Hemodilution Group Research Articles

Effects of hemodilution during controlled hypotension on hepatic, renal, and pancreatic function in humans

Study Objective: To evaluate the effects of hemodilution during controlled hypotension on the hepatic, renal, and pancreatic function in the clinical setting. Design: Randomized, prospective study. Setting: Inpatient surgery at Rosai Hospital. Patients: 20 ASA status I and II patients scheduled for total hip arthroplasty. Interventions: Hemodilution was carried out after induction of anesthesia, in which drawn blood was replaced with dextran solution to achieve final hematocrit (Hct) of 31% (Group A = mild hemodilution group, N = 10) or 23% (Group B = moderate hemodilution group, N = 10). In both groups, controlled hypotension was induced with prostaglandin E 1 (PGE 1) to maintain mean arterial blood pressure at 55 mmHg for 80 minutes. Measurements and Main Results: Measurements included arterial ketone body ratio (AKBR, aceto-acetate/3-hydroxybutyrate) for hepatic cellular function, pancreatic phospholipase A 2 (P-PLA 2) for pancreatic cellular function, and urine N-acetyl-β- dglucosaminidase (NAG index) for cellular function of the renal tubule. These indices were measured before hemodilution, after hemodilution, 80 minutes after starting hypotension, 60 minutes after recovery of normotension, and on the first postoperative day. Neither AKBR norP-PLA2 showed a significant change throughout the time course of the study in either group. Urine-NAG index showed a significant increase in moderate hemodilution group at 60 minutes after recovery of normotension (+136%) and on the first postoperative day (+149%) compared with prehemodilution value, whereas it showed no significant change in the mild hemodilution group. Blood urea nitrogen and serum creatinine measured postoperatively were within normal range. Conclusions: PGE 1-induced hypotension combined with moderate hemodilution using dextran, such as 23 % of Hct value, maintains hepatic and pancreatic function but causes damage to the renal tubular cells.

Optimal Timing of Hemodilution for Brain Protection in a Canine Model of Focal Cerebral Ischemia

Hemodilution is known to ameliorate the effects of focal ischemia when used shortly after cerebral arterial occlusion; however, it remains to be proved whether hemodilution will be effective when used at more clinically relevant times, ie, with some delay between the onset of ischemia and initiation of therapy. Thirty-two dogs were selected for inclusion in this study. Cerebral infarction was induced by permanent occlusion of the middle cerebral and the azygos anterior cerebral arteries. The animals were allocated to 1 of 4 groups of eight animals each: arterial occlusion without hemodilution (group 1); hemodilution immediately after occlusion (group 2); hemodilution 3 hours after occlusion (group 3); and hemodilution 6 hours after occlusion (group 4). Isovolemic hemodilution to a hematocrit of 30% was performed. The animals were killed 6 days after induction of ischemia, and the infarct size was determined. Groups 2 and 3 showed significant reduction of infarct size (P < .0001) when compared with group 1. The neurological grade of group 3 on postoperative days 4, 5, and 6 was significantly better than those of groups 1 and 4 (P < .01). Group 4 showed a significant increase in the incidence of hemorrhagic infarction when compared with groups 1 and 2 (P < .01). The current study indicates that hemodilution administered as much as 3 hours after ischemia is effective in reducing infarct size and improving neurological status. When administered 6 hours after ischemia, hemodilution is not helpful and may be harmful.

Isovolemic hemodilution normalizes the prolonged passage of red cells and plasma through cerebral microvessels in the partially ischemic forebrain of rats.

