Liver Blood Volume Research Articles

The Value of CT Perfusion Parameters and Apparent Diffusion Coefficient Value of Magnetic Resonance Diffusion Weighted Imaging in Diagnosis of Hepatocellular Carcinoma.

Background Hepatocellular carcinoma is one of the malignant tumors with the highest incidence in the world. According to the latest statistics of the National Cancer Center, the incidence of liver cancer ranks fifth in malignant tumors and its mortality rate ranks second in China, which seriously threatens people' s life and health. Aim To investigate the value of CT perfusion parameters and apparent diffusion coefficient (ADC) of magnetic resonance imaging (MRI) diffusion weighted imaging (DWI) in the diagnosis of hepatocellular carcinoma. Methods 43 patients with hepatocellular carcinoma and 40 patients with hepatic hemangioma treated in our hospital from August 2018 to August 2021 were selected for CT perfusion imaging and MRI examination. Results The liver blood flow (BF), liver blood volume (BV), and hepatic artery perfusion (HAP) in the hepatocellular carcinoma group were (267.38 ± 35.59) ml/(min·100 g), (30.20 ± 8.82) ml/100 g, and (0.64 ± 0.10) ml/(min·ml), respectively, which were significantly higher than those in the hepatic hemangioma group (p < 0.05). The ADC value of hepatocellular carcinoma DWI sequence was (1.20 ± 0.17) ×10−3 mm2, which was significantly lower than that of hepatic hemangioma (p < 0.05). The area under ROC curve of BF, BV, HAP, and ADC values for hepatocellular carcinoma was 0.860, 0.754, 0.804, and 0.890, respectively. The area under ROC curve of the four groups was compared (p > 0.05). Conclusion CT perfusion parameters BF, BV, HAP, and DWI sequence ADC values have certain application value in the diagnosis of hepatocellular carcinoma, and there is no significant difference between the diagnostic value of each parameter.

THE ROLE OF HYDROGEN SULFIDE IN REGULATION OF CIRCULATION BLOOD LIVER

It was shown in acute experiments on laboratory rats that intraportalinjectionof hydrogen sulfide's precursor L-cysteine (15 mg/kg)caused dilatation of the intrahepatic vessels. As a result, systemic blood pressure (SBP) and blood pressure in the portal vein (PVP) significantly decreased on 17,6 and 24,5%, respectively, and the rate of local blood flow in the liver (LF) and its blood filling (BF) increased on 28,2 and 24,4% respectively. Application of hydrogen sulfide donor NaHS (7 mg/kg) resulted in similarly directed changes: SBP and PVP decreased on 20,8% i 26,2% respectively,LF and BF increased on 16,4% and 30,9% respectively. Application of L-cysteine in the conditions of tsystationin-gamma-lyase blockade by LD-proparhilhlitsyn led to an increase in SBP on 20,4 % and PVP on 26,6% and a decrease of BF on 21,5% and LF in the liver on 11,7% comparing with baseline values of these parameters. So, blockade of tsystationin-gamma-lyase not only completely removed the effects of L-cysteine, but also inhibited synthesis of H2S from its endogenous predecessors,which led to vasoconstriction of liver's blood vessels and, consequently, to an increase of blood pressure and a decrease of liver blood flow rat's and volume of blood deposited in liver.

Comparison of volume perfusion computed tomography (VPCT) and contrast-enhanced ultrasound (CEUS) for assessment of therapeutic effect of transarterial chemoembolisation (TACE)

