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Coronary Flow and Regional Function before and after Supraarterial Myotomy for Myocardial Bridging

Myocardial bridges have been associated with clinical and metabolic evidence of ischemia, although the mechanism for this is unclear. We measured coronary blood flow and segmental function at different heart rates prior to and after release of a myocardial bridge involving the left anterior descending coronary artery in a patient with angina. Before lysis of the bridge, atrial pacing was associated with a decreased systolic flow/total flow, increased duration of systole, a lag in diastolic flow, and functional deterioration. After release of the bridge, pacing was associated with increased systolic flow/total flow and systolic interval, no diastolic flow lag, and no functional deterioration. These data imply that before bridge division, systolic flow and the initiation of diastolic flow were impeded. Functional abnormalities resulting from the flow discrepancies at heart rates of 120 to 150 beats per minute may have accounted for this patients symptoms.

The Effects of Hypothermia on Myocardial Oxygen Consumption and Transmural Coronary Blood Flow in the Potassium-arrested Heart

Hypothermia remains the primary adjunct employed to lower cellular metabolism during various cardiac procedures. In these experiments, left ventricular myocardial oxygen consumption (MVO2) and transmural blood flow (TBF) were measured during cardiopulmonary bypass with the range of temperatures used clinically. Determinations were made in empty beating normothermic hearts and after potassium cardioplegia at 37, 32, 28, 22, 18, and 15° (K+ = 15–37 meq/L: Hct 25 volumes %). Oxygen content of the total coronary sinus collection was compared with a large volume arterial sample using a Lex-O2-Con-TL analyzer (vs Van Slyke, R = 0.98). Transmural blood flow was measured at each temperature using microspheres (8μ), and perfusion was maintained at 80 mmHg. Asystole (37°) alone decreased MVO2 from 5.18 ± 0.55 to 1.85 ± 0.20 ml O2/min/100 g of left ventricle or approximately 65% (p < 0.001). With progressive cooling to 15° an additional 82% decrement in oxygen uptake occurred during asystole (p < 0.001). During asystole at 37° the decrease in MVO2 was reflected mainly by a large decrement (p < 0.01) in TBF (1.27 ± 0.19 to 0.74 ± 0.17 ml/min/g of mean left ventricular flow). However, with cooling below 32°, the arteriovenous oxygen difference narrowed progressively (p < 0.001) while TBF paradoxically returned to control levels. Endocardial/epicardial flow ratios were not altered by cooling. These data not only confirm earlier reports describing a sequential drop in MVO2 with incremental myocardial cooling, but also establish MVO2 levels for perfused hearts arrested by potassium at lower temperatures (18–15°). Moreover, as transmural blood flow becomes independent of metabolic necessity during hypothermia, coronary autoregulation appears to be impaired, possibly affecting detrimental tissue over perfusion.

The coronary pressure-flow determinants left ventricular compliance in dogs.

Displacement of the left ventricular diastolic pressure-dimension relationship (change in compliance) has been observed with alterations in coronary perfusion pressure. The relative contribution of coronary (myocardial) blood flow, as compared with the perfusion pressure at which flow occurs, was studied in 10 dogs during diastolic relaxation by potassium arrest during cardiopulmonary bypass. The normalized left ventricular pressure-dimension relationships, obtained during passive, gradual filling of the left ventricle (0–20 mm Hg) were shifted progressively to the left as coronary perfusion pressure was Increased. Myocardial blood flow was 0.06 ml/mg per min ± 0.02 ml/mg per min (mean ± SEM) at a coronary perfusion pressure of 40 mm Hg and increased to 0.38 ml/mg per min ± 0.11 ml/mg per min as the coronary perfusion pressure was raised to 120 mm Hg. Addition of adenosine significantly Increased myocardial blood flow by 109% at a coronary perfusion pressure of 80 and by 147% at a coronary perfusion pressure of 120 mm Hg, but caused no additional significant shifts in the pressure-dimension relationships, compared to the same coronary perfusion pressures without adenosine. Coronary perfusion pressure, and not coronary blood flow, is a more direct determinant of cardiac diastolic properties.

