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W E Johnston

Publications and source records attributed to W E Johnston.

At least 19 recordsLinked to original sources

Cerebral metabolic consequences of hypotensive challenges in hemodiluted pigs with and without cardiopulmonary bypass.

We tested the hypothesis that progressive aortic hypotension with bicarotid occlusion produces greater reductions in cerebral blood flow (CBF) and more flow-metabolism mismatching with hemodilution during cardiopulmonary bypass (CPB) than with hemodilution alone. In Yorkshire pigs randomized to hemodilution with CPB (n = 10) or hemodilution without CPB (control; n = 9), the effects of bicarotid ligation and graded hypotension on CBF (microspheres), the electroencephalogram (EEG), and cortical energy metabolites were examined. After bicarotid ligation, systemic flow was reduced for 15-min intervals of 80, 60, and 40 mm Hg aortic pressure, followed by a cortical brain biopsy. At baseline, CBF was lower in CPB (58 +/- 3 mL.100g-1.min-1) than control (90 +/- 3 mL.100 g-1.min-1., P < 0.05) animals, as was cerebral oxygen metabolism (3.1 +/- 0.1 vs 4.2 +/- 0.2 mL.min-1.100g-1; P < 0.05). Although CBF remained 40% lower at each level of hypotension in CPB than control animals (P < 0.05), EEG scores showed no intergroup differences, indicating similar flow-metabolism matching. Brain metabolites were similar between CPB and control groups (adenosine triphosphate, 9.6 +/- 2.4 vs 12.4 +/- 1.9 mumol/g; adenosine diphosphate, 6.0 +/- 0.7 vs 6.3 +/- 0.4 mumol/g; adenosine monophosphate, 4.8 +/- 0.9 vs 3.8 +/- 0.8 mumol/g; creatine phosphate, 8.3 +/- 1.8 vs 7.9 +/- 1.0 mumol/g; and lactate, 178.4 +/- 20.2 vs 150.8 +/- 13.9 mumol/g). Thus, despite significantly lower CBF during hypotension with bicarotid occlusion in hemodiluted animals during normothermic CPB, cortical electrical activity and the balance between flow and metabolism did not differ from those in control animals without CPB.

Adenine Nucleotides

Is calcium or ephedrine superior to placebo for emergence from cardiopulmonary bypass?

To determine whether ephedrine or CaCl2 improves hemodynamics in cardiac surgery patients emerging from cardiopulmonary bypass, three sequential doses of either CaCl2 (200 mg/dose; n = 12), ephedrine (5 mg/dose; n = 12), or placebo (n = 12) were administered in a prospective, randomized, double-blind fashion. Thermodilution volumetric catheters were used to calculate right ventricular (RV) volumes and ejection fraction. The first dose of ephedrine improved RV stroke volume from 57 +/- 3 to 63 +/- 4 mL/beat (P < 0.05) and ejection fraction from 44 +/- 2% to 49 +/- 2% (P < 0.05). Subsequent doses maintained this improvement but without further change. In contrast, placebo and CaCl2 had minimal effects on RV end-systolic volume, stroke volume, and ejection fraction. After the third injection of ephedrine, mean arterial pressure had significantly increased from 78 +/- 2 to 93 +/- 4 mmHg (P < 0.05) in contrast to insignificant increments with placebo and CaCl2. Serum ionized calcium increased by 6% to 8% after each CaCl2 bolus but remained stable in the ephedrine and placebo groups. CaCl2 failed to improve RV performance in mildly hypocalcemic patients during separation from cardiopulmonary bypass. In patients with normal preoperative ventricular function, ephedrine more effectively improved RV performance and arterial blood pressure than placebo or CaCl2, and is a suitable short-acting drug to assist separation from cardiopulmonary bypass.

Adult

Differential effects of positive end expiratory pressure and cardiac tamponade on left-right ventricular mechanical function in the dog.

