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Anesth Analg 2002;94:1120-1126
© 2002 International Anesthesia Research Society

CARDIOVASCULAR ANESTHESIA

The Effects of Acute Normovolemic Hemodilution on Left Ventricular Systolic and Diastolic Function in the Absence or Presence of ß-Adrenergic Blockade in Dogs

Junpei Nozaki, MD, Hiroshi Kitahata, MD, Katsuya Tanaka, MD, Shinji Kawahito, MD, and Shuzo Oshita, MD

Department of Anesthesiology, Tokushima University School of Medicine, Tokushima, Japan

Address correspondence and reprint requests to Junpei Nozaki, MD, Department of Anesthesiology, Tokushima University School of Medicine, 3-18-15 Kuramoto, Tokushima 770-8503, Japan. Address e-mail to jnozaki{at}clin.med.tokushima-u.ac.jp


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Acute normovolemic hemodilution (ANH) increases cardiac output because of a reduction in blood viscosity and enhancement of left ventricular (LV) contractility. The status of LV function, especially LV diastolic function during ANH, remains controversial. We therefore examined LV systolic and diastolic function during ANH. Sixteen dogs were anesthetized with isoflurane in the absence (Group 1) and presence (Group 2) of ß-adrenergic blockade (propranolol 1 mg/kg). LV contractility was quantified by the slope (Mw) of the stroke work and end-diastolic volume relation. Diastolic function was evaluated with the time constant of LV relaxation (T), chamber stiffness constant (Kc), peak LV diastolic filling rate during early filling (peak E) and atrial contraction (peak A), and ratio of peak E to peak A (E/A). Normovolemic exchange of blood (50 mL/kg) for 6% hydroxyethyl starch (ANH50) significantly increased Mw in Group 1 but not in Group 2. In both groups, ANH50 significantly decreased T. ANH50 significantly increased peak E in both groups and peak A in Group 1, and it did not change the E/A ratio or Kc in either group. ANH causes positive inotropic effects and enhances diastolic function without ß-blockade. Even after ß-adrenergic blockade, ANH improves diastolic function through the reduction of LV ejection impedance.

IMPLICATIONS: Acute normovolemic hemodilution enhances LV (left ventricular) diastolic function by alterations in the LV loading condition produced by hemodilution, which mainly contributes to a compensatory increase in cardiac output.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
The technique of acute normovolemic hemodilution (ANH) with colloid or crystalloid solutions is widely used to reduce both blood transfusion requirements and the incidence of complications of homologous blood transfusion, e.g., transfusion-transmitted disease, transfusion reaction, and immunomodulatory effects. The reduction of arterial oxygen capacity during ANH is compensated for by increased cardiac output. Previous reports noted that one factor responsible for the compensatory increase in cardiac output during ANH was a reduction in blood viscosity associated with smaller hemoglobin concentration. The lower blood viscosity leads to a decrease in systemic vascular resistance (SVR) (1) and a reduction of left ventricular (LV) ejection impedance (2,3). Another factor is the enhancement of myocardial contractility secondary to activation of the sympathetic nervous system during ANH (4,5). However, other studies showed a persistent increase in cardiac output after blockade of sympathetic response during ANH (2–4,6). We hypothesized that ANH improves LV diastolic function, which mainly contributes to an increase in cardiac output even after blockade of sympathetic response during ANH. Therefore, we investigated the effects of ANH on cardiac function, especially diastolic function, in anesthetized dogs and whether ß-adrenergic blockade by propranolol can influence the effects of ANH. The results may provide further clarification of the relevance of LV function during ANH in relation to compensatory increases in cardiac output.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
This study was approved by the Animal Care Committee of Tokushima University. Sixteen unpremedicated mongrel dogs of both sexes, weighing 9 to 16 kg, were anesthetized with thiamylal 20–25 mg/kg administered IV before tracheal intubation and were ventilated mechanically by a ventilatory pump (SN-480-3; Shinano Manufacturing Co., Tokyo, Japan) to maintain PaO2 at 100–200 mm Hg and PaCO2 at 35–45 mm Hg. Anesthesia was maintained with 1.5% isoflurane (approximately 1.2 minimum alveolar anesthetic concentration [MAC] in dogs), 50% oxygen, and 50% nitrogen. End-tidal isoflurane and carbon dioxide concentrations were monitored continuously with an HC-510 (Fukuda Denshi, Tokyo, Japan).

