Blood flow distribution in dogs during hypothermia and posthypothermia T. ANZAI, Department

M. D. TURNER, W. H. GIBSON, of Surgery, University of Mississippi

AND W. A. NEELY Medical Center, Jackson,

Mississippi

39216

ANZAI, T., M. D. TURNER, W. H. GIBSON, AND W. A.

anesthetized with thiamylal sodium by intravenous administration. After anesthesia, catheters were positioned via both femoral arteries in the distal abdominal aorta to monitor blood pressure and to withdraw blood samples. The dogs were mechanically ventilated throughout the experiment. Thereafter, thiamylal sodium was given intravenously as required. Lactated Ringer solution was given intravenously throughout the experiment. The total volume for each dog was 30 ml/kg. The left chest was opened, an electromagnetic flow probe was mounted around the ascending aorta, and a catheter was placed in the left atrium for the injection of radioactive microspheres; the chest was then closed. The systemic arterial pressure, the electrocardiogram, and the cardiac output were recorded throughout the experiment. Stroke volume and total peripheral resistance were calculated. The arterial blood samples were obtained at regular intervals during the experiment for the determination of pH, Po2, Pcoz, and hematocrit. When mean arterial pressure and cardiac output attained a steady state, the control blood microspheres flow distribution was measured by the injection of 85Srlabeled microspheres into the left atrium at 37.4 t l.OOC. Surface cooling by ice water immersion resulted DEEP HYPOTHERMIA induced by surface cooling or sur- in a fall in rectal temperature of l”C/4 min. The rectal face cooling with limited cardiopulmonary bypass is a probe was inserted to about 15 cm. At 3O”C, heparin (1 mg/kg) was given intravenously, and at 24OC the ice useful adjunct to open heart surgery for the correction of congenital defects in infants and small children (3, water was removed. The body temperature declined spontaneously until it reached about 21°C. After the 23). Many hemodynamic changes during surface-induced hypothermia and after rewarming are well estab- body temperature had remained at 20.8 t l.O°C for 30 lished (5, 20, 21, 25, 31), but little is known of blood flow min, blood flow distribution was determined by the injection of 141Ce-labeledmicrospheres. Rewarming was distribution during hypothermia and posthypothermia started by immersing the dog in warm water. When the (20, 31). Rudolph and Heymann (26) developed a method for rectal temperature reached 36°C (about 1.5 h) warming quantitating the distribution of the cardiac output to was stopped. Two hours after rewarming blood flow distribution was measured by the injection of 51Cr-ladifferent organs by the injection of radioactive microspheres. This method is useful in the determination of beled microspheres. After the experiments, samples were obtained from blood flow distribution to organs in normal and abnorthe brain, heart, lung,@liver, stomach, duodenum, jemal conditions (27). The purpose of this study was to determine the junum, colon, pancreas, kidneys, adrenal glands, and changes in blood flow distributions to various organs striated muscles. The samples were then weighed. The resulting from surface-induced deep hypothermia and tissue sample weights ranged from 1 to 3 g. Samples of from posthypothermia in dogs. The findings are to be the myocardium were obtained from the free walls of the inflow and outflow tracts of the right ventricle, from employed as base-line data for the study of vasoactive the free wall of the anterior descending area, and from drugs that may improve circulation during hypotherthe circumflex area of the left ventricle. The left ventrimia. cle samples were divided into the subepicardial and subendocardial layers by dissecting the muscle through MATERIALS AND METHODS the midpoint. Seventeen adult mongrel dogs weighing 8-15 kg were Preparation and injection of microspheres. The miBlood flow distribution in dogs during hypothermia and posthypothermia. Am. J. Physiol. 234(6): H706-H710, 1978 or Am. J. Physiol.: Heart Circ. Physiol. 3(6): H706-H710, 1978. -Blood flow distribution in tissues of mongrel dogs during hypothermia was studied with radionuclide-tagged microspheres. The animals were cooled at 21°C and rewarmed under thiamylal sodium anesthesia. During hypothermia, cardiac output fell to 20% of the control; the highest rate of blood flow relative to normothermic values was observed in the subendocardium of the left ventricle, and the lowest in the hypophysis. Each tissue showed specific reactions to hypothermia. During hypothermia the myocardial and brain-stem blood flows were about 40% of the control; almost all of the digestive tract, striated muscle, adrenal gland, and hypophysis blood flows were maintained at 20% or less of the control. After rewarming, cardiac output recovered to values significantly lower than control. The myocardium, brain, renal cortex, and striated and smooth muscle recovered to control levels; however, blood flow to the digestive organs, bronchial artery flow to the lung, and flow to the endocrine organs did not completely recover by 2 h after rewarming. NEELY.

