Effect Of Polycythemia Research Articles

Effect of Polycythemia on Serum Lipid Profile and Oxidative Stress

Polycythemia is generally known as a disorder that affects the stem cells in the bone marrow and is characterizedby a high and excessive production of red blood cells. The current study was designed to investigate andinvestigate the relationship between the serum lipid profile and oxidative stress in polycythemia patients.,The study included examining 85 blood samples from both gender, males and females, for patients comingto Shatra General Hospital. During the study period, all of (Hb, PCV, MDA, TC, TG, HDL, LDL, andVLDL) were examined for both patients and control groups.The current study showed an increase in the incidence of polycythemia in males, while it decreased infemales, and the study showed that the incidence of polycythemia increased with age until it reached itspeak in the third age group 41-50 years, then the percentage gradually decreased to a minimum in the fifthage group 61-70 years .The results of the study recorded a significant increase P <o.o5 in both the concentration of hemoglobin Hband the packed cell volume PCV in patients with polycythemia, both real and secondary, when comparedwith the control group. Also, the results of the present study showed: a significant decrease P <0.05 incholesterol concentration in the group of true polycythemia compared with the control group. A significantincrease P <0.05 in concentration of triglycerides (TG) was higher in the true polycythemia group and a highsignificant P <0.05 in the secondary polycythemia group compared with the control group.The results indicated that there was a significant decrease P <0.05 in LDL concentration in the truepolycythemia group, and a significant increase of P <0.o5 in the secondary polycythemia group comparedwith the control group. The results of the study also recorded a high significant decrease P <0.05 in the truepolycythemia group and a significant decrease P <0.o5 in the secondary polycythemia group compared tothe control group. The results also showed a significant increase P <0.05 with the concentration of VLDL inthe group of true polycythemia and high Significant p <0.05 in the secondary polycythemia group comparedwith the control group.The results showed a significant increase P <0.05 in MDA concentration in polycythemia patients comparedwith the control group.

Sex-based Approach for the Clinical Impact of the Increased Hemoglobin on Incident AF in the General Population.

Background and ObjectivesAlthough the adverse cardiovascular effect of anemia has been well described, the effect of polycythemia on the incident atrial fibrillation (AF) remain unclear. The objective of this study is to identify the association between increased hemoglobin and incident AF.MethodsThis was a retrospective-cohort study with 434,269 subjects who underwent national health examinations from the Korean National Sample Cohort. We estimated the risk of incident AF according to hemoglobin-based four-categories.ResultsDuring 3.9-year of follow-up, polycythemia group showed higher incidences of AF (hazard ratio[HR] with 95% confidence interval[CI], 1.50 [1.28–1.76] and 1.69 [1.13–2.56]; in men and women, respectively) than normal hemoglobin group (each p<0.001). In the normal hemoglobin and polycythemia groups, a 1 g/dL increase in hemoglobin level was associated with increased risks of incident AF (1.12 [1.07–1.17] and 1.18 [1.10–1.26] in men and women, each p<0.001). To investigate the specific hemoglobin concentration related to greater AF incidence, we analyzed the sensitivity/specificity of different hemoglobin levels: ≥16.0 g/dL in men and ≥14.5 g/dL in women showed the highest Youden's index, with c-indices of 0.83 and 0.82, respectively. Kaplan-Meier cumulative-event curves according to these specific hemoglobin levels (≥16.0 g/dL in men and ≥14.5 g/dL in women) also showed consistent results in both sexes (each p<0.05).ConclusionsEven in the Korean general population, increased hemoglobin was significantly associated with higher rate of incident AF. Especially, subjects with hemoglobin levels ≥14.5 g/dL in women and ≥16.0 g/dL among men were associated with increased risk of incident AF.