Each dog was placed on its right side, and an IV catheter was placed in the right femoral vein for continuous infusion of 0.9% saline (5–7 mL · kg-1 · h-1). Muscle relaxation was obtained with an initial IV injection of vecuronium 0.1 mg/kg, followed by a continuous infusion at 0.1 mg · kg-1 · h-1. Rectal temperature was monitored (CTM-303; Terumo, Tokyo, Japan) and controlled at 37°C–38°C with a water-circulating heating pad.

Polyethylene catheters were inserted into the right femoral artery for blood sampling and through the right jugular vein into the superior vena cava for ANH with 6% hydroxyethyl starch (Hespander®, average molecular weight 70,000; Kyorin Pharmaceutical Co., Tokyo, Japan) and for measurement of central venous pressure. After the heart was exposed through a left thoracotomy at the fifth or sixth intercostal space and suspended in a pericardial cradle, a 7F pressure-transducer-tipped catheter (SPC-370; Millar Instruments, Houston, TX) was inserted into the aortic root via the right carotid artery to record aortic blood pressure (RMC-1100 polygraph; Nihon Kohden, Tokyo, Japan). Heparin (300 IU) was administered IV to prevent blood coagulation in the exchange circuit. An 8-electrode 5F conductance catheter (CCS-100-6; Unique Medical, Tokyo, Japan) and a 7F pressure-transducer-tipped catheter (SPC-370) were placed in the LV through a small incision at the apex. Conductance catheter position was confirmed by verification of synchronous segmental volume signals. An 8F Fogarty occlusion catheter (62080814F; Baxter, Irvine, CA) was inserted through the left femoral vein to the inferior vena cava to create an abrupt alteration of the LV preload by inflation of the catheter’s balloon during measurement of pressure-volume loop variables. A fluid-filled catheter was placed in the pulmonary artery to inject hypertonic saline (10%; 2 mL) to determine the parallel conductance volume (Vp). After completion of the study, the dogs were killed with a bolus infusion of KCl, and all catheters were confirmed to be positioned properly.

A full description of the principles and techniques of the volume conductance catheter measurement method has appeared elsewhere, and its reliability has been confirmed (7,8). In brief, the LV volume signal from the conductance catheter and the LV pressure signal from the pressure-transducer-tipped catheter are connected to a conductance module (VPR1002; Unique Medical) that maintains a constant current (200 µA at 20 kHz) between the two outermost electrodes and measures the voltage difference between each adjacent electrode (five pairs of the intervening electrodes; interelectrode distance, 0.75 cm). These signals and the intraventricular electrocardiogram signal are digitized simultaneously (at 500 Hz) with a microcomputer (PC9821NW133D; NEC, Tokyo, Japan) interfaced with an on-line analog-to-digital converter for real-time display. In this study, data recording and storing of data analysis of the LV pressure-volume relation were performed with custom software (VPS-100; Unique Medical). Approximately 5 min before each intervention, calibration of blood conductivity was performed in a sampling cuvette incorporated into the conductance module; precalibration was performed with solutions of known conductivity (0.9% saline). Determination of the parallel conductance, Gp, of structures surrounding the ventricular cavity was by a saline calibration technique previously reported (7). The Vp is a correction term by the conductance, Gp:

equation


In this equation, {varsigma} = the blood conductivity, L = interelectrode distance, and {alpha} = the slope correction factor for conductance volume and real LV volume. We assumed that {alpha} was equal to 1. Hypertonic saline was administered in the pulmonary artery during suspended ventilation. During each measurement, Vp was subtracted from the measured volume to obtain absolute LV volume.

The dogs were assigned to one of two groups (n = 8 per group). Those in Group 1 had intact ß-adrenergic receptors during hemodilution, and those in Group 2 had their ß-adrenergic receptor pharmacologically blocked with IV propranolol (1 mg/kg).

To stabilize hemodynamic variables and adjust blood gases, baseline measurements, including Vp, were performed at least 1 h after the surgical procedure. In Group 1, ANH was performed by replacement of blood from the right femoral artery with a continuous equivalent volume of prewarmed 6% hydroxyethyl starch via the catheter in the superior vena cava. The exchange of blood with hydroxyethyl starch took approximately 10 min. The volume of this first blood exchange was 25 mL/kg. After a 10-min stabilization period, measurements were repeated (ANH25). The blood exchange was then repeated at the same volume, 25 mL/kg, with a cumulative exchange volume of 50 mL/kg (ANH50). Each measurement, including calibration of blood conductivity and Vp, and arterial blood sampling were performed after a 10-min stabilization period, and the interval between measurements was approximately 30 min. After baseline measurements, Group 2 dogs received 1 mg/kg of propranolol IV. ANH was performed according to the protocol described previously, and arterial blood sampling and measurements, including calibration of blood conductivity and Vp, were performed. Arterial blood samples were analyzed electrometrically for acid-base status, PaO2, PaCO2, serum concentrations of Na+, K+, and Ca2+ (ABL 505; Radiometer, Copenhagen, Denmark), hemoglobin concentration, oxygen saturation, and oxygen content (CO-oximeter 2500; Corning, Boston, MA).

