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Ann Thorac Surg 1998;65:993-998
© 1998 The Society of Thoracic Surgeons

Alterations in Renal Microcirculation During Cardiopulmonary Bypass

Vivek L. Pathi, FRCSaa, John Morrisonaa, Alan MacPhaden, MRCPathbb, William Martin, PhDcc, Ann-Marie McQuiston, BSccc, David J. Wheatley, MDaa

a Department of Cardiac Surgery, Royal Infirmary, Glasgow, Scotland, United Kingdom
b Department of Pathology, Royal Infirmary, Glasgow, Scotland, United Kingdom
c Department of Nuclear Medicine, Royal Infirmary, Glasgow, Scotland, United Kingdom

Accepted for publication October 21, 1997.

Address reprint requests to Dr Wheatley, Dept of Cardiac Surgery, Royal Infirmary, 10 Alexandra Parade, Glasgow G31 2ER, Scotland


   Abstract
Top
 Abstract
Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Background. This study was designed to investigate renal microvascular changes during cardiopulmonary bypass.

Methods. Kidneys were harvested from each of four groups of 6 pigs. Group A were anesthetized and heparinized only. The remaining three groups underwent cardiopulmonary bypass at 28°C, group B for 30 minutes and groups C and D for 120 minutes; group D had an additional 30 minutes of normothermic perfusion at the end of the experiment. Renal cortical blood flow was measured using radiolabeled microspheres. Microvascular morphology was defined by corrosion casting and scanning electron microscopy.

Results. In group A, renal vascular resistance was 61 ± 5.1 mm Hg · mL-1 · min-1. This value decreased to 28 ± 7.8 in group B and 25 ± 4.0 in group C (p < 0.05), and increased in group D to 40 ± 4.1 (p < 0.05 versus groups A, B, and C). Cortical thickness, as measured by microvascular casts in groups A, B, and C, was 33, 34, and 31 mm, respectively, with equal distribution of the resin to the superficial and deep cortex but was significantly reduced in group D to 22 mm (p < 0.05 versus groups A, B, and C), with failure of the resin to fill the superficial cortical layer. Diameters of glomeruli as seen on the casts were 111 ± 10.38 µm in group A, 100 ± 9.24 µm in group B, and 82 ± 4.4 µm in group C (p < 0.05 group A versus group C). The glomeruli from group D were still significantly smaller than group A (93 ± 10.35 µm, p < 0.05). Mean glomerular capillary diameters were 4.65 ± 0.26 µm in group A, 3.9 ± 0.16 µm in group B, 3.6 ± 0.19 µm in group C, and 3.65 ± 0.3 µm in group D (p < 0.05 group A versus groups B, C, and D).

Conclusions. Hypothermic nonpulsatile cardiopulmonary bypass decreased renal vascular resistance, but the superficial and deep layers of the cortex were perfused equally. Glomeruli were reduced in size because of capillary narrowing. This was consistent with diversion of blood through bypass channels. With restoration of normothermia, underperfusion of the superficial cortex occurred, with potential for damage to these nephrons during the increased metabolic demands of rewarming.


   Introduction
Top
 Abstract
 Introduction
Material and methods
 Results
 Comment
 Acknowledgments
 References
 
Multiorgan dysfunction after cardiopulmonary bypass (CPB) is well recognized [1, 2]. Reduced creatinine clearance is seen in up to 11% of patients undergoing cardiac operations, whereas overt renal failure requiring dialysis occurs in 3.7% and is associated with a mortality of 45% [3]. With detailed biochemical study the more subtle forms of fully reversible renal injury become apparent and may even be an inevitable consequence of extracorporeal circulation [4].

