X 100 g-1 X min-1), as well as a greater peak left ventricular dP/dt (P less than 0.005).

Animals↗

Myocardial recovery after hypothermic arrest: a comparison of oxygenated crystalloid to blood cardioplegia. The role of calcium.

We compared multidose crystalloid hyperkalemic cardioplegic solutions with and without added red cells in 24 canine hearts subjected to 5 hr of arrest at 10 degrees C. All cardioplegic solutions were fully oxygenated at 4 degrees C before delivery. Since blood cardioplegia contained Ca++ carried over with the red cells, Ca++ was added to the crystalloid solution in one group. The table below shows the hematocrit (HCT) and ionized Ca++ concentrations of the cardioplegic solutions, and coronary arteriovenous oxygen difference during infusion of cardioplegic solution (AVO2) (ml O2/100 ml). Recovery during reperfusion is shown as percent of prearrest left ventricular function (LVF) and prearrest myocardial ATP concentration.

Adenosine Triphosphate↗

Reduction of postischemic myocardial dysfunction by substrate repletion during reperfusion.

We studied the effect of selected metabolic substrates on recovery of myocardial function and ATP concentration when added to the reperfusate after normothermic ischemia. The hearts of 30 anesthetized, open-chest mongrel dogs were subjected to 45 min of global ischemia at 37 degrees C followed by 90 min of reperfusion. Left ventricular function curves were generated on right heart bypass before and at 30 min intervals after the ischemic period. ATP concentration was measured before, at the end of, and 90 min after the ischemic period. Experiments were randomized into five groups distinguished by the content of the myocardial reperfusate during the first 10 min of the reperfusion period. Hearts received either unmodified oxygenated pump blood (control; group I), normothermic oxygenated 28 mmol/liter potassium-blood cardioplegic solution (KBC; group II), 25 mmol/liter glutamate in KBC (group III), 250 mumol/liter adenosine with 1 mg erythro-9-(2-hydroxy-3-nonyl) adenine hydrochloride (EHNA) and glutamate in KBC (group IV), or 2 mmol/liter ribose and glutamate (group V) in KBC. Hearts reperfused with KBC showed improvement early (group II vs group I; p less than .02) but not late recovery of left ventricular function over control. Glutamate, which replenishes Krebs cycle intermediates lost during ischemia, increased functional recovery (group III vs group II; p less than .002). Ribose, which is important in purine salvage and resynthesis, added to glutamate-KBC further improved functional recovery (group V vs group III; p less than .01). Adenosine, a precursor of ATP, with EHNA, an inhibitor of rapid adenosine catabolism, added to glutamate-KBC depressed early recovery (group IV vs group III; p less than .01); however, recovery improved with time. Both glutamate and ribose with glutamate in KBC improved ATP recovery (groups III and V vs group II; p less than .002). Thus selective substrate repletion during initial reperfusion after severe normothermic ischemia can improve recovery of myocardial function and ATP concentration.

Adenosine↗

Inability of seven-pinhole myocardial tomography to obtain accurate 201Tl kinetic data.

Seven-pinhole myocardial tomography has been reported to enhance the accuracy of thallium-201 (201Tl) studies in detecting patients with coronary artery disease. To determine if this approach can accurately assess regional 201Tl kinetics, 12 dogs with temporary occlusion (mean 15 min) of either the left anterior descending (LAD) (n = 6) or left circumflex (LCX) (n = 6) coronary artery were studied. Thallium-201 was injected and serial 7-pinhole images were acquired during occlusion and following reflow (mean duration 175 min). Time-activity analysis was obtained from normal and ischemic regions of interest in the central pinhole image and the reconstructed tomographic images (TOMO-ROI). Time-activity data from corresponding normal and ischemic regions were also obtained using a circumferential graph program (TOMO-MAX). In addition, regional myocardial 201Tl activity was recorded continuously with a cadmium telluride radiation probe sutured directly to the posterior myocardial wall. Defects in 201Tl distribution with subsequent partial or complete redistribution were present in 11 of 12 central pinhole images and tomographic studies. In the normal and ischemic anterior myocardial segments the percentage change in 201Tl activity in the central pinhole image from occlusion to the end of reflow correlated well with the percentage change in activity for both TOMO-ROI (r = 0.93) and TOMO-MAX (r = 0.85). In the normal posterior segments the percentage change in 201Tl activity in the central pinhole image correlated well with TOMO-ROI (r = 0.98) and TOMO-MAX (r = 0.87).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Global and regional function in the regionally ischaemic left ventricle related to plasma ionised calcium.