OBJECTIVE: The aim was to examine the hypothesis that an increased coupling occurs between the ventricles during tamponade via a ventricular-pericardial-ventricular interaction, but that ventricular coupling would be unaltered or reduced with positive end expiratory pressure (PEEP). METHODS: An in situ arrested, canine heart preparation was used. Changes in left and right ventricular pressure (dPl, dPr) and volume (dVl, dVr) caused by increasing the volume of the other ventricle were measured at normal and at matched levels of raised pericardial pressures (Pp) caused by 20 cm H2O PEEP and by tamponade. RESULTS: With PEEP, the coupling between the ventricles was unaltered when compared to control. With tamponade, dPl/dPr, dVl/dPr, dPr/dPl, and dVr/dPl increased significantly (p less than 0.05) by 0.21 (SEM 0.03, unitless), 0.45(0.04) ml.mm Hg-1, 0.18(0.03), and 0.28(0.04) ml.mm Hg-1 respectively. CONCLUSIONS: Augmented ventricular interdependence occurs during tamponade but not with PEEP, which may help to explain the different haemodynamic patterns observed under these conditions.

Animals

Positive end-expiratory pressure potentiates the severity of canine right ventricular ischemia-reperfusion injury.

Positive end-expiratory pressure (PEEP) increases right ventricular (RV) afterload and oxygen demands. However, whether increased RV oxygen demands with high levels of PEEP can potentiate the severity of RV ischemic damage is unknown. In 20 anesthetized, closed-chest dogs randomly assigned to 0 cmH2O PEEP (ZEEP; n = 10) or 15 cmH2O PEEP (PEEP; n = 10), RV blood flow (radioactive microspheres) and segmental shortening (ultrasonic crystals) were determined during 90 min ischemia and 120 min reperfusion while mean aortic pressure was maintained above 90 mmHg. The in vivo RV area at risk (gentian violet) and area of necrosis (triphenyltetrazolium chloride) were assessed. After application of 15 cmH2O PEEP, pulmonary vascular resistance increased by 75% (P less than 0.05). During ischemia, the RV rate-pressure product remained greater with PEEP (2,403 +/- 174 mmHg.beat.min-1) than with ZEEP (1,909 +/- 94 mmHg.beat.min-1; P less than 0.05), indicating higher oxygen demands with PEEP. The area at risk from ischemia relative to RV free wall tended to be greater with PEEP (68.5 +/- 2.4%) than with ZEEP (60.0 +/- 3.9%; P = 0.08), and collateral blood flow in this risk zone was significantly lower during ischemia with PEEP (9.0 +/- 1.7 ml.min-1 x 100 g-1) than with ZEEP (18.3 +/- 3.6 ml.min-1 x 100 g-1; P less than 0.05). Accordingly, PEEP extended RV necrosis in the area at risk from 21.8 +/- 5.3% (ZEEP) to 58.1 +/- 8.4% (PEEP; P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Restraining effect of intact pericardium during acute volume loading.

To determine the effect of the intact pericardium on ventricular end-diastolic pressures (EDP) during acute volume loading, we measured left ventricular (LV) and right ventricular (RV) micromanometer pressure and LV volume using a conductance catheter in eight open-chest, anesthetized dogs. A range of LV pressure and volume was obtained by intravascular volume expansion with the pericardium intact and then over a similar range after removal of the pericardium. Pericardial pressure (Pper) was calculated using static equilibrium analysis as the difference between LVEDP with the pericardium present and absent at a constant LV volume. At the beginning of the fluid infusion (LVEDP 7.3 +/- 1.7 mmHg and RVEDP 4.4 +/- 2.6 mmHg, mean +/- SD), Pper was not different from zero (-1.0 +/- 2.3 mmHg, P not significant). The onset of pericardial restraint (Pper greater than or equal to 0 mmHg) occurred when LVEDP was 9.1 +/- 2.9 mmHg and RVEDP was 4.1 +/- 2.9 mmHg. At low cardiac volumes before fluid infusion, RV transmural pressure was positive and significantly greater than the near zero Pper. After the onset of pericardial restraint, however, RVEDP and Pper increased similarly and were related according to Pper = 1.1 (+/- 0.34) RVEDP - 4.2 (+/- 2.6) mmHg, standard deviation 0.6 +/- 0.8 mmHg, r = 0.98 +/- 0.10. These data indicate that the intact pericardium behaves in two functionally distinct ways. At low cardiac volumes, Pper is zero and the pericardium does not affect LV filling. RV transmural pressure is positive and greater than Pper.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals

Intracoronary L-arginine during reperfusion improves endothelial function and reduces infarct size.