Zielsetzung: To compare contrast-enhanced ultrasound (CEUS) and volume perfusion computed tomography (VPCT) for response evaluation of hepatocellular carcinoma (HCC) to transarterial chemoembolisation (TACE). Material und Methodik: Twenty consecutive patients with inoperable HCC underwent CEUS and VPCT in the pre- and post-TACE setting (mean, 1 day). Quality of CEUS and VPCT was rated as good/adequate/poor. Good and adequate were rated as diagnostic. We measured hepatic perfusion index (HPI), arterial liver perfusion (ALP), blood flow (BF) and blood volume (BV) at both time points by VPCT, calculated ratios and their sensitivity/specificity/negative (NPV) and positive predictive values (PPV) as well as cut-off values for these parameters as thresholds between responders and non-responders. VPCT and CEUS images were rated also according to mRECIST. Tumor response defined by mRECIST at follow-up (mean, 56 days) was accepted for validation. Ergebnisse: CEUS and VPCT yielded correct diagnosis in 20/20 cases. 10/20 patients showed at follow-up a complete response. There was a significant reduction of viable tumor tissue in all patients according to mRECIST (p 29,6% (all 100%), in BV of > 41,4% (all 100%), or in BF of > 53,1% (90%/100%/90%/100%) was indicative of response. Schlussfolgerungen: CEUS performs equally to VPCT for assessment of response to TACE in HCC. E-Mail: kaufmann.79@web.de

Colloid volume loading does not mitigate thorax, heart, and liver blood volume changes during combined heat and orthostatic stress

This study tests the hypothesis that volume loading during heat stress attenuates the reduction in regional blood volumes during an orthostatic challenge. 7 subjects underwent 30 mmHg lower-body negative pressure (LBNP) while normothermic, during heat stress (increased internal temperature ~1°C), and heat stress + colloid volume loading (12ml/kg). Relative thorax, heart, and liver blood volumes were determined by gamma camera imaging of 99mTc-labelled erythrocytes. Heat stress reduced blood volume in all regions, while subsequent volume infusion returned those values to normothermic levels. During LBNP, heat stress increased the magnitude of the reduction in blood volume (thorax=73±1, heart=72±1, liver=74±1%) compared to normothermia (thorax=22±3, heart=18±2, liver=14±63%; all P<0.001). Volume loading during heat stress did not alter the extent of the reduction in these blood volumes during LBNP (P>0.05). These data indicate that colloid volume loading during heat stress normalizes thorax, heart, and liver blood volumes but does not affect the magnitude of the subsequent reduction in blood volume in these regions during LBNP relative to heat stress alone. Supported by NIH-HL61388 & HL84072

Ethanol Predominantly Constricts Pre-sinusoids of Isolated Perfused Livers of Rat, Guinea pig and Mouse

Ethanol constricts hepatic vessels of isolated perfused livers of rats, but not dogs. However, it is not known whether ethanol constricts or dilates the hepatic vessels in other species such as guinea pigs and mice. In addition, the sites of hepatic venoconstriction induced by ethanol were not known in rat livers. We therefore studied the effects of ethanol on the segmental hepatic vascular resistance and liver weight of mice, rats and guinea pigs. The isolated livers were portally perfused with diluted blood at constant flow. The sinusoidal pressure was measured by the double occlusion method and was used to determine the pre- and post-sinusoidal resistance. The change of liver weight was also measured. Ethanol was administered cumulatively into the perfusate to gain clinically relevant concentrations of 1-300mM. Ethanol dose dependently caused predominant pre-sinusoidal constriction in livers of all three species. When compared with the livers of the guinea pigs and rats, the mouse livers were the weakest in response. Dose-dependent decreases in liver weight and bile flow accompanied predominant pre-sinusoidal constriction in guinea pigs and rats. Ethanol predominantly constricts pre-sinusoids in rat, guinea pig and mouse livers, although the mouse liver response was much weaker. Ethanol-induced pre-sinusoidal constriction is accompanied by reduction of liver blood volume in guinea pigs and rats.