To study the response of function in the regionally ischaemic left ventricle to increased and decreased concentrations of plasma ionised calcium, twenty-two anaesthetised dogs were placed on right heart bypass with constant mean aortic pressure and heart rate. Regional (sonomicrometry) and global left ventricular function were assessed before coronary artery ligation. Then, following ligation, function after 45 min stable ionised hypercalcaemia [( Ca2+] = 1.68 +/- 0.01 mmol x litre-1) and hypocalcaemia [( Ca2+] = 0.73 +/- 0.02 mmol x litre-1) were each compared to function during an immediately preceding normocalcaemic period. Control of cardiac output enabled paired comparisons to be made at matched preloads: systolic shortening from common end-diastolic chord lengths (n = 10), and stroke work at common left ventricular end-diastolic pressures (n = 22). With hypercalcaemia, systolic shortening in the ischaemic region (2.11 +/- 0.39 mm preligation) increased from -0.62 +/- 0.17 to -0.04 +/- 0.20 mm (P less than 0.01), whereas in the control region systolic shortening increased from 1.47 +/- 0.12 to 2.00 +/- 0.15 mm (P less than 0.01) reaching its preligation value (1.67 +/- 0.13 mm). Stroke work at a left ventricular end-diastolic pressure of 1.37 kPa increased (0.248 +/- 0.019 to 0.299 +/- 0.021 joules x beat-1, P less than 0.001) but not to preligation levels (0.364 +/- 0.016 joules x beat-1). Hypercalcaemia also increased myocardial oxygen consumption (by 1.0 +/- 0.3 cm3 x min-1 x 100 g-1, P less than 0.005) but not coronary blood flow. With hypocalcaemia, systolic shortening decreased in ischaemic and control regions, global function curves were markedly depressed, and myocardial oxygen consumption did not change but coronary blood flow increased. Thus hypercalcaemia improved function in ischaemic and control regions but improvement in the ischaemic region was small compared with the depression associated with ischaemia itself. Hypercalcaemia also improved global function, but not to preischaemic levels, at an increased oxygen cost.

Animals↗

Enhanced myocardial protection during ischemic arrest. Oxygenation of a crystalloid cardioplegic solution.

To determine if, during elective cardiac arrest, the myocardial protection afforded by a cold (4 degrees C) crystalloid potassium cardioplegic solution could be improved by oxygenation of the solution, we placed 16 dogs on cardiopulmonary bypass and subjected their hearts to 4 hours of cold cardioplegic arrest. Group 1 hearts (n = 8) received aerated crystalloid solution perfused through the aortic root every 20 minutes. Group 2 hearts (n = 8) were treated identically except that the crystalloid cardioplegic solution was fully oxygenated. Left ventricular function curves (ejecting heart) were generated before arrest (control) and after 45 minutes of reperfusion. A cardiac output of 1,000 ml/min could be attained in only two hearts of Group 1 after reperfusion, whereas all but one heart of Group 2 had excellent functional preservation. Mean postreperfusion adenosine triphosphate (ATP) levels in Group 1 and Group 2 hearts were 62% and 89% of control, respectively (p less than 0.01). Myocardial water content had increased significantly (p less than 0.002) after reperfusion in Group 1, but not in Group 2. During cardioplegic solution infusion, myocardial oxygen consumption (MVO2) was 1.42 +/- 0.15 ml O2/min/100 gm LV for Group 1 and 6.91 +/- 1.27 ml O2/min/100 gm LV for Group 2 (p less than 0.001). Oxygen consumed per minute of arrest was 0.027 +/- 0.003 ml O2/min/100 gm LV for Group 1 and 0.128 +/- 0.015 ml O2/min/100 gm LV for Group 2 (p less than 0.001). Postreperfusion ultrastructural evaluation of two of the Group 1 hearts revealed severe ischemic damage in contrast to the normal ultrastructural appearance of two of the Group 2 hearts. With careful attention given to maintenance of myocardial hypothermia and cardioplegic delivery methods, the myocardial protection afforded by an oxygenated crystalloid cardioplegic solution exceeds that provided by the aerated control and compares favorably with other methods of myocardial protection during ischemic arrest.

Adenine Nucleotides↗

Comparison of myocardial preservation with hypothermic potassium and nifedipine arrest.

Preservation of regional myocardial function, high-energy phosphate stores and ultrastructure were assessed in 28 canine hearts subjected to 2 hours of global ischemia at either 12 degrees C or 21 degrees C. The preservation achieved with a potassium arrest solution was simultaneously compared in the same heart with either a nifedipine arrest solution or a potassium plus nifedipine arrest solution. There were no statistically significant differences in regional function recovery between the three arrest solutions at either temperature. At 12 degrees C, slightly better functional preservation was noted for each solution. End-systolic chord length was significantly less elongated after preservation at the lower temperature (p = 0.03). The concentration of ATP and myocardial water content were not significantly better preserved with any solution at either temperature. Myocardial ultrastructure was well preserved regardless of the solution or temperature used. The degree of hypothermia appears to be more important to functional preservation than differences between the three solutions tested. We conclude that with respect to preservation of myocardial function, high-energy phosphate stores, water content and ultrastructure, nifedipine arrest offers no advantages over potassium arrest.

Adenosine Triphosphate↗

Relation between ionized calcium concentration and ventricular pump performance in the dog under hemodynamically controlled conditions.