We tested the hypothesis that intracoronary administration of L-arginine (L-Arg), the physiological nitric oxide (NO) precursor, during reperfusion would attenuate postischemic damage by L-Arg NO-pathway mechanisms. Open-chest, anesthetized dogs underwent 60 min of left anterior descending coronary arterial (LAD) occlusion followed by 270 min of reperfusion. Dogs received intracoronary 10 mM L-Arg (n = 9 dogs), intracoronary 10 mM D-arginine (D-Arg, n = 7), or saline vehicle (Veh, n = 10) in the LAD during the first 120 min of reperfusion using an extracorporeal system. After 270 min of reperfusion, segmental systolic and diastolic function were comparably impaired in all three groups. Infarct size (triphenyltetrazolium chloride) expressed as a percentage of the area at risk (An/Ar) was significantly (P < 0.05) reduced in the L-Arg group (17.7 +/- 3.2%) compared with the Veh group (34.8 +/- 2.4%); D-Arg reversed this cardioprotection (48.8 +/- 5.2%, P < 0.05 vs. L-Arg, Veh). Cardiac myeloperoxidase activity, an index of neutrophil accumulation (U/100 mg tissue), was significantly (P < 0.05) lower in the necrotic tissue of the L-Arg group (0.88 +/- 0.26) than in the Veh group (2.46 +/- 0.38). Furthermore, responses to endothelium-dependent vasodilators acetylcholine and A23187 in isolated ischemic-reperfused LAD rings were significantly (P < 0.05) greater in the L-Arg group than in the other two groups. We conclude that intracoronary infusion of L-Arg during the early phase of reperfusion reduced neutrophil accumulation and infarct size and the infusion preserved endothelial function, possibly by increasing NO release or production by the endothelium.

Animals

Myocardial protective effects of adenosine. Infarct size reduction with pretreatment and continued receptor stimulation during ischemia.

BACKGROUND: We hypothesized that 1) endogenous adenosine released during ischemia conferred an inherent cardioprotection, and 2) a pretreatment dose of adenosine before ischemia would provide additional protection independent of hemodynamic effects. METHODS AND RESULTS: Thirty-six anesthetized New Zealand White rabbits underwent 30 minutes of regional ischemia produced by coronary occlusion followed by 2 hours of reperfusion. The adenosine group (ADO, n = 9) received a 5-minute pretreatment infusion of 140 micrograms/kg/min of adenosine before ischemia. A control group (SAL, n = 9) received saline before ischemia. To separate the effects of adenosine used as a pretreatment versus the effects during ischemia, a third group (ADO+SPT, n = 9) received adenosine as pretreatment followed by 10 mg/kg 8-p-sulfophenyl theophylline (8-SPT), an A1/A2-receptor antagonist given before ischemia, thus allowing pretreatment with adenosine but antagonizing its effects during ischemia. To preclude any protection from endogenous adenosine released during ischemia, the fourth group (SAL+SPT, n = 9) received saline as pretreatment and 8-SPT before ischemia. Area of necrosis within the area at risk (infarct size) was determined with tetrazolium and Evans blue stains, and transmural blood flow was measured using radioactive microspheres. Collateral blood flow in the area at risk was similar in all groups, as was the size of the area at risk. Infarct size was reduced by adenosine pretreatment (ADO, 8.4 +/- 7.2%) in contrast to saline vehicle (SAL, 27.8 +/- 6.3%; p less than 0.05 versus ADO). alpha 1/alpha 2-Receptor blockade after adenosine pretreatment abolished the ischemic protection provided by pretreatment adenosine (ADO+SPT, 42.7 +/- 8.3%; p less than 0.05 versus ADO). Finally, receptor blockade of endogenously released adenosine without adenosine pretreatment increased infarct size by 24% over the nonpretreated saline group (SAL+SPT, 51.5 +/- 9.0%; p less than 0.05 versus SAL). CONCLUSIONS: We conclude that 1) endogenous adenosine building up during ischemia is cardioprotective, and 2) pretreatment with adenosine confers cardioprotection independent of hemodynamic effects. Whether pretreatment effects of adenosine subsequently modulate the effects of endogenous adenosine (through alterations in receptor population or sensitivity) or endogenous and exogenous adenosine represent additive compartments is unclear.