Effect of Polycythemia on Percutaneous Coronary Intervention Outcome

Effect of Polycythemia on Percutaneous Coronary Intervention Outcome

P5660Clinical impact of polycythemia on cardiovascular outcome from the general population: a nationwide cohort study

Abstract Background Although adverse effect of anemia had been reported, effect of polycythemia on cardiovascular outcome from the general population had not been revealed yet. Methods We included 451,107 subjects who received national health examinations from the Korean National Health Insurance Service-based National Sample Cohort from 2009–2013. Medical records were screened from January 2002 to investigate the subjects' disease-free baseline period. They were followed until December 2013. We divided male and female subjects into four categories each based on hemoglobin level (normal, moderate to severe and mild anemia, polycythemia) to assess each outcome. Results During 1,735,964 person·years, 12,107 major adverse cardiovascular and cerebrovascular events (MACCE), 862 incident acute myocardial infarction (MI), 5,850 incident ischemic stroke, and 2,430 incident atrial fibrillation (AF) were observed. Compared to normal hemoglobin range group, polycythemia group showed higher MACCE (HR=1.23 [1.12–1.35] in male, HR=1.79 [1.20–2.67] in female, each p&lt;0.001), incident MI (HR=1.37 [1.05–1.79] in male, HR=3.46 [1.06–14.00] in female, each p&lt;0.001), incident ischemic stroke (HR=1.27 [1.10–1.46] in male, HR=1.72 [1.02–2.91] in female, each p&lt;0.001), and incident AF (HR=1.46 [1.21–1.74] in male, HR=2.13 [1.03–4.77] in female, each p&lt;0.001). Each outcome was linearly increased with the increase of hemoglobin among subjects with polycythemia (p&lt;0.001), and with the decrease of hemoglobin among subjects with anemia (each p&lt;0.001, U-shaped relationship). These relationship was more profound in obese female younger than 60-year-old. Conclusion Not only anemia but also polycythemia were significantly associated with higher rate of MACCE including death, incident MI, ischemic stroke, and AF among the general population.

Hemodynamic alterations associated with polycythemia and partial exchange transfusion

Polycythemia hyperviscosity syndrome has been associated with multiple systemic effects. There is dearth of data on the effects of polycythemia on cardiac function. This case presents a newborn infant with symptomatic polycythemia in whom detailed myocardial function analysis for systolic and diastolic performance, as well as end-organ perfusion assessment was carried out using transthoracic echocardiography. Hemodynamic information in polycythemic infants before and after partial exchange could improve our understanding of the impact on myocardial performance.

Effects of polycythemia on systemic endothelial function in chronic hypoxic lung disease

Chronic obstructive pulmonary disease (COPD) is a major risk factor for cardiovascular disease. Polycythemia, a common complication of hypoxic COPD, may affect systemic vascular function by altering blood viscosity, vessel wall shear stress (WSS), and endothelium-derived nitric oxide (NO) release. Here, we evaluated the effects of hypoxia-related polycythemia on systemic endothelial function in patients with COPD. We investigated blood viscosity, WSS, and endothelial function in 15 polycythemic and 13 normocythemic patients with COPD of equal severity, by recording brachial artery diameter variations in response to hyperemia and by using venous occlusion plethysmography (VOP) to measure forearm blood flow (FBF) responses to a brachial artery infusion of acetylcholine (ACh), bradykinin (BK), sodium nitroprusside (SNP), substance P (SP), isoptin, and N-monomethyl-L-arginine (L-NMMA). At baseline, polycythemic patients had higher blood viscosity and larger brachial artery diameter than normocythemic patients but similar calculated WSS. Flow-mediated brachial artery vasodilation was increased in the polycythemic patients, in proportion to the hemoglobin levels. ACh-induced vasodilation was markedly impaired in the polycythemic patients and negatively correlated with hemoglobin levels. FBF responses to endothelium- (BK, SP) and non-endothelium-dependent (SNP, isoptin) vasodilators were not significantly different between the two groups. L-NMMA infusion induced a similar vasoconstrictor response in both groups, in accordance with their similar baseline WSS. In conclusion, systemic arteries in polycythemic patients adjust appropriately to chronic or acute WSS elevations by appropriate basal and stimulated NO release. Overall, our results suggest that moderate polycythemia has no adverse effect on vascular function in COPD.