H706

0363.6135/78/O(rOO-OOOO$Ol.25 Copyright

0

1978 the American

Physiological

Society

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BLOOD

FLOW

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HYPOTHERMIA

crospheres (3M Co.) were 15 t 3 pm in diameter, and labeled with “*Sr (10 mCi/g), 141Ce(10 mCi/g), or >lCr (35 mCi/g). The microspheres, ultrasonicated before injection, were suspended in 10% dextran solution containing one drop of Tween-20 to prevent particle aggregation. The volume of each injection was about 1 ml, approximately 400,000 microspheres contained in a hollow glass mixing sphere. The microspheres were washed rapidly from the sphere into the atrium with 10 ml of saline. The injection was usually about 8 s. The reference blood samples were withdrawn into a heparinized syringe from the arterial catheter at a rate of 12 ml for 90 s in the three conditions; the withdrawal was started 8 s before the microsphere injection into the left atrium. After completion of the experiment, the radioactivity of the tissue samples and reference blood samples was analyzed by gamma ray spectrometry. Each sample was counted at gamma energy peaks specific for each of the three radionuclides: 514 keV for *“ST, 320 keV for ;‘lCr, and 145 keV for 14Ce. We compared three withdrawal speeds for a 12-ml sample: 90, 120, and 180 s in control and hypothermic periods. There was no significant difference in the three rates; thus we used 12 ml/90 s as the withdrawal rate. The blood flow of the tissues was determined from the equation: tissue blood flow/activity of tissue = reference sample flow/activity of reference sample, according to the method of Rudolph and Heymann (26). These values were calculated with the aid of a digital computer. All data were analyzed for their significance by Student’s t test. Results are presented as means t SD. RESULTS

Cardiac output fell to 20% of the control during hypothermia. The blood flow declined during hypothermia in all of the tissues studied. The flow did not decrease to the same degree in the various tissues. Blood flow to the subendocardial layer of the left ventricle decreased to a mean of 43.6% of control, whereas the flow to the hypophysis fell to 8.6%. In Fig. 1 the mean control blood flows are set at 100% and the mean hypothermic and posthypothermic blood flows are shown as a percentage of control. Brain blood flow in hypothermia declined to almost 25% of control with the exception of the brain stem in which flow was maintained at almost 38% of control, significantly higher than cerebellar and anterior and posterior cortical flows. Posthypothermic brain blood flow levels returned to near initial control values. Myocardial blood flow during hypothermia was maintained at about 40% of control and returned to almost 100% by 2 h posthypothermia. Flow to the full thickness layer of the stomach antrum, jejunum, and colon fell to almost 20% of control, whereas flow to the duodenum remained significantly higher, at about 28%. The gastric antrum exhibited slower posthypothermic recovery, with a flow of 78% of control at 2 h. Hepatic artery and bronchial artery flows both declined to about 25% of control in hypothermia and were slow to recover, with blood flows of 63% and 67% of control, respectively, 2 h after hypothermia. Renal cortical flow, depressed to 26% of control,

0

25

50

75

100

125%

CEREBELLUM BRAINSTEM

BRAIN

ANT. LOBE THALAMUS RV OUTFLOW

MYOCARDIUM

LVAO

SUBEPI.