The objective of this study was to determine whether hemodilution could normalize the mean transit times of red blood cells (Tr) and plasma (Tp) through cerebral microvessels in a partially ischemic brain. Wistar-Kyoto (WKY) rats, aged 30-40 weeks, were divided randomly into three groups. The first group was the nonocclusion, nonhemodilution (NN) normal control group. The second group was the occlusion, nonhemodilution (ON) group, in which animals were treated with bilateral carotid artery ligation. The third group was the occlusion-hemodilution (OH) group, in which animals were treated with bilateral common carotid artery ligation and, then, isovolemic hemodilution by replacing blood with the same volume of 3% modified fluid gelatin. Local cerebral blood flow (lCBF) and microvascular volumes of red blood cells (Vr) and plasma (Vp) in 14 brain structures were measured using 14C-iodoantipyrine, iron-55 labeled red blood cells, and 14C-inulin, respectively. The amount of oxygen delivered to local brain structures (OD), cerebral microvascular blood volume (Vb), mean transit time of blood (Tb), Tr, and Tp through cerebral microvessels were calculated from the data. Two hours after carotid artery ligation, lCBF decreased by approximately 38% in forebrain structures, 22% in rostral hindbrain areas, and 8% in the caudal hindbrain (29% for all 14 structures). The decreases in ODs were parallel with those of lCBFs, at 33, 17, and 2% in the three regions, respectively (24% for all structures). In contrast, Vb increased by 68, 37, and 16% in the three regions, respectively (48% for all structures). Tr and Tp were markedly prolonged (180% for Tr and 154% for Tp) in the forebrain regions, moderately (91% for Tr and 73% for Tp) in the rostral hindbrain, and mildly (60% for Tr and 13% for Tp) in the caudal hindbrain, with a mean increase of 136% for Tr and 111% for Tp in all structures. When data in the OH and NN groups were compared, lCBF values tended to be slightly higher and Vb values were significantly higher (p < 0.05) in the OH group. ODs in the eight forebrain structures were all significantly less (p < 0.05) in the OH group than the NN group. Tr and Tp values in the forebrain were similar between the OH and the NN groups. In conclusion, occlusion of the bilateral common carotid arteries in WKY rats causes partial forebrain ischemia, in which both Tr and Tp are prolonged. These prolongations of Tr and Tp can be normalized by isovolemic hemodilution. However, the ischemic forebrain remains hypoxic after hemodilution.

Alteration of Cerebral Microcirculation by Hemodilution with Hemosome in Awake Rats

Our study showed that hemodilution with modified fluid gelatin resulted in an increase in local cerebral blood flow (LCBF), but no change at all in local cerebral oxygen delivery (LCOD) in rats. Hemosome, a lecithin encapsulated hemoglobin having the oxygen-carrying capacity, was developed to improve LCOD by hemodilution. Therefore, we have hypothesized that LCBF & LCOD would be increased by hemodilution with hemosome. To test this hypothesis, adult male Sprague-Dawley rats weighing approximately 350g were used and divided into the hemodilution and the control groups. Hemosome was made from pig red blood cells and lecithin. It's mean diameter was approximately 0.3 um and hemoglobin concentration was approximately 4g/dl. Isovolemic hemodilution, which lowered the systemic hematocrit from approximately 50% to approximately 30%, was achieved by rapidly replacing blood with the same volume of hemosome. Ten min later, LCBF in 14 brain structures were measured using the 14C-iodoantipyrine technique. Our results showed that LCBF of the control group ranged from 115 +/- 11 ml/100g/min in the medulla to 260 +/- 31 ml/100g/min in the occipital cortex. LCBFs were generally higher (p < 0.05, MANOVA) by 16% in the hemodilution group than in the control group. However LCODs were generally decreased (p < 0.05, MANOVA) by 18% in the hemodilution group than in the control. In conclusion, hemodilution with hemosome indeed improves LCBF but lowers LCOD in awake rats.

Hemodilution accelerates the passage of plasma (not red cells) through cerebral microvessels in rats.

Hemodilution lowers the total circulatory red cell mass and blood viscosity and thereby may alter the time of passage of red cells and plasma through cerebral microvessels. This study was designed to clarify this question. Adult Wistar-Kyoto rats, aged approximately 32 weeks, were divided into hemodilution and control groups. Local cerebral blood flow and microvascular red cell and plasma volumes in 14 brain structures were measured with the use of [14C]iodoantipyrine, 55Fe-labeled red cells, and [14C]inulin, respectively. In the control group, the hematocrit in cerebral microvessels ranged from 0.29 to 0.45 with a mean of 0.36, which was 71% of the systemic hematocrit (0.51). The mean transit times of blood, red cells, and plasma through microvessels were 0.62 to 1.77 seconds (mean, 0.92 second), 0.44 to 1.15 seconds (mean, 0.65 second), and 0.78 to 2.5 seconds (mean, 1.25 seconds), respectively. In the hemodilution group, the mean hematocrit in microvessels was 0.28, which was 89% of the systemic hematocrit (0.32). Local cerebral blood flow was approximately 59% higher (P < .01) than that of the control animals. The rate of oxygen delivered to the brain was slightly increased (9%) after hemodilution. Blood volume in cerebral microvessels was similar to that of the control group. Mean transit time of blood was 0.62 second (68% of the control), transit time of red cells was 0.53 second (85% of the control), and transit time of plasma was 0.67 second (54% of the control). These findings indicate that isovolemic hemodilution accelerates the plasma (not red cell) flow velocity in cerebral microvessels.