In this study, LV contractility was assessed by the slope (Mw) of the stroke work and the end-diastolic volume relation. During each ANH stage, LV stroke work was calculated as the area of various loops that were obtained by transient occlusion of the inferior vena cava resulting in approximately a 30 mm Hg decline in LV pressure during 10–15 cardiac cycles. Then LV stroke work was plotted against the corresponding end-diastolic volume, and linear regression analysis was used to calculate Mw (9). LV relaxation was evaluated with a time constant (T) of LV pressure decline during isovolemic relation. T was evaluated assuming a nonzero asymptote of ventricular decline (10). LV diastolic filling was evaluated by determining the peak value of the first derivative of the LV volume-time curve (dV/dt) during early diastolic filling (peak E) and atrial contraction (peak A), and the ratio of peak E to peak A (E/A ratio) (11). Passive indices of diastolic function were evaluated with the LV chamber stiffness constant (Kc) derived from the LV diastolic pressure volume relation (12). Figure 1 shows LV pressure and volume wave forms and a series of LV pressure-volume diagrams obtained in a typical experiment.



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  		Figure 1. Left ventricular (LV) pressure and volume wave forms obtained in a typical experiment (A). LVP = LV pressure; LVV = LV volume; dV/dt = the first derivative of the LV volume-time curve; peak E = the peak dV/dt during early diastolic filling; peak A = the peak dV/dt during atrial contraction; ECG = electrocardiogram. A series of LV pressure-volume diagrams during preload reduction by vena caval balloon occlusion before (B) and after (C) 50 mL/kg colloid-for-blood exchange.

 
Data are presented as mean ± SD. Analyses of differences within each group were made by one-way analysis of variance for repeated measures, and post hoc analyses were made with Student’s t-test with Bonferroni’s correction. Analyses of differences between groups were performed by analysis of variance for repeated measures followed by the Student’s t-test. P values of <0.05 were considered significant.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
The arterial blood analysis and cardiac hemodynamic variables obtained during ANH both in the absence and presence of ß-adrenergic blockade are summarized in Tables 1 and 2. There were no significant differences between the two groups in any variables except for LV end-systolic volume and SVR at baseline. ANH reduced hemoglobin concentrations from 13.4 ± 3.0 g/dL at baseline to 8.8 ± 2.2 g/dL at ANH25 and 6.1 ± 1.4 g/dL at ANH50 (n = 16, both groups). In Group 1, heart rate (HR), LV end-diastolic pressure, stroke volume, and cardiac output increased, and SVR decreased significantly after stepwise ANH. LV end-systolic volume, however, did not increase significantly, and LV end-diastolic volume slightly increased, but not significantly, after each stage of ANH. In Group 2, after ß-adrenergic blockade, HR significantly decreased and then did not change throughout stepwise ANH. The difference between the two groups in HR was significant. LV end-diastolic pressure and volume increased significantly after ANH. Stroke volume and cardiac output decreased after the administration of propranolol; however, they then increased significantly after ANH50. LV end-systolic volume and SVR increased significantly after the administration of propranolol, and LV end-systolic volume did not change during stepwise ANH; however, SVR decreased significantly after ANH50. Mean aortic blood pressure and central venous pressure in both groups remained stable throughout the experimental protocol.


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  		Table 1. Arterial Blood Analysis During Acute Normovolemic Hemodilution (ANH) Both in the Absence and Presence of ß-Adrenergic Blockade (BB)
 

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  		Table 2. Hemodynamic Data and Vp During Acute Normovolemic Hemodilution (ANH) Both in the Absence and Presence of ß-Adrenergic Blockade (BB)
 
There were no significant differences between the two groups in Mw, T, peak E, peak A, or E/A ratio during baseline. In the absence of ß-adrenergic blockade, ANH caused a significant increase in Mw (74 ± 15 mm Hg at baseline to 88 ± 27 mm Hg at ANH50; Fig. 2). ANH caused significant decreases in T (34 ± 4 ms at baseline to 27 ± 2 ms at ANH50; Fig. 3) and significant increases in peak E (100 ± 52 mL/s at baseline to 153 ± 47 mL/s at ANH50; Fig. 4) and peak A (60 ± 31 mL/s at baseline to 82 ± 25 mL/s at ANH50; Fig. 4). No changes in E/A ratio (Fig. 4) or Kc (0.268 ± 0.185 at baseline to 0.276 ± 0.312 at ANH50) were produced by ANH in the absence of ß-adrenergic blockade.