The anatomic site of this injury has so far evaded detection [5, 6]. The use of pulsatile, as opposed to nonpulsatile, perfusion may improve distribution of intrarenal blood flow, with preferential perfusion of parts of the cortex, suggesting that changes in the microcirculation may be of importance in this pathology [7]. The superiority of increased pump flow rate as opposed to vasoconstriction as a means of increasing renal perfusion has been demonstrated recently in pigs [8]. In this study, vasoconstriction despite producing increased systemic arterial pressure did not increase renal perfusion.

The effects of CPB on the blood vessels of the kidney were studied in a porcine model using CPB, hypothermia, and rewarming. Blood flow within the different layers of the renal cortex was measured using radioactive microspheres. Microvascular corrosion casting was used to delineate the exact distribution of intrarenal blood flow. Scanning electron microscopy of the resin casts was used to elucidate changes at the glomerular level. This technique has been used extensively in the past to reproduce the state of the renal microvasculature in many species [9, 10].


   Material and methods
Top
 Abstract
 Introduction
 Material and methods
Results
 Comment
 Acknowledgments
 References
 
Landrace pigs weighing 24 to 28 kg were anesthetized with isoflurane 1% to 3% and mechanically ventilated with an Oxford-Penlon (Abingdon, England) volume cycled ventilator, maintaining arterial oxygen tension at 15 to 20 kPa and carbon dioxide tension at 4 to 5 kPa. NaHCO3 was added to keep arterial pH at 7.4 to 7.5. Four groups of kidneys were removed during the operations [11]: group A, after anesthesia and heparin administration only; group B, after 30 minutes of CPB at 28°C; group C, after 120 minutes of hypothermic CPB, the final 90 minutes involving cross-clamping the ascending aorta and inducing cold crystalloid cardioplegic arrest; and group D, animals underwent 120 minutes of CPB at 28°C with aortic clamping and cardioplegia identical to group C, but were then rewarmed at 36°C for 30 minutes.

The CPB was set up between bicaval cannulas for venous drainage (Gambro 36/51 whistle tip) and an aortic cannula for arterial return (Bardic 16F catheter). The electrocardiogram and arterial and venous pressures were continuously monitored with a Sirecust 404 monitor and polygraph. The bypass circuit comprised a Safe II membrane oxygenator (Polystan, Wilford, England) and a Stockert-Shiley roller pump (Stockert-Shiley, Midhurst, England). One liter of crystalloid prime was used and flows were maintained at 80 mL · kg-1 · min-1 at 28°C. In groups C and D, the aorta and pulmonary artery were cross-clamped and 10 mL/kg body weight cold St. Thomas’ crystalloid cardioplegia was instilled into the aortic root every 30 minutes. In group D, the animals were rewarmed for the final 30 minutes to 36°C. At the end of the experiment, the animals were killed by 10-mg bolus doses of morphine and midazolam followed by exsanguination into the venous reservoir. This study was approved by the University of Glasgow ethical committee. All animals received humane care in compliance with the European convention on animal care and in accordance with the guidelines of "The Animals (Scientific Procedures) Act" 1986.

Measurement of tissue blood flow
Tissue perfusion was measured using 15-µm microspheres, radiolabeled with cobalt or chromium. The 1.0 to 1.5 x 106 microspheres were agitated on a roller to ensure complete mixing and then injected rapidly. Blood was withdrawn from the femoral arterial line using a controlled rate aspiration pump set at 7.5 mL/min commencing 30 seconds before and continuing for 1 minute after the injection. The sample was divided into counting vials and radionuclide activity assessed.

Regional blood flow per 100 grams of tissue (RBF) was calculated according to the formula: , where Ct is the activity per gram of tissue sample, WR is the rate of pump withdrawal (7.5 mL/min), and Cr is the activity in the reference blood sample. Renal vascular resistance (RVR), expressed as mm Hg · mL-1 · min per 100 g, was calculated as: .