Evaluation of the tolerance to hemorrhagic shock — Comparison between hemodilution and non-hemodilution: Jpn. J. Anesthesiol. 1994; 43/11: 1680–1685

We induced various degrees of bleedings in adult mongrel dogs to determine their tolerance to bleedings. The dogs were divided into two groups: the hemodilution group (Group A: Hct 11.1 +/- 1.9%) and the non-hemodilution group (Group B: Hct 36.8 +/- 6.6%). The Group A tended to show higher tolerance to bleedings than the Group B, although the difference was not significant. Throughout the period of increasing degrees of bleedings, MAP remained higher in Group B than in Group A, but CI was higher in Group A than Group B. DO2I was kept higher in Group B than in Group A. Both PaO2 and PaCO2 showed no difference between the two groups. The results of our study indicate that hemodilution group tends to be more tolerant to bleeding than non-hemodilution group. The reason is probably that under hemodilution the oxygen delivery is maintained through an increase in cardiac output in the presence of decreased arterial oxygen content. In addition, it is considered that the safety is obtained through various factors such as preferential blood distribution to important organs (in particular to the myocardium), more efficient extraction of oxygen from the blood, and the decreased work load resulting from a reduced blood viscosity.

Pial microvascular hemodynamics in anemia

Isovolemic hemodilution and subsequent anemia increase cerebral blood flow (CBF). We hypothesized that pial microvascular pressure also increases with hemodilution and that arteriolar diameter varies concurrently as a myogenic autoregulatory response. First- and second-order arterioles (31-92 microns, n = 29) and large venules (65-215 microns, n = 17) were studied in thiopental-anesthetized rats. Microvascular pressure was determined using the servo-null technique, and vessel diameters were obtained directly from a video monitoring system. We measured the increase in CBF (radiolabeled microspheres) that accompanies hemodilution in a separate group of animals (n = 20). Hematocrit was reduced to 16-36% with homologous plasma (hemodilution group, n = 13) or held constant with homologous whole blood (control group, n = 4). In control animals, arteriolar and venular diameter varied +/- 1-2 microns from baseline values, and microvascular pressure remained unchanged from baseline. In the hemodilution group, CBF increased, but there was no systematic pial vasodilation. Furthermore, intraluminal pressure did not increase in pial microvessels, suggesting that proximal vasodilation was negligible even at the lowest hematocrit studied. Vascular resistance fell proportionately in both large vessel and microvascular segments. We conclude that experimental anemia does not produce alterations in microvascular pressure in rats, and the hyperemia accompanying hemodilution is largely viscosity mediated.

Comparison of single-dose antithrombotic agents in the prevention of microvascular thrombosis

A model of thrombosis was used to evaluate the efficacy of single-dose heparin, hemodilution, and 40,000 milliwatts dextran in the prevention of microvascular thrombosis. Forty Lewis rats (275 gm body weight) were divided into four groups (n = 10): hemodilution (6 ml NS), single-dose heparin (1 μ/gm), 40,000 mw dextran (0.3 gm/100 gm), and control (0.275 ml NS). After exposure of the superficial femoral arteries, a model of arterial crush with arteriotomy followed by an intimal abrasion was used. The animals randomly received one of the four solutions above. Experimental results included patency rates of 90% at 20 minutes and 10% at 24 hours in the hemodilution group, 100% at 20 minutes, and 70% at 24 hours in the single-dose heparin group, and 100% at both 20 minutes and 24 hours in the dextran group. A 100% thrombosis rate was observed in the control group at 20 minutes and 24 hours. Single-dose heparin and dextran significantly improved patency in comparison to both the control and hemodilution groups at 24 hours ( p < 0.01). Scanning electron microscopy of the vessels revealed thrombus deposition consistent with these findings. These results indicate that single-dose heparin and single-dose dextran reduce thrombosis in this model of microvascular injury.