The effect of plasma ionized calcium concentration on left ventricular function was studied in the canine heart on right heart bypass. Stroke volume, mean arterial pressure and heart rate were controlled. Plasma ionized calcium was lowered to 0.58 +/- 0.01 mM by citrate infusion and raised to 1.70 +/- 0.01 mM by calcium chloride infusion in random order in each dog. Left ventricular function at each of these ionized calcium levels was compared with that in an immediately preceding normocalcemic period. At a constant stroke work (16.9 +/- 0.2 g-m), sustained hypercalcemia was associated with a small decrease in left ventricular end-diastolic pressure (1.7 +/- 0.7 cm H2O, p less than 0.05) despite a marked increase in peak left ventricular dP/dt (first derivative of ventricular pressure) averaging 34 percent (p less than 0.001). Coronary blood flow, tension-time index and myocardial oxygen consumption were not significantly altered. Stroke work determined at a left ventricular end-diastolic pressure of 14 cm H2O, by interpolation in left ventricular function curves, was 11 +/- 4.4 percent above that at control normocalcemia (p less than 0.05). At a constant stroke work (16.9 +/- 0.2 g-m), sustained hypocalcemia was associated with a marked depression of left ventricular function as demonstrated by a substantial increase (from 4.9 +/- 0.3 to 12.7 +/- 1.1 cm H2O, p less than 0.0001) in left ventricular end-diastolic pressure (p less than 0.0001), decreased mean systolic ejection rate (p less than 0.01) and decreased peak left ventricular dP/dt (p less than 0.0001). Coronary blood flow increased (p less than 0.05) whereas myocardial oxygen consumption did not change significantly. A marked displacement of left ventricular function curves to the right (compared with curves obtained during normocalcemia) was observed, and stroke work determined at a left ventricular end-diastolic pressure of 14 cm H2O was 52 +/- 5.4 percent below control level (p less than 0.001). It appears that hypercalcemia, when initiated from a normal control level, provides only a small enhancement of ventricular pump performance (as indexed by the stroke work-left ventricular end-diastolic pressure relation) despite a marked increase in peak left ventricular dP/dt, whereas marked improvement of left ventricular performance may be expected when calcium infusion is initiated from an ionized calcium level that is below normal.

Animals↗

Regional myocardial protection during aortic cross-lamp ischemia in dogs: calcium-containing crystalloid solutions.

To study the effects of calcium in cardioplegic solutions, an in situ dog heart model was used that allowed infusion of two different cardioplegic solutions into separate regions of the same heart. Two concentrations of ionized calcium, 1.0 mM and 0.5 mM, in a cold, potassium-containing solution were tested in two groups of dogs and compared with the same cold, potassium-containing solution but without the calcium, during 100 minutes of global myocardial ischemia induced by aortic clamping. Results were evaluated in terms of percent change of regional systolic shortening measured with ultrasonic piezoelectric crystals, percent change of regional myocardial blood flow, and change of regional left ventricular myocardial diastolic distensibility. No significant differences were found between myocardial regions protected with calcium of either concentration and regions protected with calcium of either concentration and regions protected without calcium. This study could demonstrate no beneficial or adverse effects of including calcium in this type of crystalloid cardioplegic solution applied to an in situ dog heart model.

Animals↗

Regional myocardial protection: use of a new method to compare cold potassium cardioplegia with hypothermic coronary perfusion.

A new canine model was developed to compare two cardiplegic agents using each heart as its own control. Paired piezoelectric crystals were implanted into the left anterior descending and circumflex regions. The percentage of shortening (systolic shortening/end-diastolic segment length X 100) was assessed in each region on right-heart bypass over a range of cardiac outputs. Durng 100 minutes of ischemic arrest the left anterior descending and circumflex regions were perfused separately every 20 minutes with either cold buffered saline or cold KCl cardioplegia solutions. After recovery, the percentage of shortening after ischemic arrest was determined. The percentage of shortening in the region protected by KCl was unchanged (12.5 +/- 5.0 to 13.0 +/- 4.6%) after arrest, but was markedly decreased in the buffered saline region (11.3 +/- 5.9 to 3.2 +/- 4.9%) (p < 0.001, n = 6). This model should facilitate the comparison of two cardioplegic solutions.

Animals↗

Ventricular performance and myocardial water content during hemodilution in dogs.

In dogs anesthetized with chloralose-urethan on right heart bypass, left ventricular (LV) performance was assessed at constant LV stroke work before and for up to 2.5 h after crystalloid hemodilution was established. Lowering the hematocrit from 43.3 +/- 1.3% to 13.6 +/- 1.7% (SE) did not significantly change LV end-diastolic pressure (LVEDP) initially. After 80 min LVEDP increased slightly by 1.7 +/- 0.6 cmH2O (P less than 0.05) at a stroke work of 17.3 +/- 2.3 g.m. The value of dP/dt did not change significantly throughout. When LV function curves were generated by increasing cardiac output, the stroke work attained at an LVEDP of 10 cmH2O decreased with hemodilution from 23.9 +/- 3.5 to 20.8 +/- 3.9 g.m (NS). LV wall water content increased with hemodilution, from which it could be calculated that there was an 18.6% increase in LV mass. Thus, despite an increase in LV external girth demonstrated by LV circumferential gauges, it is possible that increased wall thickness due to the water gain resulted in little change or an actual decrease in LV end-diastolic volume. Thus, profound hemodilution can be attained with only slight depression of LV performance.

Anemia↗