Corrosion casting and scanning electron microscopy
After excision of the kidneys, the superior polar renal artery was catheterized with a 5F cannula and flushed with heparinized saline until free of blood. Batson’s No. 17 methylmethacrylate monomer solution (1:1.25, Batson’s monomer to methylmethacrylate; Park Scientific, Northampton, England) was injected at controlled pressure of 50 to 70 mm Hg (measured on the inlet side) until it was seen to be flowing freely from the renal veins. The preparation was left at room temperature for 2 hours to allow polymerization before being bisected coronally to visualize the intrarenal anatomy. The blocks were immersed in alternate baths of 20% potassium hydroxide and water every 48 hours, until completely macerated of all organic material. Any residual fat adherent to the resin skeleton was dissolved by detergent solution.

The vascular casts were mounted on aluminium blocks with silver paste, coated in a gold/palladium Polaron SE 5000 sputter-coater (Electron Microscopy Services, London, England) and viewed under a scanning electron microscope (Jeol UK Ltd, Welwyn Garden, England). The working distance was standardized at 48 mm and the accelerating voltage at 5 keV. An overview was obtained of the distribution of renal blood flow by scanning at x10 magnification, and measuring the cortical width from the arcuate artery to the edge of the cortical vasculature. Specimens were also viewed at a neutral angle and at 15 degrees clockwise and counterclockwise under a magnification of x400 to x700 in a random blinded manner. Afferent arterioles were followed to their glomeruli and subsequent transformation into the efferent arterioles and peritubular capillary plexus. Bypass channels were defined as large diameter vessels directly linking afferent arteriole and efferent arteriole or capillary plexus, without forming a glomerulus. Glomeruli were scanned onto an image analysis system and the following parameters measured using a digitizing pad (Fig 1): polar diameter, distance parallel to the vascular pole; transverse diameter, the distance perpendicular to PD; afferent arteriole, the diameter 10 µm proximal to the vascular pole; and glomerular capillaries, average diameter of 10 vessels per glomerulus.



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  		Fig 1. Glomerulus from group A. Well-filled capillaries with clear definition of glomerular anatomy. (AA = afferent arteriole; EA = efferent arteriole; GC = glomerular capillaries; PD = polar diameter.)

 
Statistical analysis
All measures are expressed as mean ± standard deviation. For glomerular diameters and cortical widths, the mean of all the measurements from each animal were used to produce summary statistics. Analysis of variance with Bonferroni correction was used to compare the four groups and statistical significance taken at a p value less than 0.05. Partial correlation analysis was used to ascertain the influences of several related factors such as temperature, time on cardiopulmonary bypass, hemoglobin concentration, potassium and hydrogen ion levels on renal vascular resistance, and cortical thickness. This allowed certain confounding factors to be controlled to uncover relationships between other variables. In the first-order analysis the group was used as the controlling factor.


   Results
Top
 Abstract
 Introduction
 Material and methods
 Results
Comment
 Acknowledgments
 References
 
Hemodynamics and renal vascular resistance
Results from six animals were analyzed for each group. The absolute values for temperatures, hemoglobin, bypass times, renal blood flow, and perfusion pressures are shown in Table 1. The blood pressure and hemoglobin level were significantly higher for the non-bypass group A when compared with the three bypass groups (p < 0.01).


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  		Table 1. Hemodynamic and Biochemical Parameters in the Four Groups of Pigs

 
The renal vascular resistances (RVR) for the four groups are shown in Figure 2. In group A, the mean RVR was 61 ± 5.1 mm Hg · mL-1 · min-1. In groups B and C the RVR was much lower at 28 ± 7.8 and 25 ± 4.0 mm Hg · mL-1 · min-1, respectively (p < 0.05, group A versus groups B and C). In group D animals, RVR was 40 ± 4.1 mm Hg · mL-1 · min-1, which was significantly different from groups A, B, and C. Partial correlation coefficients controlling for group revealed significant relationships with temperature (r = 0.838, p < 0.0001) and hemoglobin levels (r = 0.890, p < 0.0001). No significant relationships were found with hydrogen ion, potassium ion, and CPB time.