Circulatory Effects of Verapamil During Normovolemic Hemodilution in Anesthetized Rats

Patients who have undergone perioperative normovolemic hemodilution may require calcium channel blockers for the treatment of myocardial ischemia and/or supraventricular tachyarrhythmias. The purpose of this rodent study was to examine the effect of intravenous verapamil on the hyperdynamic circulatory response to acute normovolemic hemodilution (hematocrit 20%). Anesthetized animals were randomly divided into four groups equal in number: (1) controls (no hemodilution, no drug); (2) hemodilution only; (3) verapamil only; and (4) hemodilution followed by verapamil. Cardiac output was recorded using an electromagnetic flow probe. Pre- and afterload tests were performed, the former consisting of rapid infusion of blood adjusted for hematocrit, the latter consisting of an aortic clamp technique. Animals in group 2 had significantly (P less than 0.05) greater percent increases in cardiac index, stroke volume index, and dP/dt, and greater percent decreases in mean arterial pressure, systemic vascular resistance, and oxygen delivery than did control animals (group 1). Infusion of verapamil after hemodilution (group 4) did not interfere with the compensatory increases in cardiac index and stroke volume index seen in group 2, nor did it reduce the peak stroke volume index in response to preload stress, although it did reduce resting dP/dt, mean arterial pressure and systemic vascular resistance, and peak cardiac index and "left ventricular developed pressure" after preload and afterload stress, respectively. We conclude that reduced ventricular function after verapamil administration does not interfere with the compensatory increase in stroke volume index after normovolemic hemodilution.

Neurological deterioration under isovolemic hemodilution with hydroxyethyl starch in acute cerebral ischemia.

In a prospective study, we randomly allocated 70 patients with acute ischemic stroke to two therapy groups. Up to interim analysis, 33 patients underwent bloodletting, with simultaneous infusion of an identical volume of hydroxyethyl starch (10%, 200/0.5). The target hematocrit was 35%. A control group of 37 patients did not receive hemodilution. Apart from an unequal sex distribution, the two groups were comparable with regard to age, cardiovascular risk factors, and medical history. In the hemodilution group, the mean hematocrit fell from 44.4% to 37.7%. After 14 days, improvement on the neurological score scale was 3.3 points in the hemodilution group compared with 6.5 points in the control group (p = 0.12). Subgroups with early inclusion (less than 12 hours) or pronounced lowering of hematocrit (greater than 15% of initial hematocrit) also did not profit from hemodilution. Clinical deterioration observed in eight hemodilution group patients (p less than 0.01) led to discontinuation of the study for ethical reasons.

Adjusted hypervolemic hemodilution in acute ischemic stroke.

We prospectively randomized 47 patients with acute ischemic stroke of the middle cerebral artery of less than 24 hours' duration to either adjusted hypervolemic hemodilution or control treatment and followed them up for 90 days. Rapid hemodilution to a target hematocrit of 30-35% as monitored with bedside determinations was achieved by using infusions of dextran 40, venesections, and infusions of additional crystalloid solution when necessary. There was no difference in the death rate between the two treatment groups. Of these 47 patients, 37 (19 in the hemodilution group and 18 in the control group) could be followed up for the entire study period of 3 months. The relative improvement in neurologic function from day 1 to days 8, 21, and 90 was significantly better in the hemodilution group than in the control group. In accordance, special tests for fine motor control of the paretic arm disclosed better performance in the hemodilution group. The frequency of patients with severe disability was significantly lower in the hemodilution group on days 8 and 21. Plasma viscosity (measured in 11 patients) was not affected by infusions of dextran 40. Vigorous hypervolemic hemodilution in patients with acute ischemic stroke is well tolerated and improves early neurologic outcome with an effect lasting at least 3 months.