Clinical study on the effect of polycythemia on retinopathy of prematurity

Objective To explore the effect of polycythemia on retinopathy of prematurity (ROP).Methods The clinical data of 262 premature cases was analyzed retrospectively in Xi'an Children Hospital from January 2005 to January 2009. Polycythemia was found in 46 cases (17. 56 %), including 27 males and 19 females. In 216 infants without polycythemia (82.46%), 155 were male and 61 were female. The difference of the birth weight (t = 0. 730, P = 0. 466), gestational age (t= 1. 603, P= 0. 110), oxygen inhalation numbers (χ2 =0. 04 ,P>0. 90) and times (t= 1. 225, P= 0. 223), and concentration (t= 1. 823,P=0. 071) between polycythemia group and no polycythemia group were not significant. In order to diagnose ROP, the ocular fundus of all premature infants was examined with binocular indirect ophthalmoscope, and the stage of ROP was assessed. Results In all the premature infants, ROP was found in 120 cases (45.80%). In 46 cases of polycythemia, ROP was found in 25 cases (54.34%); in 216 infants without polycythemia, ROP was found in 95 cases (43.98%); the difference of ROP incidence betweenthe two groups was not significant (χ2=1.64, P>0. 1). In 120 ROP patients, 104 cases (86.67%) with ROP 0. 05). Conclusion Polycythemia may not affect the incidence of ROP, but impact on the severity of ROP. Key words: Retinopathy of prematurity/etiology; Polycythemia/complications

Polycythemia and hyperviscosity in the newborn.

Research from the past 15 to 20 years has led to a comprehensive understanding of the etiology and effects of polycythemia and hyperviscosity in the newborn. Polycythemia and hyperviscosity are generally a result of a poor intrauterine environment or hypoxic complications during labor and delivery. Changes in blood viscosity are a direct result of changes in hematocrit because the plasma viscosity in the newborn is virtually always normal. Polycythemia and hyperviscosity are associated with decreases in blood flow to the brain, heart, lung, intestines, and carcass. Renal blood flow is not affected, but renal plasma flow is diminished, resulting in a lower glomerular filtration rate (GFR). The elevated hemoglobin and hematocrit are associated with an increase in the arterial oxygen content. It is the increase in arterial oxygen content, not the hyperviscosity, that is directly responsible for the decreased blood flow in the brain and heart as well as cardiac output. As a result, brain and cardiac oxygenation is normal. Decreased pulmonary blood flow appears to be the result of hyperviscosity and can result in system hypoxia. This can be corrected by a partial exchange transfusion to lower the hematocrit and viscosity. This will also improve renal function by increasing plasma flow. Because the abnormalities in brain function are due to a primary hypoxia event and not reduced cerebral blood flow, a partial exchange transfusion will not improve short-term or long-term abnormalities in neurological functioning.

Cardiac function, microvascular structure, and capillary hematocrit in hearts of polycythemic rats.

The effect of polycythemia on the coronary microcirculation was studied in young male rats. Two experimental models of polycythemia were employed: cobalt-induced polycythemia, which mimics hypoxia-induced changes, and erythropoietin-induced polycythemia, which circumvents these changes. In both models, baseline left ventricular function was normal, whereas maximal systolic and developed pressures were decreased. In cobalt-treated rats the left ventricular functional reserve was also compromised. Morphometric analysis of the left ventricle confirmed previously described improved geometric conditions for oxygen supply at the distal portions of capillaries (smaller domain areas and shorter capillary segments). In cobalt-treated but not in erythropoietin-treated rats, increased capillary angiogenesis was also detected. In the hearts from rats with both types of polycythemia, a small but significant increase in the formation of arterioles was found. Capillary linear hematocrit was within the normal range in both types of polycythemia despite sizeable increases in systemic hematocrit. Significant differences in red blood cell distribution within capillaries were found between proximal and distal portions in all experimental groups.