LVAO SUBENOO. STOMACH

DIGESTIVE ORGAN

ANTRUM DUODENUM JEJUNUM

HEPATIC

LUNG

BRONCHIAL

ART. CORTEX

KIDNEY ENDOCRINE GLAND

ART

MEDULLA ADRENAL HYPOPHYSIS STRIATED

MUSCLE

SMOOTH I

0

I

Control

I::"'

Hypothermia

1

25 m

I

I

50

75

I

100

I

125%

Post-Hypothermia

FIG. 1. Changes in blood flow distribution in major organs and tissue during hypothermia and posthypothermia. Mean control blood flows are set at lOO%, and mean hypothermic and posthypothermic blood flows are shown as a percentage of control.

recovered to control levels in the hypothermic period. The adrenal gland and the hypophysis blood flows were severely depressed during hypothermia. The flows to these endocrine organs remained significantly lower than control 2 h after rewarming. Blood flow to skeletal muscle was also strikingly low during hypothermia, about 10% of control. Table 1 gives the actual mean blood flow data obtained in the tissues studied during the three conditions. The hypothermic and posthypothermic blood flows significantly different from the normothermic control period are indicated by superscript symbols. Student’s t test was used to determine significance, and a probability value of 0.05 or less was considered to be significant. Table 2 gives the blood flow ratios in layers of the myocardium and the kidney. The subendocardiall subepicardial ratio in both the anterior descending and the circumflex areas of the left ventricle remained normal during hypothermia and posthypothermia. Blood flow in the renal medulla during hypothermia exhibited a somewhat greater decrease in flow than the renal cortex. The flow ratio between the two areas returned toward normal on rewarming but medullary perfusion remained depressed. Blood gas analysis and hematocrit. During the control period, blood gases exhibited a pH of 7.4 t 0.07, a PO, of 359 t 132, and a PcoB of 27.5 t 4.5. Arterial PO,

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ANZAI,

H708

was high because the animals were respired with high oxygen concentration during the experiment. The mean hematocrit was 38.8 t 5.3%. In the hypothermic period, the mean values for the arterial blood gases were pH, 7.32 t 0.15; PoZ, 422 t 134; and PcoZ 34.1 t 7.7. These measurements were made at a blood temperature of 37OC. The hematocrit rose to 45.8 t 8.6%. The mean values for blood gases in the posthypothermic period were pH, 7.29 t 0.10; PO,, 351 t 113; and PcoZ, 39.7 t 6.6. The mean hematocrit fell to 39.6 t 7.6%. Hemodynamics. Changes in hemodynamics are summarized in Table 3. The cardiac output decreased to 19.8 TABLE 1. Tissue blood flow during hypothermia and posthypothermia Control

Brain Cerebellum Brain stem Ant lobe Post lobe Thalamus Hypothalamus Myocardium RV inflow RV outflow LV AD subepi LV AD subendo LV circ subepi LV circ subendo Stomach Corp full thickness Corp mucosal layer Corp muscular layer Antr full thickness Antr mucosal layer Antr muscular layer

Hypothermia

31.3 20.1 40.9 41.4 28.0 14.5

Ik It ir: z!I 2 2

8.9 5.8 11.0 11.9 7.8 3.3

87.3 85.8 81.3 87.7 93.0 101.2

+ + -+ + + +

24.1 24.1 21.2 28.5 27.5 28.3

7.4 7.7 9.4 7.3 7.5 4.3

-t f + + + Ir

3.0* 1.7* 3.6* 2.6* 1.6* 0.7*

31.8 2 12.2* 35.0 + 10.6* 34.4 + 8.2* 41.0 iI 11.0* 37.4 + 15.1* 37.9 z!I 9.5*

Posthypothermia

36.8 24.1 39.1 42.2 31.7 13.8

78.1 86.4 79.8 87.4 97.7 103.7

k 10.3 + 8.7 + 13.1 rfr 12.8 AZ 9.1 + 5.3

iz e + + 2 +

25.4 31.4 24.8 32.4 38.9 31.6

28.2 + 13.2

5.2 + 2.9”