Effects of terlipressin and somatostatin on liver and thorax blood volumes in patients with cirrhosis

Variceal bleeding in cirrhosis can cause liver ischaemia and deteriorate the hyperdynamic state; thus, the effects of vasoconstrictor therapy on liver blood volume (LBV) and thorax blood volume (ThBV) are important. To evaluate and compare the effects of terlipressin and somatostatin on LBV and ThBV in stable patients with cirrhosis and portal hypertension. Twenty patients were studied (Child-Pugh class A/B/C: 5/8/7). The radioactivities in the liver region (LRR) and the thorax region (ThRR) by single-head gamma camera technique, as indicators of LBV and ThBV, respectively, and systemic haemodynamics were measured at baseline and after intravenous infusion of 2 mg of terlipressin (n=10) or somatostatin 250 mg/h after an initial bolus of 250 mg (n=10). LRR and ThRR decreased significantly with increasing severity of cirrhosis. Thirty minutes after terlipressin infusion, LRR and ThRR increased by 7.8 ± 4.4% (NS) and 14 ± 5.3% (P=0.01) compared with baseline values; the increase in ThRR was significantly related to the increase in LRR (r=0.682, P=0.03). In contrast, somatostatin reduced LRR and ThRR by 13.3 ± 6.5% (P=0.07) and 1 ± 4% (NS) respectively. LRR and ThRR increased significantly in the terlipressin group compared with the somatostatin group (P=0.01 and P=0.02 respectively). Terlipressin reduced cardiac output and heart rate (both P=0.01) and increased the mean arterial pressure (MAP) and systemic vascular resistance (P=0.009 and P=0.002 respectively); MAP decreased after somatostatin infusion (P=0.03). Terlipressin, but not somatostatin, maintains LBV, increases ThBV and improves the hyperdynamic state in cirrhosis. These effects can be beneficial in variceal bleeding, particularly in patients with advanced liver disease.

Effect of terlipressin on blood volume distribution in patients with cirrhosis

Background: Patients with cirrhosis and portal hypertension have an altered blood volume distribution and a hyperdynamic systemic circulation. Terlipressin is known to reduce portal pressure by decreasing splanchnic inflow, but its effect on the blood volume distribution is unknown. The aim of the study was to investigate changes in regional blood volume distribution and systemic haemodynamics after administration of terlipressin to patients with cirrhosis. Methods: Blood volume distribution was determined in 13 patients with cirrhosis and portal hypertension by a dual‐head gamma‐camera technique and systemic haemodynamics was measured before and after intravenous administration of terlipressin (2 mg). Results: Terlipressin increased the blood volume in the thorax region (+6.0%, P < 0.002) and the liver region (+12.2%, P < 0.002), whereas blood volume in the splanchnic region remained unchanged. Systemic vascular resistance (SVR) and mean arterial blood pressure increased after terlipressin (+34 and +21%, P < 0.001). The increase in liver blood volume correlated directly with the increase in SVR (r = 0.88, P < 0.001). Conclusions: Terlipressin ameliorates the hyperdynamic circulation, increases thorax and liver blood volumes, but produces no effect on the splanchnic blood volume. Besides decreasing the splanchnic inflow, terlipressin may affect portal pressure by causing vasodilatation of intrahepatic vessels.

Improving MR quantification of regional blood volume with intravascular T1 contrast agents: accuracy, precision, and water exchange.

The goal of this work was to develop a comprehensive understanding of the relationship between vascular proton exchange rates and the accuracy and precision of tissue blood volume estimates using intravascular T1 contrast agents. Using computer simulations, the effects of vascular proton exchange and experimental pulse sequence parameters on measurement accuracy were quantified. T1 and signal measurements made in a rat model implanted with R3230 mammary adenocarcinoma tumors demonstrated that the theoretical findings are biologically relevant; data demonstrated that over-simplified exchange models may result in measures of tumor, muscle, and liver blood volume fractions that depend on experimental parameters such as the vascular contrast concentration. As a solution to the measurement of blood volume in tissues with exchange that is unknown, methods that minimize exchange rate dependence were examined. Simulations that estimated both the accuracy and precision of such methods indicated that both the inversion recovery and the transverse-spoiled gradient echo methods using a "no-exchange" model provide the best trade-off between accuracy and precision.