The effect of polycythemia on skin blood flow in hypertensive rats

Polycythemia has marked effects on blood flow through large arteries, but there has been little study of microvascular flow properties, particularly in the hypertensive state. We have previously shown that skin blood flow in the rat had properties very similar to those in man. We used laser Doppler techniques to determine the effect of erythropoietin-induced polycythemia on skin blood flow in 12 Spontaneously Hypertensive Rats (SHR) as compared with 12 normotensive Wistar-Kyoto (WKY) rats. We contrasted flow values at the back and base of tail, nutritively (NUTR) perfused skin sites, with those at the plantar surface of the paw, a site with substantial arteriovenous anastomotic (AVA) perfusion. Erythropoietin treatment produced a substantially greater hematocrit response in the SHR rats, rising from 47 ± 1 to 64 ± 1, than in the WKY animals, who showed an increase from 46 ± 1 to 55 ± 1. Blood pressure was higher in the EPO-treated WKY and SHR rats: 157 ± 4 mm Hg as compared to 148 ± 2 mmg Hg in the WKY animals and 228 ± 4 mm Hg as compared to 201 ± 3 mm Hg, respectively (both p < 0.03). Erythropoietin treatment had very little effect on basal skin blood flow in either WKY or SHR rats. However, there was significantly lower heat-stimulated flow at the plantar surface of the paw in the EPO treated rats (WKY: 27.3 ± 1.9 ml/min/100 gm vs 35.5 ± 1.5 ml/min/100 gm in the untreated state; p < 0.02; SHR: 32.7 ± 2.6 ml/min/100 gm vs 45.4 ± 2.3 ml/min/100 gm in the untreated state; p < 0.01). In contrast, there was little difference at the back or tail. We conclude that erythropoietin-induced polycythemia affects flow in AVA rather than NUTR microvessels. Although raised vascular pressure has produced microvascular flow in our previous studies, the rise in pressure associated with high hematocrit appears to result from an increase in microvascular resistance, decreasing flow. Our study helps clarify clinical observations on the hemodynamic consequences of hematocrit elevation.

Effects of polycythaemia and haemodilution on circulation in neonates.

Haemodilution in nine neonates resulted in significant mean (SEM) decrease of packed cell volume (0.67 (0.01) to 0.55 (0.01)) and increases in cardiac output (250 (16) to 308 (25) ml/min/kg) and blood flow velocities of the internal carotid artery and the coeliac artery (+20%). However, red cell flows in the aorta, carotid and coeliac arteries did not change during haemodilution, thereby indicating that haemodilution did not improve oxygen transport.

The effect of polycythemia and hypoxia on urinary N-acetyl- β-D-glucosaminidase activity in newborns

Urinary N-acetyl- β-D-glucosaminidase activity was assayed in fullterm and preterm polycythemic neonates, in preterm infants with hypoxia, and in healthy newborns. There were no significant differences between fullterm and preterm babies or between appropriate for gestational age and small for gestational age neonates in the normal group. N-acetyl- β-D-glucosaminidase excretion on the first day of life was significantly raised in polycythemic newborns ( P < 0.01). Fourteen days after partial plasma exchange the enzyme activity returned to normal. N-acetyl- β-D-glucosaminidase activities in preterm babies with respiratory distress syndrome were significantly ( P < 0.01) raised on the 1st, 2nd, 4th days and fell sharply to the 14th day. N-acetyl- β-D-glucosaminidase isoenzyme studies revealed that urine samples taken from preterm babies with respiratory distress syndrome in the first week after birth contained increased amounts of intermediate and B isoenzyme forms while there was a concomitant reduction in the amount of the A form present.