Adenosine

High-performance computing, high-speed networks, and configurable computing environments: progress toward fully distributed computing.

The next several years will see the maturing of a collection of technologies that will enable fully and transparently distributed computing environments. Networks will be used to configure independent computing, storage, and I/O elements into "virtual systems" that are optimal for solving a particular problem. This environment will make the most powerful computing systems those that are logically assembled from network-based components and will also make those systems available to a widespread audience. Anticipating that the necessary technology and communications infrastructure will be available in the next 3 to 5 years, we are developing and demonstrating prototype applications that test and exercise the currently available elements of this configurable environment. The Lawrence Berkeley Laboratory (LBL) Information and Computing Sciences and Research Medicine Divisions have collaborated with the Pittsburgh Supercomputer Center to demonstrate one distributed application that illuminates the issues and potential of using networks to configure virtual systems. This application allows the interactive visualization of large three-dimensional (3D) scalar fields (voxel data sets) by using a network-based configuration of heterogeneous supercomputers and workstations. The specific test case is visualization of 3D magnetic resonance imaging (MRI) data. The virtual system architecture consists of a Connection Machine-2 (CM-2) that performs surface reconstruction from the voxel data, a Cray Y-MP that renders the resulting geometric data into an image, and a workstation that provides the display of the image and the user interface for specifying the parameters for the geometry generation and 3D viewing. These three elements are configured into a virtual system by using several different network technologies. This paper reviews the current status of the software, hardware, and communications technologies that are needed to enable this configurable environment. These interdependent technologies include: (1) user interface and application program construction methodologies, (2) the interprocess communication (IPC) mechanisms used to connect the software modules of the application, (3) the network protocols and interface hardware used by the IPC for communicating between modules running on separate and independent computing system elements, (4) the telecommunications infrastructure that provides the low-level data transfer functions for the networks that connect the geographically distributed elements used by the application, and (5) the nature of the functional elements that will be connected to form virtual systems.

Computer Communication Networks

Cerebral perfusion during canine hypothermic cardiopulmonary bypass: effect of arterial carbon dioxide tension.

Cerebral blood flow (radioactive microspheres), intracranial pressure (subdural bolt), and retinal histopathology were examined in 20 dogs undergoing 150 minutes of hypothermic (28 degrees C) cardiopulmonary bypass to compare alpha-stat (arterial carbon dioxide tension, 40 +/- 1 mm Hg; n = 10) and pH-stat (arterial carbon dioxide tension, 61 +/- 1 mm Hg; n = 10) techniques of arterial carbon dioxide tension management. Pump flow (80 mL.kg-1.min-1), mean aortic pressure (78 +/- 2 mm Hg), and hemoglobin level (87 +/- 3 g/L [8.7 +/- 0.3 g/dL]) were maintained constant. During bypass, intracranial pressure progressively increased in the alpha-stat group from 6.0 +/- 1.0 to 13.9 +/- 1.8 mm Hg (p less than 0.05) and in the pH-stat group from 7.7 +/- 1.1 to 14.7 +/- 1.4 mm Hg (p less than 0.05), although there was no evidence of loss of intracranial compliance or intracranial edema formation as assessed by brain water content. With cooling, cerebral blood flow decreased by 56% to 62% in the alpha-stat group (p less than 0.05) and by 48% to 56% in the pH-stat group (p less than 0.05). However, 30 minutes after rewarming to 37 degrees C, cerebral blood flow in both groups failed to increase and remained significantly depressed compared with baseline values. Both groups showed similar amounts of ischemic retinal damage, with degeneration of bipolar cells found in the inner nuclear layer in 67% of animals. We conclude that, independent of the arterial carbon dioxide tension management technique, (1) cerebral perfusion decreased comparably during prolonged hypothermic bypass, (2) intracranial pressure increases progressively, (3) ischemic damage to retinal cells occurs despite maintenance of aortic pressure and flow, and (4) a significant reduction in cerebral perfusion persists after rewarming.