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  		Fig 2. Renal vascular resistance values for the four groups.

 
Corrosion casting
Cortical thickness, as measured on the microvascular corrosion casts of groups A, B, and C were 33, 34, and 31 mm, respectively (p = not significant). Equal perfusion of superficial and deep cortex was seen in these three groups. In group D the cortical thickness values were significantly lower, at 22 mm (p < 0.05 group D versus groups A, B, and C). There was reduced filling of the superficial layer of the cortex when compared with the other three groups, although the juxtamedullary layer was normally filled(Figs 3 and 4). When controlled for group, cortical thickness was significantly related to RVR (r = -0.577, p = 0.004) and hemoglobin levels (r = -0.515, p = 0.012). When controlled for group and bypass time, temperature became an additional significant correlate (r = -0.612, p = 0.003), although when controlling for group and temperature, bypass time did not achieve any significance.



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  		Fig 3. Corrosion cast of kidney in group A, revealing even filling of the entire renal cortex, with clear definition of the corticomedullary junction. (C = cortex; M = medulla.)

 


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  		Fig 4. Corrosion cast of kidney from group D revealing a lack of filling of the superficial cortex.

 
Scanning electron microscopy
Results of glomerular measurements by scanning electron microscopy are shown in Table 2. Polar diameters of glomeruli were 111 ± 10.38 µm in group A, 100 ± 9.24 µm in group B, and 82 ± 4.4 µm in group C (p < 0.05 groups A and B versus group C). Diameters for group D were 93 ± 10.35 µm, which were still significantly lower than for group A (p < 0.05 group A versus group D). Despite a trend toward lower transverse diameters of glomeruli in group C compared with the other three groups, this did not reach statistical significance. Mean glomerular capillary diameters were 4.65 ± 0.26 µm in group A, which was significantly higher than values for group B (3.9 ± 0.16 µm), group C (3.6 ± 0.19 µm), and group D (3.65 ± 0.3 µm). Despite a trend for lower afferent arteriolar diameters in group C versus groups A, B, and D, this did not reach statistical significance.


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  		Table 2. Glomerular Vascular Measurements Obtained by Scanning Electron Microscopy of Corrosion Casts

 
Glomerular morphology
Glomeruli from group A kidneys were well formed, with clear definition of the afferent and efferent arterioles and intervening glomerular capillaries (see Fig 1). In group B the anatomic structure of the nephron remained intact, although there was some narrowing of the capillaries with increase of intercapillary spaces (Fig 5). Major changes in morphology of the glomeruli were seen in group C kidneys, with many glomeruli being represented by simple capillary loops (Fig 6). There were large areas where glomeruli were not easily discernible. After rewarming in group D, there was a return of glomerular anatomy in the juxtamedullary region similar to groups A and B, although the glomerular capillaries were severely narrowed (Fig 7). There was little filling of the superficial cortex of these kidneys by injected resin.



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  		Fig 5. Glomerulus from group B. Smaller glomerulus with narrowed capillaries suggesting diversion of flow through alternative channels.

 


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  		Fig 6. Glomerulus from group C. Severe reduction in size of glomerulus with complete loss of functional unit. These act as shunts between afferent and efferent arteriolar systems.

 


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  		Fig 7. Glomerulus from group D. Some recovery of anatomy of the functional unit, although shunting of blood past the nephrons is still evident. Narrowing of the capillaries and increase in intercapillary spaces suggest interstitial edema.

 

   Comment
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
Acknowledgments
 References
 
Clinical studies have demonstrated the deleterious effects of extracorporeal circulation on renal function, but the majority of patients undergoing open heart operations suffer no obvious deficit [12–14]. Despite extensive biochemical investigation, there is little information on the morphology of the microvasculature during hypothermic CPB [7, 15]. The aim of this study was the definition of blood flow patterns in the renal cortex after hypothermic CPB and subsequent rewarming to normothermia during a simulated cardiac operation.