Comparison of crystalloids and colloids for hemodilution in a model of focal cerebral ischemia

Forty dogs were subjected to 6 hours of occlusion of the left internal carotid and middle cerebral arteries. They were divided into two "hemodilution groups" of 13 dogs each and a control "nonhemodiluted group" of 14 dogs. Thirty minutes after arterial occlusion, isovolemic hemodilution was performed by phlebotomy and infusions of low-molecular weight (MW) dextran in one group and of lactated Ringer's solution in the other group. The animals were sacrificed 1 week after temporary arterial occlusion. Hemodilution reduced the hematocrit to a level of 33% to 34%, which lasted throughout the week in both groups. After hemodilution there was a very significant reduction in blood viscosity, plasma total protein content, and fibrinogen levels in both groups in the acute stage; these levels gradually returned to baseline by the end of the week. In the group with lactated Ringer's solution hemodilution, both osmotic and oncotic pressures were decreased by hemodilution in the acute stage. In the control and low-MW dextran groups, osmotic and oncotic pressure remained unaltered throughout the week. Hemodilution resulted in a slight decrease in mean arterial blood pressure in all groups in the acute stage, but there were no significant changes in central venous, pulmonary arterial, or pulmonary wedge pressures. During the week of study, there were no differences in the cardiac index and total blood volume between the groups, and no significant changes in hematological parameters with the exception of a slight increase in bleeding time immediately after hemodilution with low-MW dextran. Daily neurological assessment showed consistently poorer condition during the first 5 days in the group with lactated Ringer's solution compared to either the control group or the group receiving low-MW dextran. Based on Mann-Whitney U-testing, the infarct volume of the lactated Ringer's solution recipients, expressed as a percentage of the total volume of that hemisphere (median 15.7%, range 6.6% to 25.2%) was significantly larger than that of the group receiving low-MW dextran (median 2.2%, range 0% to 15.8%) and that of the control group (median 11.9%, range 0% to 39.9%). The results indicate that, in this model, hemodilution with colloids was beneficial, whereas hemodilution with crystalloids was deleterious. It is likely that the decrease in oncotic pressure observed after hemodilution with lactated Ringer's solution is one of the most important reasons for its detrimental effect.

Hemodilution and hypertension effects on cerebral hemorrhage in cerebral ischemia in rats.

We determined the effect of hemodilution and hypertension on cerebral hemorrhage and brain injury in 32 rats subjected to 180 minutes of middle cerebral artery occlusion and 120 minutes of reperfusion. We divided the rats into four groups. In the control group (n = 8) neither hematocrit nor blood pressure was manipulated during occlusion, in the hemodilution group (n = 8) 5% albumin was administered to maintain a hematocrit of 30% during occlusion, in the hypertension group (n = 8) mean arterial blood pressure was increased to 30 mm Hg above baseline during occlusion with phenylephrine, and in the hemodilution/hypertension group (n = 8) albumin and phenylephrine were employed simultaneously during occlusion. We assessed the amount of cerebral hemorrhage (as concentration of extravasated hemoglobin) spectrophotometrically and the extent of ischemic injury (as percentage of the hemisphere with deficient staining) histochemically using 2,3,5-triphenyltetrazolium chloride. Mean +/- SD hemoglobin concentration in the hemisphere ipsilateral to the occlusion in the hemodilution/hypertension group (71 +/- 14 micrograms/g brain tissue) was significantly (p less than 0.05) greater than that in the hemodilution and hypertension groups (25 +/- 5 and 29 +/- 7 micrograms/g, respectively), hemoglobin concentrations in these two groups were in turn significantly (p less than 0.05) greater than that in the control group (2 +/- 3 micrograms/g). Mean +/- SD percentage of the ipsilateral hemisphere with deficient staining was significantly (p less than 0.05) less in the hypertension and hemodilution hypertension groups (8 +/- 3% and 11 +/- 6%, respectively) than in the control and hemodilution groups (26 +/- 8% and 26 +/- 7%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Hypertension and hemodilution during cerebral ischemia reduce brain injury and edema