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  		Figure 2. Effects of acute normovolemic hemodilution (ANH) on the slope (Mw) of the preload recruitable stroke work relation in the absence (open bars) or presence (solid bars) of ß-adrenergic blockade at baseline, after the administration of propranolol (BB; 1 mg/kg IV), and after stepwise ANH. Cumulative exchange blood volumes with 6% hydroxyethyl starch are 25 mL/kg (ANH25) and 50 mL/kg (ANH50). Data are presented as mean ± SD. *P < 0.05 compared with baseline within group; {dagger}P < 0.05 between the group without and with ß-adrenergic blockade.

 


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  		Figure 3. Effects of acute normovolemic hemodilution (ANH) on the time constant (T) of left ventricle relaxation in the absence (open bars) or presence (solid bars) of ß-adrenergic blockade at baseline, after the administration of propranolol (BB; 1 mg/kg IV), and after stepwise ANH. Cumulative exchange blood volumes with 6% hydroxyethyl starch are 25 mL/kg (ANH25) and 50 mL/kg (ANH50). Data are presented as mean ± SD. *P < 0.05 compared with baseline within group; #P < 0.05 compared with BB.

 


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  		Figure 4. Effects of acute normovolemic hemodilution (ANH) on the peak left ventricular diastolic filling rate during (A) early filling (peak E) and (B) atrial contraction (peak A), and (C) the ratio of peak E to peak A (E/A) in the absence (open bars) or presence (solid bars) of ß-adrenergic blockade at baseline, after the administration of propranolol (BB; 1 mg/kg IV), and after stepwise ANH. Cumulative exchange blood volumes with 6% hydroxyethyl starch are 25 mL/kg (ANH25) and 50 mL/kg (ANH50). Data are presented as mean ± SD. *P < 0.05 compared with baseline within group; #P < 0.05 compared with BB; §P < 0.05 compared with ANH25; {dagger}P < 0.05 between the groups without and with ß-adrenergic blockade.

 
The administration of propranolol produced significant decreases in Mw (81 ± 21 mm Hg at baseline to 51 ± 24 mm Hg after ß-adrenergic blockade), and Mw showed no change during two-step ANH (Fig. 2). ß-Adrenergic blockade produced significant increases in T (27 ± 3 ms at baseline to 39 ± 10 ms after ß-adrenergic blockade; Fig. 3), and ANH then significantly decreased T (30 ± 4 ms at ANH50; Fig. 3). Blockade of the ß-adrenergic receptor decreased peak E and increased peak A only slightly, and two-step ANH produced significant increases in peak E (108 ± 32 mL/s after ß-adrenergic blockade to 183 ± 41 mL/s at ANH50) and increased peak A, but not significantly (54 ± 29 mL/s after ß-adrenergic blockade to 63 ± 29 mL/s at ANH50). ANH did not increase the E/A ratio significantly (2.5 ± 1.5 after ß-adrenergic blockade to 3.3 ± 1.2 at ANH50), but there was a significant difference between the two groups in the E/A ratio during ANH50 (Fig. 4). Kc did not change significantly after ß-adrenergic blockade and stepwise ANH (0.230 ± 0.156 at baseline, 0.120 ± 0.059 after ß-adrenergic blockade, and 0.145 ± 0.106 after ANH50).


   Discussion
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 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
Our results indicate that, in dogs, the increase in cardiac output in intact ß-adrenergic receptors was responsible for an increase in stroke volume and HR, whereas after ß-adrenergic blockade, the increase in cardiac output was associated only with the increase in stroke volume. However, the percentage increase in cardiac output over pre-ANH values was nearly the same in both conditions (151% vs 143% after ANH50). These results were similar to those of previous studies (2,3,6).