The finding of reduced renal vascular resistance during nonpulsatile perfusion at 28°C may have two explanations. First, there may be uncontrolled dilatation of afferent and efferent arterioles as compensation for the nonpulsatile low pressure arterial waveform and hypothermia. Andersson and colleagues [5] demonstrated renal blood flow (measured by thermodilution) to be correlated more strongly with pump flow rates than with systemic arterial pressure. This suggests that control of the renal circulation during CPB may be at the level of the bypass pump, rather than at a vascular level. Although the systemic arterial pressures maintained in our study were low, the addition of vasoconstrictors to elevate these may not have altered perfusion patterns as recently demonstrated by O’Dwyer and colleagues [8].

Second, a state of fixed vasodilatation can be hypothesized in the afferent and efferent arterioles resulting in unimpeded flow through all cortical glomeruli, with filtration pressures across the glomerular capillary membrane directly dependent on systemic perfusion pressure. This has been shown previously to be the case by Urzua [13] and Badner [16] and their colleagues. They reported a direct relationship of both urine output and glomerular filtration rate with systemic perfusion pressure. This may also explain the failure of urine output during CPB to predict postoperative renal function [12]. One can speculate on the presence of a "functional" circulation maintaining glomerular filtration and urine output, and a "nutritional" circulation maintaining tissue perfusion and viability. Although the two may normally be identical, they may become separate entities during the abnormal hemodynamics of hypothermic CPB. With rewarming in group D, despite nonpulsatile perfusion, the renal vascular resistance increased again and may be a reflection of the reduction in renal vascular bed available at this stage, as the cortical cast thickness in these kidneys was reduced. This was primarily attributable to decreased blood flow through the superficial cortical nephrons, although blood flow through the juxtamedullary nephrons was preserved. The increase in mean size of the glomeruli seen in group D kidneys may be attributable to increased interstitial edema, which may play a part in increasing vascular resistance. Although this has not been demonstrated directly, the finding of unchanged mean capillary size in the casts of group D glomeruli would indicate an increase in the extravascular space as the major contributor to the larger glomeruli. It can only be speculated that this is attributable to rewarming and not the extra period of bypass as a warm bypass group was not included in the study.

The strong correlation of renal vascular resistance with hemoglobin levels would be expected to occur due to the well recognized effect of hemodilution on blood viscosity and tissue perfusion [17]. Although the degree of hemodilution achieved during this study was excessive, the confounding effects of blood transfusion were avoided. Our results would also indicate a major role for hypothermia, although the hemoglobin levels remained low in group D, the RVR was higher than in groups B and C. It may be that some degree of vascular smooth muscle action may be regained after return to normothermia, allowing the renal vascular resistance to increase despite the low systemic pressures and reach the level seen in group D animals. There may be some heterogeneity in this effect among different nephrons, some displaying preglomerular vasoconstriction and others remaining dilated [18, 19]. The potential for ischemic damage to some poorly perfused nephrons during this stage of increased metabolic demand is clearly apparent. This may be the crucial time when manipulations aimed at improving renal cortical perfusion, such as dopamine and mannitol, could be instituted. Further studies using a warm bypass group may clarify whether it is the hypothermia or the length of bypass that sets the stage for the poor perfusion of the superficial cortex during subsequent rewarming.

An alternative explanation for the low RVR during CPB may be that thoroughfare vascular channels exist within the kidneys allowing blood to bypass the high resistance glomeruli partially or completely. The afferent arterioles of hibernating animals whose renal blood flow can be reduced dramatically during winter sleep are known to be controlled by sphincters in the preglomerular vessels [20]. This may be analogous to the conditions found during hypothermic CPB. The maintenance of the distribution of perfusion to the entire thickness of the cortex seen in the corrosion casts of the hypothermic bypass groups B and C, compared with group A, would favor flow through these "aglomerular" bypass channels as a possible explanation for the reduced renal vascular resistance.