Animals

Heart rate-right ventricular stroke volume relation with myocardial revascularization.

Whether increasing pacing frequency in cardiac surgical patients effectively improves right ventricular cardiac index depends on the interrelationships between heart rate, stroke volume index, and end-diastolic volume index. If an inverse relation exists between heart rate and right ventricular volume then the decrease in right ventricular ejection fraction described after bypass may be due, in part, to changes in heart rate. We evaluated the effects of pacing at 80, 95, and 110 beats/min using a thermodilution volumetric catheter in 16 patients undergoing myocardial revascularization. End-diastolic volume index, stroke volume index, and stroke work index were significantly greater after bypass than before bypass, whereas right ventricular ejection fraction remained constant. Before and after bypass, sequentially increasing pacing frequency from 80 to 110 beats/min decreased stroke volume index by 28% to 35% (p less than 0.001), end-diastolic volume index by 12% to 14% (p less than 0.001), and right ventricular ejection fraction by 18% to 24% (p less than 0.001). Right ventricular performance, assessed by comparing the stroke volume index to end-diastolic volume index and stroke work index to end-diastolic volume index relations generated during pacing, was not altered by bypass. We conclude that sequentially increasing heart rate from 80 to 110 beats/min fails to improve stroke volume index and consequently cardiac index before or after cardiac operations. Intraoperatively, in patients with normal left ventricular function, increasing pacing frequency decreases right ventricular ejection fraction due to simultaneous reductions in stroke volume index and end-diastolic volume index.

Adult

Efficacy of myocardial protection with hypothermic blood cardioplegia depends on oxygen.

The role of oxygen (O2) in blood cardioplegia (BCP) remains controversial. On the one hand, O2 reduces ischemic injury between BCP infusions by maintaining energy production through oxidative pathways. On the other hand, O2 carried by blood may not be released to the tissue at 4 degrees C or potentially provides substrate for deleterious O2 radical species. This study tests the hypothesis that O2 is a critical component in myocardial protection afforded by BCP. In 17 anesthetized dogs, left ventricular performance was measured by left ventricular end-systolic pressure-volume relations using the position of the end-systolic pressure-volume relation quantitated by the left ventricular midrange volume intercept at 100 mm Hg (V100) to describe performance. After 30 minutes of global normothermic ischemia, hearts were protected with multidose 4 degrees C BCP for 1 hour of arrest. Oxygen content in BCP was adjusted to 1.1 +/- 0.2 vol% (n = 7; desaturated BCP group), 4.3 +/- 0.5 vol% (n = 5; intermediate oxygenated BCP group), or 10.2 +/- 0.6 vol% (n = 5; saturated BCP group) using a membrane oxygenator interposed in the BCP circuit and aerated with an appropriate mixture of O2, nitrogen, and carbon dioxide. After 1 hour of 37 degrees C reperfusion, 3 of the 7 dogs in the desaturated BCP group failed to generate sufficient cardiac output to discontinue bypass. In the remaining 4 dogs, severe left ventricular depression caused a rightward shift in V100 from 17 +/- 4 to 47 +/- 9 mL (p = 0.02). With intermediate BCP, all hearts were weaned from bypass with marginal left ventricular depression (V100, 20 +/- 5 versus 46 +/- 16 mL; p = 0.10). In contrast, hearts protected with saturated BCP showed no significant increase in V100 (13 +/- 4 versus 24 +/- 13 mL; p = 0.23). We conclude that O2 in BCP is critical to its myocardial protective properties.