Changes in regional vascular capacitance during prostacyclin-induced cardiac vagal reflex in pigs.

The purpose of this study was to determine the effects of the prostaglandin I2 (prostacyclin; PGI2)-induced cardiac vagal reflex on intestinal and liver blood volumes and the intestinal vascular pressure-volume (P-V) relationship. In anesthetized pigs, blood volumes were measured by blood-pool scintigraphy. Portal venous pressure was varied by graded inflation of a portal vein constrictor to determine the intestinal vascular P-V relationship. Proximal right coronary infusion of PGI2 at a rate of 0.15 micrograms.kg-1.min-1 for 6 min increased intestinal blood volume by 7.0 +/- 1.2% (P < 0.01, means +/- SE) and shifted the intestinal vascular P-V relationship away from the pressure axis (i.e., a volume increase at a given venous pressure). This change was associated with decreases in liver blood volume and left ventricular end-diastolic pressure by 4.5 +/- 1.2 (P < 0.01) and 17 +/- 2% (P < 0.05), respectively. PGI2 also reduced central venous pressure by 16 +/- 2% from 3.2 +/- 0.5 mmHg (P < 0.05) and portal venous pressure by 7.0 +/- 0.6% from 7.6 +/- 0.6 mmHg (P < 0.05). These responses were abolished by bilateral vagotomy. The results demonstrate that intracoronary PGI2 infusion increases intestinal blood volume. This increase is mediated by a cardiac vagal reflex. The PGI2-induced shift in the intestinal vascular P-V relationship suggests that intestinal blood volume increases by an active change in vascular capacitance, whereas reductions in liver blood volume and left ventricular end-diastolic pressure appear to be due to passive mechanisms related to the shift of blood volume to the intestinal circulation.

Blockade of reflex venous capacitance responses in liver and spleen by hexamethonium, atropine, and surgical section

Since hexamethonium and surgical section have been used to prevent reflex splanchnic capacitance responses, we examined the effectiveness of these procedures in blocking responses to direct stimulation of preganglionic fibres in the splanchnic nerves. Liver blood volume was measured by plethysmography and splenic blood volume by weighing in cats anesthetized by pentobarbital. The cats were adrenalectomized to prevent adrenal catecholamine secretion in response to splanchnic nerve stimulation. Hexamethonium (10 and 20 mg/kg) alone or atropine (1 mg/kg) alone caused only a small variable block of the responses to preganglionic nerve stimulation. A combination of the two drugs essentially produced a complete block of the liver capacitance response, but a significant response still persisted in the spleen. Surgical section of the postganglionic nerve bundles around the hepatic and splenic arteries completely abolished the responses to preganglionic stimulation. It is concluded that a relatively complete block of reflex splanchnic capacitance responses requires either a combination of hexamethonium and atropine or surgical section of the postganglionic nerves.

Changes in hepatic blood volume on galactose and indocyanine green uptake by cat liver.

The liver has important functions as a blood volume reserve and in uptake and metabolism of many substrates. This study examines whether changes in hepatic blood volume modify the uptakes of model substrates galactose and indocyanine green (ICG) in cats anesthetized with pentobarbital sodium. A hepatic venous long-circuit technique with an extracorporeal reservoir was used to control hepatic flow and venous pressure and to allow repeated sampling of arterial, portal, and hepatic venous blood without depletion of the cat's blood volume. Hepatic blood volume was measured by plethysmography. Galactose and ICG were infused intravenously at constant rates for 200 min in each of three series of experiments. The first series were time controls. In the second series, hepatic blood volume was increased by raising hepatic venous pressure. In the third series hepatic blood volume was decreased by hepatic nerve stimulation and infusions of norepinephrine and angiotensin. Hepatic congestion resulted in small increases in blood galactose levels, suggesting mild impairment of hepatic galactose metabolism. Decreases in liver blood volume did not modify hepatic galactose metabolism. Increases in hepatic blood volume facilitated while decreases inhibited ICG uptake, but the effects were small. Sinusoidal velocity and transit time have minor effects on uptake even for protein-bound substrates. In summary, large changes in hepatic blood volume had minor effects on galactose and ICG blood concentrations, suggesting that the metabolic functions of the liver are essentially independent of the blood reservoir function.