The effect of cell-free and erythrocyte-containing perfusion in rat livers

Abstract The isolated perfused rat liver (IPRL) has been used to evaluate various aspects of hepatic metabolism. However, varying perfusion compositions, specifically differing concentrations of erythrocytes (RBC), make comparisons difficult. We evaluated oxygen and glucose consumption, sodium and potassium release, and hepatic enzyme release in rat livers perfused with either cell-free (CF) or 10% RBC-containing perfusates for 90 min. Perfusate oxygen content and hepatic oxygen consumption were increased in RBC vs CF perfusion ( VO 2 = 0.0208 ± 0.002 (RBC) vs 0.0107 ± 0.001 (CF) ml O 2 /min/g). Glucose consumption was increased in CF perfusion (0.295 ± 0.048 (CF) vs 0.173 ± 0.065 (RBC) mg/min/g). Sodium, potassium, and alkaline phosphatase release were not increased in either CF or RBC perfusion. SGOT and SGPT release occurred in both perfusion systems, although significantly greater elevations were documented by 75 min in CF perfusion. Bile flow was significantly elevated with RBC perfusion. High-power light microscopy and electron microscopy documented more cellular and subcellular injury in CF perfusion. We conclude that perfusion with 10% RBCs is associated with less cellular injury and enhanced oxygen delivery to the isolated perfused rat liver.

Comparison of Nonpulsatile and Pulsatile Extracorporeal Circulation on Renal Cortical Blood Flow

Radioactive microspheres were used to compare renal cortical blood flow with pulsatile and nonpulsatile extracorporeal perfusion in mongrel dogs. No difference was found in total renal cortical flow or in flow distribution using pulsatile compared with nonpulsatile perfusion when mean perfusion pressure was held constant at a high (80 mm Hg) or low (50 mm Hg) level. Although the present investigation does not resolve the question of whether pulsatile perfusion has advantages over nonpulsatile perfusion in maintaining renal function, the data indicate that any differences between the two techniques must be explained by a mechanism other than increased total cortical blood flow or by redistribution of cortical flow.

An Improved Technique for Producing Ventricular Hypertrophy with a Subcoronary Valvular Aortic Stenosis Model

Although techniques for producing aortic valve stenosis proximal to the ostia of the coronary arteries have been described in experimental animals, only moderate left ventricular hypertrophy has been obtained. A technique for plicating the noncoronary sinus of Valsalva in puppies is presented that has enabled us to achieve levels of ventricular hypertrophy not previously reported with methods for subcoronary aortic stenosis.

Protection of mitochondrial function during ischemia by potassium cardioplegia: correlation with ischemic contracture.

The effect of potassium cardioplegia on mitochondrial function was evaluated in the ischemic isolated rat heart. Mitochondrial function as well as adenosine triphosphate (ATP) levels were determined at the initiation of ischemic contracture, at the completion of ischemic contracture, and 20 minutes following contracture completion. Group I received no cardioplegia prior to ischemia, while Group II received potassium cardioplegia prior to the onset of ischemia. The respiratory control index (RCI), which is the primary measure of the intactness of mitochondrial function, was calculated with both a NAD (nicotinamide adenine dinucleotide)-linked substrate and a FAD (flavin adenine dinucleotide)-linked substrate. Potassium cardioplegia significantly delayed ischemic contracture initiation and completion. Although the RCI and ATP levels decreased significantly at successive levels of contracture, there was no difference in the RCI or ATP content between Group I and Group II at contracture initiation or completion. Unlike previous investigations that have used a time-base to examine mitochondrial function and acute cardiac ischemic injury, we correlated mitochondrial function with the measurable physiologic event ischemic contracture. The data indicated that potassium cardioplegia preserved ATP content and mitochondrial function, and that contracture initiation and completion correlate well with specific ATP levels and mitochondrial respiratory control. The relationship between mitochondrial function and ATP content indicates that the beneficial effect of potassium cardioplegia on mitochondrial function may be secondary to the preservation of high-energy phosphate levels which provide energy for mitochondrial maintenance.