Animals

Variable non-linearity in end systolic pressure-volume relationships results from interaction between end diastolic and developed pressure-volume relations.

OBJECTIVE: The aim was to determine the contributions of diastolic pressure to the shape of the relationship of total systolic left ventricular pressure with volume (pressure-volume relationship). STUDY DESIGN: The pressure-volume relationship was approximated (by least squares fit) to a parabola P = aV2 + bV + C. Non-linearity was indicated by values "a" significantly different from zero. Negative values indicated concavity to the volume axis, positive values convexity to the volume axis. MATERIALS: Langendorff perfused rabbit hearts (n = 8) with intraventricular balloon were used. Balloon pressure was measured for varying balloon volumes. RESULTS: The total systolic pressure-volume relationship was concave towards the volume axis at 2.4 mM extracellular calcium ions concentrations ([Cae++]) a = -47.2 (SD 5.4), p less than 0.05. It was nearly linear at [Cae++] = 0.6 mM; a = -0.8(5.8), p greater than 0.05. It was convex at [Cae++] = 0.3 mM; a = 25.3(4.0), p less than 0.01. The diastolic pressure-volume relationship was always convex: a = 30.1(6.7), 33.5(7.6), 42.2(6.6) for [Cae++] = 2.4, 0.6, and 0.3 mM respectively. When these diastolic values were subtracted from the total pressures, pressure-volume curves for developed pressure were obtained which were always concave: a = -76.9(10.2), -33.5(3.7), -16.3(2.9) for [Cae++] = 2.4, 0.6, and 0.3 mM. CONCLUSIONS: The true systolic pressure-volume relationship of the left ventricle is not linear but concave to the volume axis. The slope is therefore variable and not an index of contractility. Apparently linearity or convexity is due to inappropriate addition of the diastolic pressure-volume properties.

Animals

Clinical utility of a position-monitoring catheter in the pulmonary artery.

Unsuspected distal migration of the tip of the pulmonary artery catheter may cause life-threatening complications. We prospectively evaluated the clinical utility of the PA Watch Catheter in 25 patients after cardiac surgery by hourly measurements of pulmonary artery (distal lumen), right ventricular (middle lumen), and central venous (proximal lumen) pressures. The catheter was considered to be in the proper position when the middle lumen port, located 10 cm from the tip, transmitted a right ventricular pressure waveform. Satisfactory initial catheter placement was obtained in 24 of 25 patients. During the 28.4 +/- 1.8 h of postoperative monitoring, clinically unsuspected distal catheter migration, indicated by the presence of a pulmonary artery pressure waveform in the middle lumen port, occurred in 12 of the 25 patients (48%). In these patients, 20 episodes occurred and required catheter withdrawal distances of 1.8 +/- 0.3 cm (range 1-6 cm). The PA Watch Catheter proved to be a useful indicator of unsuspected distal catheter migration in the postoperative period. The PA Watch Catheter allows assessment of catheter tip placement in the proximal pulmonary artery and may decrease catheter-induced complications.

Adult

ULFS-49 causes bradycardia without decreasing right ventricular systolic and diastolic performance.