23.6 + 14.0

45.7 + 16.1

8.5 It 3.0*

34.3 + 12.2

6.6 iI 3.4

1.3 iz 0.9*

7.5 + 2.8

41.3 + 25.1

7.6 + 1.8*

34.1 t 16.9

65.3 IL 40.7

10.5 It 5.0*

52.0 + 24.7

7.6 2 3.4

1.6 + 1.2*

7.9 * 4.1

Intestinal tract Duodenum Jejunum Colon

77.9 + 20.5 74.5 2 22.1 61.7 IL 29.3

21.7 + 12.3* 11.8 + 6.5* 14.1 Ik 4.9*

73.2 t 23.2 65.9 t 26.8 50.4 + 22.6

Hepatic artery Pancreas Bronchial artery

43.6 + 19.9 28.5 t 10.0 60.7 + 35.2

10.2 rt 6.5” 6.6 + 2.6” 14.7 k 5.6*

27.8 AI 16.67 25.8 + 13.9 38.6 + 29.6-f

Kidney Cortex Medulla

451.9 Ik 99.7 7.2 t 6.1

127.6 + 40.7* 1.4 2 1.7”

446.8 ix 129.4 5.2 + 4.9

Endocrine Adrenal Hypophysis

398.3 219.0

45.9 2 34.7* 14.8 + 9.6*

289.6 t 91.3* 67.8 + 20.2*

0.9 2 0.7*

12.2 * 4.7

Striated

muscle

5 183.5 2 134.2

10.1 Ifr 0.3

Values are means ~fr SD (n = 17; hypophysis, n = 5). Blood flow was measured in ml/min 100 g. AD, area supplied by anterior descending branches of the left coronary artery; circ, area supplied * P < 0.01 by circumflex branches of the left coronary artery. compared to control value (paired t test). t P < 0.05 compared to control value (paired t test).

TURNER,

GIBSON,

AND

NEELY

TABLE 2. Blood flow ratios in the different layers of the myocardium and the kidney ---____ Control

Myocardium (left ventricle) AD subendocardium/ subepicardium Circ subendocardium/ subepicardium Kidney Medulla/tort,-u (X 100)

1.09

Hypothermia

1.09 kO.23

1.13 kO.21 1.11 to.35

1.66 + 1.37

0.95 +0.87*

kO.29

Posthypothermia

1.07 kO.34 1.07 kO.23

1.30 k1.05 --Values are means + SD (n = 17). AD, area supplied by anterior descending branches of the left coronary artery; circ, area supplied by circumflex branches of the left coronary artery. ‘“P < 0.01 compared to control value (paired t test).

TABLE 3. Hemodynamic changes during hypothermia and posthypothermia Control

Temperature, “C Pulse rate, beats/min Mean arterial pressure, mmHg Cardiac output, ml/ min. 10 kg Stroke volume, ml/ beat 10 kg Total peripheral resistante, units

Hypothermia

Posthypothermia

37.4 t 0.8 132 + 22 125 + 16

20.8 I!I 1.0* 42 + 7* 70 + 16*

35.6 + 0.5 151 t 16 124 + 16

913 +- 142

186 + 40*

787 ?I 112-l

7.2 + 1.8

4.3 Ii 1.5*

5.2 + 1.2*

147 + 53

447 z!z 153*

183 -+ 40

l

Values are means + SD (n = 17). * P < 0.01 compared to control value (paired t test). t P < 0.05 compared to control value (paired t test).

t 5.2% of the control during hypothermia, and it recovered to 86.0 t 14.1% in the posthypothermic period, significantly lower than that of the control (P < 0.05). This indicates a trend for incomplete recovery 2 h after a return to the euthermic condition. The calculated total peripheral resistance increased significantly to 304% of the control in the hypothermic period and returned to near the control level in the posthypothermic period. DISCUSSION