Estimation of postoperative fluid requirements in infants and children.

A quadrant scheme is presented for estimating postoperative fluid volumes for replacement of internal fluid shifts (third space losses) in pediatric surgical patients undergoing major intraabdominal surgery. The benefits derived from using a prescribed postoperative fluid management program that includes this quadrant scheme are determined by analyzing a series of 50 consecutive patients managed by five senior general and thoracic surgical house officers. Although the program tended to overestimate the fluid needs of the patients relative to a predetermined optimal urine output level, all but two patients with septic complications were hemodynamically stable and none had complications due to the fluid administration program.

Myocardial Blood Flow and Oxygen Consumption in the Empty-Beating, Fibrillating, and Potassium-Arrested Hypertrophied Canine Heart

Myocardial oxygen consumption and blood flow distribution were examined in severely hypertrophied canine hearts in the empty-beating, fibrillating, and pharmacologically arrested states. Hypertrophy was produced using a subcoronary valvular aortic stenosis model that mimics the clinical situation of aortic valvular stenosis. Oxygen content of the total coronary sinus collection was compared with a large volume arterial sample using a Lex-O2-Con-TL analyzer, which had been validated by the Van Slyke-Neill method. Transmural blood flow was measured in each state using microspheres, and perfusion pressure was maintained at 80 mm Hg. Oxygen consumption in the empty-beating hypertrophied heart was found to be the same as that previously reported for normal hearts. Blood flow was evenly distributed in the empty-beating heart, with an endocardial/epicardial ratio of 0.99 +/- 0.15 (SEM) milliliters per minute per gram of left ventricular weight. Oxygen consumption failed to increase significantly with fibrillation; however, blood flow distribution favored the subepicardium, suggesting that oxygen consumption determinations in the fibrillating hypertrophied heart may not accurately reflect metabolic demand. Basal oxygen consumption of the hypertrophied heart as determined by the potassium-arrested, blood-perfused model was the same as that previously described for normal hearts. Blood flow during potassium arrest favored the subendocardium (endocardial/epicardial ratio = 1.14 +/- 0.27 ml/min/gm LV weight).

The effects of intermittent ischemic arrest on the perfusion of myocardium supplied by collateral coronary arteries.

Six weeks after placement of an ameroid constrictor on the circumflex coronary artery, blood flow in a collateral region was compared with flow in myocardium supplied by normal arteries during cardiopulmonary bypass (80 mm Hg). Myocardial blood flow was determined using radionuclide-labeled microspheres (8 to 10 mu) before 10 minutes of ischemic arrest and after 1, 5, and 10 minutes of reperfusion. The retrograde circumflex pressure was monitored continuously and served as an additional index of perfusion of the collateral region. During reperfusion, endocardial flow in the collateral region remained unchanged despite a threefold increase in a similar layer having normal arteries (p less than 0.01). Following ischemic arrest, mean transmural and subendocardial hyperemic responses both persisted for longer than 10 minutes in normal regions. Simultaneously, peripheral circumflex pressures decreased at 1 and 5 minutes of reperfusion (p less than 0.001) but returned to control within 10 minutes. Persistently elevated endocardial flow in the normal arteries and the absence of a hyperemic response in the collateral region during an associated decrement in retrograde circumflex pressure may indicate incomplete flow repayment even after 10 minutes of reperfusion. Marked transmural flow imbalances despite adequate coronary perfusion pressures suggest that intermittent ischemic arrest may cause cumulative ischemia, and this occurrence may be detrimental especially in collateral regions of myocardium.