The effects of ULFS-49, a new calcium channel blocker, on right ventricular (RV) systolic and diastolic performance were evaluated in nine anesthetized, closed-chest dogs by load-insensitive indexes. ULFS-49 (0.3 mg/kg) decreased heart rate (HR) from 76 +/- 25 to 47 +/- 11 beats/min (p less than 0.01) and cardiac output (CO) from 1.89 +/- 0.62 to 1.42 +/- 0.72 L/min (p less than 0.01), as RV free wall end-diastolic area increased from 486 +/- 126 to 581 +/- 45 mm2 (p less than 0.01) and RV end-diastolic volume increased from 66.6 +/- 26.4 to 85.3 +/- 28.5 ml (p less than 0.05). Pacing at 100 beats/min ablated these hemodynamic and dimensional changes. RV free wall contractility was assessed by the slope and midrange intercept values of the relation between RV end-systolic pressure (Pes) and end-systolic free wall area (Aes) and between RV free wall segmental work (SW) and end-diastolic area (Aed). RV free wall stiffness was measured by exponential fit of the RV end-diastolic pressure (Ped)-Aed points during caval occlusion. With pacing at 100 beats/min, the slope of the Pes-Aes relationship was unchanged by ULFS-49 (0.52 +/- 0.29 vs. 0.60 +/- 0.35 mm Hg/mm2) as was the midrange intercept (382.3 +/- 114.7 vs. 387.1 +/- 121.5 mm2). After administration of ULFS-49, the slope of the SW-Aed relation increased from 31.8 +/- 14.4 to 37.3 +/- 17.7 mm Hg.mm2 (p less than 0.05) without changing the midrange intercept (410.5 +/- 108.1 mm2 vs. 413.0 +/- 107.0 mm2). Similarly, neither the position nor curvature of the Ped-Aed relation was changed by ULFS-49. These data demonstrate that ULFS-49 causes significant bradycardia and increases the size of the right ventricle without directly depressing RV free wall systolic or diastolic performance.

Animals

Nonlinearity of indexes of left ventricular performance: effects on estimation of slope and diameter axis intercepts.

The slope and diameter axis intercept (D0) of the linear indexes end-systolic pressure-diameter relation (ESPDR), maximum of the first derivative of left ventricular pressure (dP/dtmax)-end-diastolic diameter relation (dP/dtmax-Ded), and dimensional preload-recruitable stroke work relation (PRDSW) are used to describe left ventricular performance. We tested the hypothesis that nonlinearity in these indexes would preclude accurate estimation of slope and D0. In nine pentobarbital-anesthetized dogs, right heart bypass was used to obtain a wide range of pressure-minor axis diameter (sonomicrometry) points from which the three indexes were derived. For ESPDR and dP/dtmax-Ded, a nonlinear fit (y = ax2 + bx + c) approximated the data better than a linear fit, with significant nonlinearity toward the diameter axis (a = -10.28 +/- 3.42 and -111.2 +/- 26.2, respectively, P less than 0.05). Although linear D0 was significantly less than nonlinear D0, this difference was overcome by the diameter intercept at a midrange value of end-systolic pressure or dP/dtmax. PRDSW demonstrated no significant nonlinearity (a = -4.40 +/- 3.53, P = 0.86) but extrapolation to D0 demonstrated linear and nonlinear differences. We conclude that 1) ESPDR and dP/dtmax-Ded demonstrate significant nonlinearity, while PRDSW is well-approximated by a linear fit over a large range of data points; and 2) extrapolation of D0 is inaccurate in all three indexes, while a midrange intercept is independent of the model used to fit the data. Left ventricular performance may be more accurately described by linear slope and midrange diameter intercept over comparable ranges of data.

Animals

Regional function, blood flow, and oxygen utilization relations in repetitively occluded-reperfused canine myocardium.