At a body temperature of 21°C one would expect, in the face of a greatly decreased cardiac output, a decline in blood flow to the various organs. The observed decline, however, was found to benonuniform among the vascular beds analyzed. The patterns of blood flow distributions during hypothermia and posthypothermia differed from that observed during the initial normothermic control period. The brain blood flow at 21°C averaged about 25% of control. The brain-stem flow, however, was maintained at 38% of control. In phenoxybenzamine (POB)-treated dogs, Kawashima et al. (20) found total brain blood flow to be 19.3% of the control at a body temperature of 24OC. On rewarming we observed prompt return of brain blood flows to control levels. The values for brain blood flow obtained under normothermic conditions agreed closely with those reported by others (12, 27). In the areas of the myocardium measured, the subendocardial layer of the

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BLOOD

FLOW

DISTRIBUTION

DURING

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HYPOTHERMIA

circumflex region of the left ventricle exhibited the highest blood flow rate, and the free wall of the right ventricle the lowest. In hypothermia, the average myocardial blood flow was maintained at about 40% of control, whereas the cardiac output fell to 20%. Blair (6) also found myocardial flow to be well maintained during hypothermia. The blood flow ratio of the subendocardium/subepicardium during hypothermia remained within the normal range, near 1.10 (8). Both the brain stem and the myocardium maintained considerably higher blood flows in hypothermia than the other tissues studied as well as disproportionally high flows relative to the decline in cardiac output. In POB-treated dogs Kawashima et al. (20) reported total myocardial flow to be 28.4% of control at 24OC. Myocardial blood flow returned to near control values when the dogs were rewarmed to a normal body temperature. Studies on the in situ hypothermic heart indicate that it still requires relatively more oxygen than other tissues (29). Other studies show that at ZO-25°C the oxygen supply to the myocardium is adequate (24). The rblatively high blood flow in the hypothermic myocardium seen in the present study appears to demonstrate that blood flow to a tissue 1s regulated by oxygen demand at least down to 21°C. Blood flows in all areas of the digestive tract studied, including the mucosal layer of the gastric antrum and corpus, fell to low levels during hypothermia. Perfusion in the full thickness layer of the duodenum, however, remained somewhat1 higher than the other digestive tract tissue. The normothermic blood flows found for the stomach (1, 10, 12, 13, ZO), duodenum (10, 12>, and small and large intestines (10, 20) were in agreement with those reported by others. Zarins and Skinner (31) using a mechanical assist device, reported that the blood flow rate of the gastrointestinal tract remained at 70% or less of control value in posthypothermia. In our studies, however, the posthypothermic blood flows in the digestive tract, although somewhat lower, were not significantly different from control levels. Hepatic artery and bronchial artery blood flows were significantly short of control 2 h after rewarming. These flows may later recover to normal; at any rate, no adverse effects on liver or lung have been reported in animals subjected to short-term hypothermia. The slow recovery of hepatic artery flow is in agreement with the results of Zarins and Skinner (31); however, these authors observed a large increase in bronchial artery flow on rewarming. Normothermic renal cortical blood flow agreed closely with the results of others (7, 28) averaging 451.9 t 99.7 ml/100 gemin. This value fell to 127.6 t 40.7 ml/l00 gemin at a body temperature of 21”, a 73.6% decrease. In POB-treated dogs, Kawashima et al. (20) found an 81% decrease in total renal blood flow. The two endocrine organs studied, the adrenal gland and the hypophysis, exhibited severely depressed blood flows at 21°C and, along with striated muscle, were the tissues with the lowest flow relative to control. The mean normothermic adrenal blood flow, 398.3 t 183.5 ml/100 g. min, was in the range of that reported by others (13, 20). Blood flow in this tissue decreased by 87.5% during hypothermia and although flow greatly