Ventilation-perfusion relationships during induced normovolemic polycythemia in dogs.

Previous studies on normal subjects and patients with polycythemia have given conflicting results of the effect of polycythemia on pulmonary gas exchange. We studied acutely induced normovolemic polycythemia in the dog and measured arterial blood gases and ventilation-perfusion (VA/Q) relationships using the multiple inert gas elimination technique. The mean base-line hematocrit of 43 +/- 5% was increased to 57 +/- 4 and 68 +/- 8%, respectively, after two exchange transfusions of packed erythrocytes. Subsequent plasma exchange transfusions returned the mean hematocrit to 44 +/- 4%. Polycythemia caused no significant arterial hypoxemia; indeed there was a slight improvement in the alveolar-arterial PO2 difference. The multiple inert gas elimination measurements showed no increase in VA/Q inhomogeneity with no increase in log SD ventilation (V) or log SD blood flow (Q). There was a shift of mean V and mean Q to high VA/Q areas because of a decrease in cardiac output, presumably caused by increased blood viscosity. This study showed no deleterious effects on pulmonary gas exchange within the hematocrit range of 36-76%.

1436 EFFECT OF POLYCYTHEMIA ON FIBRINOGEN DISAPPEARANCE RATE IN PUPPIES

I have shown in previous work that polycythemia in the newborn dog will cause a disease similar pathologically to necrotizing enterocolitis(NEC) in human infants. To explore the patho-physiology of this disease, the effect of polycythemia on fibrinogen disappearance rate was studied in 38 puppies (3-14d). All pups received an exchange transfusion removing 65cc/kg of blood and transfusing 85cc/kg of either whole blood (control, C, resulting Hct.=37), or packed red blood cells(polycythemia, P, resulting Hct.=68). NEC was found in 15 of 19 P and 4 of 19 C pups(p<.01). The concentration of Fibrinogen degradation products measured by tanned red cells hemagglutination inhibition at 2 & 4hr. post transfusion was 36% higher in the P than the C pups (NS). 1251 Fibrinogen and Evan's blue (an albumin marker) were injected 2hr after transfusion and the concentration of clottable labelled fibrinogen and albumin tracer were measured at ½ hr & 2 hrs after injection. The fraction of the tracer that disappeared over the 1½hr period was calculated. In previous experiments pups have been shown to have stable plasma volumes during this period. In the P group 45±18 SD% of the clottable fibrinogen disappeared vs only 28±15% in the C group (2p<.01). In the P group 36±21% of the albumin tracer disappeared vs 31±12% in the C group(NS). Thus polycythemia in the newborn dog is associated with an increased disappearance of clottable fibrinogen not associated with a general increase in protein disappearance rate. The most sensative currently available test for fibrinogen degredation products was inadequate to demonstrate this event.

Effect of polycythemia on gastrointestinal blood flow and oxygenation in piglets.

Gastrointestinal blood flow and oxygenation were measured before and after the induction of polycythemia in newborn piglets. Sixty minutes after exchange transfusion with age-matched packed red blood cells, hematocrit and in vitro whole blood viscosity increased, while 51Cr-measured blood volume did not change. Cardiac output and total gastrointestinal blood flow (the sum of stomach, jejunum, ileum, and colon blood flows) decreased a similar degree after exchange transfusion, although the reduction in total gastrointestinal blood flow was not uniform in all regions of the gastrointestinal tract. Specifically, blood flow to the stomach and mucosa-submucosa layer of the small bowel decreased, whereas that to the colon and muscularis-serosa layer of the small bowel remained unchanged. Gastrointestinal O2 delivery increased after exchange transfusion because of the increase in arterial O2 content consequent to polycythemia. The arteriovenous O2 content difference remained unchanged following exchange transfusion, and gastrointestinal O2 consumption thus decreased 49 +/- 2%. After a test meal, postprandial values for gastrointestinal blood flow and oxygenation in polycythemic piglets increased to levels similar to postprandial values reported previously in normal newborn piglets.