The extent of cerebral injury and edema was determined in isoflurane-anesthetized rats (n = 32) after 180 min of middle cerebral artery occlusion (MCAO) and 120 min of reperfusion. One of the following was employed during the occlusion period only: 1) control, mean arterial pressure [MAP = 131 +/- 7 (SD) mmHg] and hematocrit (43 +/- 2%) were not manipulated; 2) hemodilution, the hematocrit was reduced to 30% with 5% albumin (MAP = 104 +/- 19 mmHg); 3) hemodilution-normotension, hemodilution was established, and MAP was maintained at 131 +/- 9 mmHg with phenylephrine; 4) hemodilution-hypertension, hemodilution was established, and MAP increased to 161 +/- 2 mmHg with phenylephrine. Brain injury was determined with 2,3,5-triphenyltetrazolium chloride, and cerebral edema was assessed by microgravimetry. Brain injury and cerebral edema were less in both phenylephrine groups, compared with the control and hemodilution groups (P less than 0.05). These results are consistent with the premise that if normotension is maintained, hemodilution reduces ischemic brain injury and edema. They also indicate that the addition of phenylephrine-induced hypertension to hemodilution therapy results in a further reduction of ischemic injury without exacerbating cerebral edema.

Isovolemic hemodilution in experimental focal cerebral ischemia. Part 1: Effects on hemodynamics, hemorheology, and intracranial pressure.

A total of 76 splenectomized dogs were entered in a study of the value and effects of isovolemic hemodilution. Of these, seven were not included in the analysis because of technical errors. Of the remaining 69 dogs, 35 were treated with hemodilution; 28 were subjected to a 6-hour period of temporary occlusion of the distal internal carotid artery and the proximal middle cerebral artery, and seven underwent a sham operation only, with arterial manipulation but no occlusion. The other 34 dogs were not subjected to hemodilution; 26 of these underwent temporary arterial occlusion and eight had a sham operation only. In each group the animals were about equally divided into 1) an acute protocol with regional cerebral blood flow measurements by a radioactive microsphere technique and sacrifice at the end of the acute experiment, and 2) a chronic protocol with survival for 1 week to permit daily neurological assessment and final histopathological examination but without blood flow measurements. Isovolemic hemodilution was performed about 1 hour after the arterial occlusion or sham operation and was accomplished by phlebotomy and infusions of low molecular weight dextran to bring the hematocrit to a level of 30% to 32%. This treatment resulted in a very significant reduction in viscosity and fibrinogen levels. The decrease in hematocrit lasted throughout the week in the animals in the chronic protocol. The decrease in viscosity correlated almost linearly with the decrease in hematocrit. There was a slight decrease in systemic arterial pressure with hemodilution but there were no significant changes in central venous pressure or in pulmonary arterial or wedge pressure. There was a slight decrease in cardiac index in both the hemodilution and control groups, which may have been due to the effects of barbiturate anesthesia. There was a slight increase in the measured blood volume in both groups, which was probably artifactual and related to the method of calculation. Intracranial pressure increased significantly with time in all animals subjected to arterial occlusion, but this increase was less severe in the hemodilution group. There was no significant change in intracranial pressure in sham-operated animals, whether hemodiluted or not. The results of cerebral blood flow measurements, assessment of neurological conditions, and measurement of infarct size are given in Part 2 of this report.

Reperfusion injury induced by augumented oxygen uptake in the initial reperfusion period: Possible efficacy of extreme hemodilution

This study was designed to investigate the relationship between myocardial oxygen consumption and oxygen-induced myocardial injury. Dog hearts were exposed to 40 min normothermic ischemia and then reperfused for 10 min with three oxygenated perfusates containing different hemoglobin concentrations and with moderate hemodilution. The experimental groups consist of a moderate hemodilution group (Group M) receiving 8 g/dl of hemoglobin, an extreme hemodilution group (Group E) given 4 g/dl of hemoglobin, and a hemoglobin-free autologous plasma group (Group F). Hearts in the non-ischemic control group (Group C) were also perfused with moderate hemodilution throughout. In Group C, Group M and Group E, the O2 tension of perfusates was maintained at about 100 mmHg and in Group F, at over 300 mmHg. Oxygen extraction at 5 min after reperfusion in Group C was 14%, in Group M and Group E less than 10%, but in Group F 70%. Oxygen consumption in Group F was more than twice that in Group E and surpassed that in Group C. Group M also showed a significant increase in oxygen consumption compared with Group E at 5 min after reperfusion. Among the ischemic groups, Group E showed improvement of left ventricular function almost comparable to Group C accompanied by a rapid decrease in myocardial lactate, improved preservation of myocardial adenine nucleotides and prevention of myocardial lipid peroxidation. In contrast, Group F showed persistently higher values of lipid peroxides and lactate, the poorest recovery of adenine nucleotides, and impairment of left ventricular function.(ABSTRACT TRUNCATED AT 250 WORDS)