increased on rewarming it remained significantly below the initial level. The hypophyseal blood flows are of doubtful value for several reasons. First, as reported by Goldman and Sapirstein (14), the anterior hYPOPhY sis of the rat is perfused not by the internal carotid artery but by the hypophyseal portal system. Therefore the total blood flow to the hypophysis should be greater than our results indicate. Second, the blood flow was calculated on the basis of the total organ weight instead of the weight of the posterior lobe. Finally, the small size of this organ probably resulted in low accuracy because of the small number of microspheres present. The normal striated muscle blood flow found in this study agreed with that reported by others (12, 20). At 21°C muscle blood flow decreased 90%. Considering the large muscle mass of the body, it appears likely that the lactic acidosis observed during hypothermia may result from inadequate perfusion of this tissue. Identification of hypothermic vascular beds with low perfusion rates and improvement in perfusion of such beds should lead to safer long-term deep hypothermia. In surface-induced deep hypothermia, ether is considered by several investigators (21, 23), to be the best anesthetic drug, since serious arrhythmias rarely occur and the animals are easily resuscitated from total circulatory arrest. However, Bigelow et al. (5), Rittenhouse et al. (25), Zarins and Skinner (31), and Kawashima et al. (20) did not use ether during surface-induced hypothermia and experienced no difficulty. In the study described here thiamylal sodium was the only anesthetic agent used and it appeared to be satisfactory. The blood pH decreased somewhat during hypothermia, possibly indicating a moderate metabolic acidosis. We believe that hemodynamics were not greatly affected by this moderately disturbed acid-base balance. However, as reported by Harper and Glass (17), the cerebral blood flow is highly sensitive to arterial Pco,; similarly, coronary blood flow is, as shown by Wang and Katz (30) and McConnell et al. (22), sensitive to changes in blood

PH.

During hypothermia the blood volume decreases (4, 9) and the hematocrit rises (24). Although a total of 30 ml/kg of lactated Ri .nger solution was infused throughout the experiment, we observed some hemoconcentration. The lactated Ringer solution was given in an attempt to maintain a relatively normal hematocrit and blood volume. The total volume of fluid given was low and should have had little effect on the parameters studied. The decreased bl.ood volume and the accompanying hemoconcentration in hypothermia have not been fully explained but are probably due to several different mechanisms. Increased circulating catecholamines due to surgical stress (16) may have caused splenic contraction which would contribute to the hemoconcentration observed in our animals. The 15 t 3 pm-diameter microspheres used in this study, although not ideal ,a .ppeared to be the optimum size for use in the variety of tissues analyzed ( 1, 11, 19). With the exception of the hypophysis, the tissue sample weights ranged from 1 to 3 g, and most samples, other than the adrenals and the hypophysis, weighed 2-3 g. Approximately 400,000 microspheres were given in each

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H710 blood flow determination. Although the number of microspheres was not counted in tissue samples, a study was performed in hypothermic and normothermic dogs to determine reproducibility of blood flow among three microsphere injections given at lo-min intervals. These data, although they did not measure accuracy, did show close agreement among the sequential measurements. A principal objective of this study was to determine, in a variety of tissue types, whether areas of disproportionally low blood flows were present. It would appear from the greatly increased total peripheral resistance during hypothermia that such areas exist. We have found in recent studies that this high resistance is relieved by adenosine triphosphate and by a combination of nitroprusside and low-dose epinephrine; thus, this resistance is not due entirely to hemoconcentration and increased blood viscosity. The tissues showing the lowest relative flows were

ANZAI,

TURNER,

GIBSON,

AND

NEELY

striated muscle and the adrenal gland. However, most tissues exhibited about an 80% or greater decrease in blood flow. Only the blood flows in the myocardium and brain stem were maintained at a relatively high level. Several tissues were slow to recover perfusion to the initial values by 2 h after rewarming. Johansson and Huttunen (18) found that hypothermia may induce intravascular sludging and capillary occlusion. This may explain why certain vascular beds recovered slowly after hypothermia. In the short-term hypothermia em-ployed-in this study, only a mild acid-base imbalance was observed. In long-term induced hypothermia, this imbalance, unlike the case of true hibernation (2, E), becomes severe. This work HL-11730. Received

was supported

for publication

in part 9 May

by Public

Health

Service

Grant

1977.