Temporary coronary occlusion followed by reperfusion severely reduces contractile function in the involved segment. We tested whether an uncoupling exists between O2 utilization (MVO2) and systolic shortening in the ischemic-reperfused segment subjected to repetitive coronary occlusion and reperfusion. In 10 anesthetized open-chest dogs, left ventricular pressure and segment length (sonomicrometry) relations were measured in the left anterior descending (LAD, ischemic-reperfused) segment and circumflex coronary artery (nonischemic segment). Four 12-min LAD occlusions were each followed by 30 min reperfusion. MVO2 was determined in both segments by transmural blood flow (15 microns microspheres) and regional coronary arterial-venous O2 extraction after each occlusion-reperfusion period. The four occlusion-reperfusion periods did not produce necrosis by staining with triphenyltetrazolium chloride. LAD occlusion produced dyskinesis [control = 16 +/- 3.0% systolic shortening (SS) vs. -8.8 +/- 1.5%, P less than 0.0001]. The first reperfusion restored SS only to 2.3 +/- 2.0%, which progressively deteriorated to -3.9 +/- 1.1% (P less than 0.05) with subsequent occlusion-reperfusion episodes. Relative to the nonischemic segment, MVO2 in the ischemic-reperfused segment decreased by only 18% despite dyskinesis. Pressure-length analysis showed systolic stiffening during reperfusion with displacement of the passive ischemic pressure-length loop to the left. Segment work (integral of each loop) continued to be generated at 34.5% of control levels after the last occlusion-reperfusion event in contrast to the negative SS. We conclude that 1) MVO2 in the ischemic-reperfused segment without necrosis remains elevated despite severe reductions in systolic shortening, and 2) the discrepancy between systolic shortening and MVO2 is partially due to persistent development of segment work.

Animals

Preoperative and intraoperative predictors of inotropic support and long-term outcome in patients having coronary artery bypass grafting.

The prognostic value of preoperative symptoms, preoperative left ventricular function, and intraoperative factors as related to postoperative outcome in coronary artery bypass grafting is unclear. This study was performed to identify risk factors that could be used as markers to predict immediate and long-term outcome, knowledge of which might allow physicians to modify these factors to decrease the likelihood of an adverse outcome. We retrospectively evaluated preoperative factors (including age, sex, New York Heart Association [NYHA] classification of symptoms, ejection fraction [EF], wall motion abnormalities, baseline left ventricular end-diastolic pressure [LVEDP], postradiographic contrast injection LVEDP, change in LVEDP with contrast injection, cardiac enlargement, and collateral vessels) and intraoperative factors (duration of bypass and aortic cross-clamp time) in 128 patients. The need for inotropic drug support was used as a marker of immediate outcome. A 36-mo follow-up used death and the postoperative NYHA classification of symptoms as markers of long-term outcome. The various factors associated with the use of inotropes and immediate outcome were analyzed by logistic regression. The factors related to inotrope use (and presumed adverse short-term outcome) in order of decreasing significance were lower EF, older age, cardiac enlargement, female sex, and higher baseline and postcontrast LVEDP. Patients with EF greater than or equal to 55%, but also having wall motion abnormalities and LVEDP change greater than or equal to 10 mm Hg, and all patients with EF less than 55% were more likely to require inotropic drug stimulation after cardiopulmonary bypass. Neither the change in LVEDP nor the presence of wall motion abnormalities independently predicted the need for postoperative inotropic support.(ABSTRACT TRUNCATED AT 250 WORDS)

Age Factors

Brain microemboli during cardiac surgery or aortography.

We have observed many focal dilatations or very small aneurysms in terminal arterioles and capillaries of 4 of 5 patients and 6 dogs who had recently undergone cardiopulmonary bypass. A smaller number of sausagelike dilatations distended medium-sized arterioles. Two other patients had a small number of the same microvascular changes following proximal aortography. Thirty-four patients and 6 dogs not undergoing cardiopulmonary bypass had none. (A 35th patient who had not undergone cardiopulmonary bypass or aortography showed a small number of dilatations; mediastinal air was a suggested source.) Some of the dilatations exhibited various forms of birefringence. Because most of the dilatations appear empty, we speculate that they are the sites of gas bubbles or fat emboli that have been removed by the solvents used in processing. These microvascular events, occurring only in conjunction with major arterial interventions, may be the anatomical correlate of the neurological deficits or moderate to severe intellectual dysfunction seen in at least 24% of patients after cardiac surgical procedures assisted by cardiopulmonary bypass.

Adult