In this study, ANH produced an inotropic cardiac response in the absence of ß-adrenergic blockade. This inotropic cardiac response during ANH has been reported previously (2,4–6) and could contribute to the compensatory increase in cardiac output. Several researchers, using maximal LV dP/dt as an indicator, have studied the effects of ANH on LV contractility in anesthetized, ß-adrenergic-intact dogs and pigs (13–15). In these studies, LV contractility was unchanged or increased by ANH. LV dP/dtmax is highly sensitive to inotropic stimulants but has a significant dependence on preload and afterload (16). Thus, LV dP/dtmax may be unsuitable for evaluation of myocardial contractility during ANH, because the reduction of blood viscosity during ANH increases venous return (17) and causes decreased SVR. In this study, LV myocardial contractility was assessed by Mw, which is independent of preload and afterload and is sensi-tive to changes in contractile states (9). Our finding that ANH enhanced LV contractility with intact ß-adrenergic receptors was consistent with that of Habler et al. (18). They also observed an enhancement of myocardial contractility assessed by Ees (left ventricular elastance) and Mw. We, however, found that ANH did not increase LV contractility after ß-adrenergic blockade. Our results suggest that an enhancement in LV myocardial contractility during ANH is mainly due to an increase in ß-adrenergic stimulation of the heart and that ANH does not have a direct effect on LV contractility when the secondary activation of sympathetic stimulation is blocked.

We examined the effects of ANH on LV diastolic function both in the absence and presence of ß-adrenergic blockade. The major factors determining the time constant of LV relaxation, which reflects the ability of the sarcoplasmic reticulum to sequester cytosolic calcium and release action-myosin cross-bridges, include rate of inactivation, loading conditions, and nonuniformity of LV function (19). Gaasch et al. (20) indicated that the time constant of LV relaxation is not influenced by acute changes in preload; systolic load, however, is an important determinant of the time constant of LV relaxation. The timing of LV ejection and the systolic pressure profile also determine the rate of LV relaxation (19). An early peak in systolic pressure is associated with rapid LV relaxation. We observed that a decreased blood viscosity during ANH resulted in a decrease in peripheral vascular resistance and a reduction of LV ejection impedance, thereby altering the timing of LV ejection to an earlier peak in systolic pressure. Therefore, the mechanisms related to an increase in the rate of LV relaxation during ANH may be associated with altered loading conditions, especially decreased afterload. The activation of the sympathetic stimulation during ANH also causes a decrease in the time constant of LV relaxation (21). However, our findings that ANH, even in the presence of ß-adrenergic blockade, decreased the time constant of the LV relaxation suggest that the activation of the sympathetic stimulation during ANH does not play an important role for the enhancement of LV relaxation. On the contrary, the reduction of LV ejection impedance during ANH is a major mechanism related to the enhancement of LV relaxation.

We assessed the phase of LV diastolic filling by the peak filling rate, as evaluated by determining dV/dt with a conductance catheter. The peak filling rate during early diastole depends on the early diastolic pressure gradient between the left atrium and LV. In the results of several prior studies, increases in preload resulted in increases in both filling rates without altering the E/A ratio (22). The relatively rapid rate of LV relaxation caused by the reduction of afterload and the increase in preload during ANH in our study might produce the large atrioventricular pressure gradient and the resulting increased peak E and peak A, without a change in the E/A ratio.

The subjects of this study were anesthetized with 1.5% (approximately 1.2 MAC in dogs) isoflurane. One major reason that we chose isoflurane as the anesthetic is that maintaining the level of anesthesia during hemodilution is difficult with IV anesthetics, including opioids. Cardiac function (LV contractility) is decreased less by isoflurane than by other volatile anesthetics, such as halothane, enflurane, and sevoflurane. However, in one study, isoflurane, but not the equivalent halothane or sevoflurane, reduced total arterial resistance (23). Furthermore, small doses of isoflurane increased the rate of LV relaxation in dogs with pacing-induced cardiomyopathy because of declines in LV end-diastolic pressure (24). Thus, isoflurane may have influenced LV diastolic function during ANH in our study. There were significant differences in baseline SVR and LV end-systolic volume between our groups with and without ß-adrenergic blockade. The reason for the differences between the two groups is unclear, because the depth of anesthesia and the characteristics of all subjects were quite similar. We believe that the baseline differences in SVR and LV end-systolic volume do not pose a potential problem for evaluation of the hemodynamic responses in the two groups during ANH because our statistical analyses were focused on the changes of variables during ANH within a group rather than between groups.

In summary, these results show that ANH causes positive inotropic effects and enhances LV diastolic function in the intact sympathetic nervous system in dogs. Even after ß-adrenergic blockade, ANH improves the rate of LV relaxation and diastolic filling through the reduction of LV ejection impedance caused by decreased blood viscosity and results in increased cardiac output to the same extent without ß-adrenergic blockade. These results suggest that decreased blood viscosity produced by ANH enhances LV diastolic function and plays an important role in the mechanisms responsible for the compensatory increase in cardiac output.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

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Accepted for publication December 20, 2001.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press