REFERENCES 1. ARCHIBALD, L. H., F. G. MOODY, AND M. SIMONS. Measurement of gastric blood flow with radioactive microspheres. J. Appl. Physiol. 38: 1051-1056, 1975. 2. AXELROD, D. R., AND D. E. BASS. Electrolytes and acid-base balance in hypothermia. Am. J. Physiol. 186: 31-34, 1956. 3. BARETT-BOYES, B. G., M. SIMPSON, AND J. M- NEUTZ. Intracardiac surgery in neonates and infants using deep hypothermia with surface cooling and limited cardiopulmonary bypass. Circukztion 43, Suppl. 1: 25-30, 1971. 4. BARLOW, G., G. B. SPURR, AND R. L. BOWE. Circulating levels of 17-hydroxycorticosterone in prolonged hypothermia. J. AppZ. Physiol. 14: 777-780, 1959. 5. BIGELOW, W. D., W. K. LINDSAY, AND W. F. GREENWOOD. Hypothermia: its possible role in cardiac surgery; an investigation of factors governing survival in dogs at low body temperatures. Ann. Surg. 132: 849-866, 1950. 6. BLAIR, E. CZinicaZ Hypothermia. New York: McGraw, 1964, p. 19, 36. 7. CARRIERE, S., G. D. THORBURN, C. C. C. O’MORCHOE, AND A. C. BARGER. Intrarenal distribution of blood flow in dogs during hemorrhagic hypotension. CircuZation Res. 19: 167-179, 1966. 8. COBB, F. R., R. J. BACHE, AND J. C. GREENFIELD, JR. Regional myocardial blood flow in awake dogs. J. CZin. Invest. 53: 16181625, 1974. 9. D’AMATO, H. E., AND A. H. HEGNAUER. Blood volume in the hypothermic dog. Am. J. PhysioZ. 173: 100-102, 1953. 10. DELANEY, J. P., AND J. CUSTER. Gastro-intestinal blood flow in the dog. CircuZation Res. 17: 394-402, 1965. 11. DOMENCH, R. J., J. I. E. HOFFMAN, M. I. M. NOBLE, K. B. SAUNDERS, J. R. HENSON, AND S. SUBIJANTO. Total and regional coronary blood flow measured by radioactive microspheres in conscious and anesthetized dogs. CircuZation Res. 25: 581-596, 1969. 12. ERICSSON, B. F. Effect of pentobarbital sodium anesthesia, as judged with aid of radioactive carbonized microspheres, on cardiac output and its fractional distribution in the dogs. Acta Chir. &and. 137: 613-620, 1971. 13. FORSYTH, R. P., A. S. NIES, F. WYLER, J. NEUTZ, AND K. L. MELMON. Normal distribution of cardiac output in the unanesthetized restrained rhesus monkey. J. AppZ. Physiol. 25: 736741, 1968. 14. GOLDMAN, H., AND L. A. SAPIRSTEIN. Nature of the hypophyseal blood supply in the rat. Endocrinology 71: 857-858, 1962. 15. GOODRICH, C. A. Acid-base balance in euthermic and hibernating marmots. Am. J. Physiol. 224: 1185-1189, 1973. 16. HARDY, J. D., T. CARTER, AND M. D. TURNER. Catecholamine metabolism. Surgery 150: 666-683, 1959. 17. HARPER, A. H., AND H. I. GLASS. Effect of alterations in the arterial carbon dioxide tension on the blood flow through V the

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Blood flow distribution in dogs during hypothermia and posthypothermia.

Blood flow distribution in dogs during hypothermia and posthypothermia T. ANZAI, Department M. D. TURNER, W. H. GIBSON, of Surgery, University of Mis...
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