Myocardial Oxygen Balance during Hemodilution in Patients Undergoing Coronary Artery Bypass Grafting

The myocardial (arterial-coronary sinus) balance of oxygen and lactate was studied before a cardiopulmonary bypass and during the first 5 min of a normothermic bypass in two patient groups undergoing coronary revascularization for multiple coronary artery disease. The hemodilution (HD) group was hemodiluted before the bypass with dextran 70 (15 ml/kg; resulting mean hematocrit 32%) and further at the beginning of the bypass due to nonhemic priming of the oxygenator (mean hematocrit 15%). The control (C) group was not diluted before the bypass, and four units of red blood cells were included in the oxygenator priming (mean hematocrit 27% after the beginning of the bypass). The preoperative dilution produced a decline in the coronary sinus blood oxygen tension and oxygen saturation, but no change in the arterial-coronary sinus lactate balance. After the first 5 min of the bypass, the heart produced lactate in both the HD group and the C group, but the lactate production was more pronounced in the HD group. At the same time, the coronary sinus blood oxygen saturation was lower in the HD group than in the C group. Hypotension frequently accompanied the beginning of the bypass in both groups. It is concluded that the hemodilution to a hematocrit level of 32% in patients undergoing coronary revascularization for multiple stable coronary artery disease produces compensatory changes in myocardial oxygen extraction, but no changes of a generalized ischemia can be demonstrated. The hemodilution to a hematocrit level of 15% produces myocardial ischemia in patients with a normothermic unloaded heart, adding to the effect of hypotension at the beginning of the bypass.

Moderate and Extreme Hemodilution in Open-Heart Surgery: Fluid Balance and Acid-Base Studies

Two groups of patients underwent aortic valve replacement. Fifteen patients received moderate hemodilution (mean hematocrit, 27%) with 40% donor blood in the priming solution. Extreme hemodilution was used in 14 patients (mean hematocrit, 18%) with a nonhemic prime and withdrawal of blood at the start of operation. Both groups were given more than 7 liters of fluid during operation; donor blood was primarily used in the moderately diluted patients, and Ringer's acetate was primarily given to the other group. The diuretic response to this fluid load was much more pronounced in the extreme than in the moderate hemodilution group. Eighteen hours postoperatively, patients in the moderate and extreme hemodilution groups had an excess of about 2 and 1.5 liters of water, respectively. In the patients who had moderate dilution an average of 1,000 ml of erythrocytes disappeared from circulation; no such disappearance could be found in the other group. The moderate group showed significantly lower arterial Po 2 postoperatively than the extreme group. There were, however, no differences between the two groups in mixed venous Po 2 during perfusion or in acid-base and osmolality values.

Oxygen transport of colloidal fluorocarbon suspensions in asanguineous rabbits.

In anesthetized, oxygen-breathing rabbits, the entire blood volume was exchanged with a 20% colloidal fluorocarbon fluid suspension of high gas solubility. In contrast to the control animals with acute isovolemic and hypervolemic hemodilution, the fluorocarbon suspension prevented the decrease in arterial oxygen content below a hematocrit of 13%. However, the more pronounced effect of the fluorocarbon suspension on oxygen delivery occurred at higher hematocrits and was due to its efficiency as a plasma expander, since it increased the cardiac output even above the level of the hypervolemic hemodilution group. The fluorocarbon suspension also raised arterial blood pressure and total peripheral resistance due to its increased viscosity. Thus, in mild hemodilution, the fluorocarbon suspension kept oxygen utilization in the normal range by increasing cardiac output, and in extreme hemodilution it improved oxygen utilization by also raising the arterial oxygen content and arterial blood pressure. The survival time of the isovolemic control animals was 31.6 min, it was extended to 57.8 min in the hypervolemic control animals, and the rabbits with the fluorocarbon suspension lived for 124.8 min.