Effect of polycythemia on vascular volume in the newborn dog.

The effect of polycythemia [hematocrit (Hct) 64-80] on blood volume (BV) was studied in 27 unanesthetized, splenectomized newborn dogs (age 6-14 days, postsplenectomy 5-13 days). Normovolemic polycythemia (N) was induced in nine pups by exchange transfusion with 75 ml/kg of adult, packed (to Hct 95) red blood cells (RBC). Hypervolemic polycythemia (H) was induced in 11 pups by transfusion of RBC (50 ml/kg). Seven pups received exchange transfusion with 75 ml/kg of whole blood and served as controls (C). Red cell volume (RCV, 51CrRBC) and plasma volume (PV, 125I-fibrinogen and Evans blue) were measured prior to and at 1, 2, and 4 h after transfusion, before the pups received fluid orally. The pups were fed 8 ml X kg-1 X h-1 after 4 h, and measurements were repeated at 8 and 24 h. BV fell in C prior to 4 h by 10 +/- 4% (SD) (P less than 0.01) and then rose to initial levels. BV rose in the N pups by 17 +/- 9 (P less than 0.01), 14 +/- 5 (P less than 0.01), 9 +/- 10 (P less than 0.1), 17 +/- 9 (P less than 0.01), and 31 +/- 17% (P less than 0.01) at 1, 2, 4, 8, and 24 h post transfusion. BV rose in the H pups by 41 +/- 8, 35 +/- 10, 23 +/- 11, 27 +/- 6, and 43 +/- 9% (all P less than 0.01). Thus newborn dogs with induced N or H equilibrate rapidly to a BV significantly higher than C levels.(ABSTRACT TRUNCATED AT 250 WORDS)

THE EFFECT OF POLYCYTHEMIA ON PLASMA VOLUME IN NEWBORN DOGS

The effect of polycythemia(Hct 64-80) on plasma volume(PV) was studied in 27 unanesthetized, splenectomized puppies (age:6-14,post-spenectomy:5-13d). Normovolemic polycythemia(N) was induced in 9 pups by exchange transfusion(ExN) with 75cc/kg of red blood cells (RBC). Hypervolemic polycythemia(H) was induced in 11 pups by transfusion of 50cc/kg of RBC. 7 pups received ExT with 75cc/kg of whole blood and served as controls(C). PV(125I Fibrinogen) and red cell volume(RCV, by 51Cr) were measured prior to and 1,2, and 4hrs after transfusion, with the pups receiving no oral intake.Pups were fed 8cc/kg/hr after 4hrs, and measurements were repeated at 8 and 24hrs.RCV rose with transfusion in N and H and remained elevated throughout the experiment. RCV did not change in C. PV fell slightly in the C group prior to 4hrs and then rose to initial levels. PV rose in the N pups from -50±7%SD to -35±10%(p<.001),-37±8%,-38±9%, and after feeding to -29±13 and 1±18(p<.001),1,2,4,8 and 24hrs post-transfusion.PV fell in the H pups from 4±2% to -24±12(p<.001),-35±14, -37±14, and then rose after feeding to -32±9 and 0±15(p<.001). At 1,2,4 and 8hrs PV in H and N was different from that in C(p< .01).Thus pups with induced N or H equilibrate rapidly to a PV determined primarily by the Hct and not initial PV.Since the increase in PV in N prior to feeding was rapid and occurred during a period of no fluid ingestion, it must be due to a decrease in capillary pressure secondary to the induced change in viscosity. A further increase in PV to control levels occurs when the pups are fed, which is probably caused by renal solute retention.

High-altitude adaptation and maximum work performance.