The existence of four anatomically distinct aglomerular pathways was first suggested by Cassellas and colleagues in 1979 and may act as bypass pathways through the mesangium after blockage of the glomerular capillaries [21–23]. These channels may exist in all kidneys as a potential source of nutritional perfusion during periods of altered hemodynamics or embolic occlusion that may occur during CPB. This divergence in nutritional and functional perfusion may explain the failure of high systemic arterial pressure during CPB to improve subsequent renal function [12]. It may be that increasing arterial blood pressure increases flow through the glomeruli, thus increasing filtration rates. Low pressures may continue to allow flow through the nutritional circulation, while increasing efferent arteriolar tone to maintain filtration.

The changes in the sizes of the glomeruli would again support the hypothesis of blood flow diversion through bypass pathways during hypothermic CPB. If all blood flow were to pass through the glomeruli, then the decrease in RVR would be expected to increase the sizes of the glomerular capillaries to accommodate the increased flow. If the glomerular capillaries were bypassed, however, their volume would not be increased.

Renal dysfunction after CPB is a common occurrence. The reversibility of this dysfunction would favor a vascular change as an explanation. Although renal vascular resistance decreases during hypothermic CPB, the increased flow may pass through channels other than through the glomeruli. This could be analogous to hibernating animals where, although renal perfusion and viability are maintained, little or no urine is produced during winter sleep. With return of normothermia (and pulsatile perfusion), these changes may gradually reverse, thereby allowing return of normal renal function. During the critical phase of rewarming, however, nephrons with incomplete return of perfusion, particularly in the superficial cortex, may be at risk of ischemic damage. Under conditions of prolonged hypoxia or hypotension associated with low cardiac output, however, this damage may be compounded and lead to clinically apparent and permanent dysfunction.


   Acknowledgments
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
References
 
This work was supported by a grant from the British Heart Foundation.


   References
Top
 Abstract
 Introduction
 Material and methods
 Results
 Comment
 Acknowledgments
 References
 

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  8. O’Dwyer C., Woodson L.C., Conroy B.P., et al. Regional perfusion abnormalities with phenylephrine during normothermic bypass. Ann Thorac Surg 1997;63:728-735.[Abstract/Free Full Text]
  9. Gattone V.H., Sale R.D. Quantitative vascular casting of the post-ischemic hydronephrotic kidney. Scan Electron Microscopy 1986;2:549-556.
  10. Gomez-Campdera F.J., Maroto-Alvaro E., Galinanes M., Garcia E., Duarte J., Rengel-Aranda M. Acute renal failure associated with cardiac surgery. Child Nephrol Urol 1988;9:138-143.[Medline]
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  12. Fukae K., Tominaga R., Tokunaga S., Kawachi Y., Imaizumi T., Yasui H. The effects of pulsatile and nonpulsatile systemic perfusion on renal sympathetic nerve activity in anesthetized dogs. J Thorac Cardiovasc Surg 1996;111:478-484.[Abstract/Free Full Text]
  13. Urzua J., Troncoso S., Bugedo G., et al. Renal function and cardiopulmonary bypass: effect of perfusion pressure. J Cardiothorac Vasc Anesthesia 1992;6:299-303.[Medline]
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  16. Badner NH, Murkin JM, Lok P. Differences in pH management and pulsatile/nonpulsatile perfusion during cardiopulmonary bypass do not influence renal function. Anesth Analg 1992:696–701.
  17. Tobias M.A., Fryer J.M. Which priming fluids?. In: Longmore D.B., ed. Towards safer cardiac surgery. Lancaster: MTP Press, 1980:401-426.
  18. Kelleher S.P., Robinette J.B., Conger J.D. Sympathetic nervous system in the loss of autoregulation in acute renal failure. Am J Physiol 1984;246:F379-F386.
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