The treadmill work performance of rats at sea level with normal or elevated hematocrits was compared with that of rats conditioned in a hypobaric chamber at 450 Torr for 3 wk with similar hematocrit adjustments. A mean increase in hematocrit to 62 significantly improved the work performance of rats at sea level and at ambient O2 tensions of 100, 75, and 35 Torr. By contrast, rats conditioned in a hypobaric chamber with mean hematocrits of 40 and 58 performed similarly at all O2 tensions compared with sea-level rats with hematocrits of 43. Thus, although an increase in O2-carrying capacity of the blood of sea-level animals increased work capacity, altitude adaptation did not appear to result in any positive effect on work capacity, and indeed, seemed to interfere with the beneficial effect of polycythemia on maximum work performance.

The effect of polycythemia on blood flow in working and non‐working skeletal muscle

The effect of acutely induced polycythemia on blood flow and viscosity in the vasodilated vascular bed of working and non-working skeletal muscle was studied. In 12 mongrel dogs anesthetized with thiopental sodium the calf muscle of one hind limb was isolated. Vasodilation was induced either by sciatic stimulation setting the muscle at maximal work or by i.a. infusion of papaverine. Blood flow was measured at different perfusion pressure before and after infusion of 300 ml packed homologous red cells. Blood viscosity in vitro was determined in a coneplate viscometer. Apparent viscosity in vivo was analyzed by comparing pressure-flow relationships for blood and a reference solution. Polycythemia decreased blood flow by 35% in the non-working muscle but less than 10% in the working muscle at comparable perfusion pressures. Blood viscosity in vitro increased by 35% at low shear rates. Apparent viscosity in vivo increased by 35% in the non-working muscle but less than 10% in the working muscle. The flow impairment induced by polycythemia was far more pronounced in the non-working skeletal muscle indicating a flow facilitation by the rhythmic muscle contractions. Erythrocyte flow in fact increased in the working muscle after induced polycythemia while decreased in the non-working muscle.

Myocardial blood flow and its distribution in anesthetized polycythemic dogs.

SUMMARY Decreased cardiac output, coronary blood flow, and systemic oxygen transport in polycythemia are attributed to increased blood viscosity and regarded as potentially harmful. We studied the effects of isovolemic polycythemia on these variables as well as on myocardial oxygen consumption and regional myocardial blood flow in 31 anesthetized dogs, seven with cannulated left main coronary arteries. Measurements were made at rest, during hypoxemia or adenosine infusions, and with aortic stenosis, pacing, or an aorto-atrial fistula. When hematocrit increased from 42% to 66%, it reduced cardiac output by 36% and systemic oxygen transport by 8%; with hypoxemia, cardiac output rose in polycythemic dogs. Normoxemic polycythemia decreased myocardial blood flow by 46% and increased mean coronary resistance by 54%, slightly decreased myocardial oxygen transport and consumption, and did not alter coronary sinus oxygen tension or myocardial oxygen extraction. Cardiac stress, hypoxemia, and adenosine infusion lowered coronary resistance in polycythemic dogs. Left ventricular myocardial oxygen transport was dependent on pressure work and not on arterial oxygen content or hematocrit. With maximal coronary vasodilation, coronary vascular resistance at hematocrits of 66% was 1.5 times that at 42%. Polycythemia per se did not alter the even distribution of flows across the left ventricular wall, but subendocardial underperfusion began at higher perfusion pressures in polycythemic than in normocythemic dogs. We conclude that autoregulation plays a role in regulating flows and oxygen transport in polycythemia. With maximal coronary vasodilation, however, the increased viscosity of polycythemic blood could be an important factor reducing the amount of myocardial blood flow and oxygen transport. THE EFFECTS of polycythemia on the circulation depend in part on whether there is an associated increase in blood volume 1 which is usually elevated in most forms of polycythemia in man. 2 5 Because of the raised blood volume, cardiac output is usually increased, unless there is heart failure. Systemic oxygen transport (cardiac output times arterial oxygen content) is therefore increased above normal when arterial oxygen saturation is normal 4 and may be normal or only moderately reduced when