Hepatic venous resistance site in the dog: localization and validation of intrahepatic pressure measurements.

Intrahepatic pressure (9.4 +/- 0.3 mmHg; 1 mmHg = 133.32 Pa), measured proximal to a hepatic venous resistance site, was insignificantly different from portal venous pressure (9.6 +/- 0.4 mmHg). This lobar venous pressure is not wedged hepatic venous pressure as it is measured from side holes in a catheter with a sealed tip. Validation of the lobar venous pressure measurement was done in a variety of ways and using different sizes and configurations of catheters. The site of hepatic venous resistance in the dog is localized to a narrow sphincterlike region about 0.5 cm in length and within 1-2 cm (usually within 1 cm) of the junction of the vena cava and hepatic veins. Sinusoidal and portal venous resistance appears insignificant in the basal state and large increases in liver blood volume (histamine infusion or passive vena caval occlusion) or large decreases in liver blood volume (passive vascular occlusion) do not alter the insignificant pressure gradient between portal and lobar venous pressures. Norepinephrine infusion (1.25 microgram X kg-1 X min-1 intraportal) and hepatic sympathetic nerve stimulation (10 Hz) led to a significantly greater rise in portal venous pressure than in lobar venous pressure, indicating some presinusoidal (and (or) sinusoidal) constriction and this indicates that lobar venous pressure cannot be assumed under all conditions to accurately reflect portal pressure. However, most of the rise in portal venous pressure induced by intraportal infusion of norepinephrine or nerve stimulation and virtually all of the pressure rise induced by histamine could be attributed to the postsinusoidal resistance site.(ABSTRACT TRUNCATED AT 250 WORDS)

Mechanism and role of intrinsic regulation of hepatic arterial blood flow: hepatic arterial buffer response.

Hepatic parenchymal cell metabolic status does not control the hepatic arterial blood flow. Portal blood flow is a major intrinsic regulator of hepatic arterial tone. Hepatic arterial blood flow changes so as to buffer the impact of portal flow alterations on total hepatic blood flow, thus tending to regulate total hepatic flow at a constant level. This response is called the "hepatic arterial buffer response." The mechanism of the arterial buffer response seems to depend on portal blood flow washing away local concentrations of adenosine (production may be constant) from the area of the arterial resistance site. If portal flow decreases, less adenosine is washed away and the local concentration rises resulting in arterial dilation. Putative roles. Hepatic clearance of many hormones and endogenous compounds is blood flow limited. Constancy of total hepatic blood flow is crucial to homeostasis, and severe changes in the magnitude of flow can rapidly alter plasma concentrations of such compounds. The buffer may also prevent portal flow changes from severely altering intrahepatic blood pressures and liver blood volume. Pathological implications. If the O2 supply-to-demand ratio becomes too low, as in the case of a hypermetabolic liver (chronic alcohol exposure), a state of tissue hypoxia can exist without producing hepatic arterial dilation. Therapeutic implications. Livers show protection and improved recovery from several toxic agents, including alcohol, if the O2 supply-to-demand ratio can be increased. Arterial dilation by means of intra-arterial or intra-portal adenosine may prove useful.

The comparative effect of administration of substances via the hepatic artery or portal vein on hepatic arterial resistance, liver blood volume and hepatic extraction in cats.

Compounds reaching the liver do so via either the hepatic artery or the portal vein. This paper reports on the effectiveness of administration of compounds into these alternate routes for their effects on the hepatic parenchymal cells, the hepatic arterial resistance vessels (blood flow) and hepatic capacitance (blood volume responses). All tests were done on cats under pentobarbital anesthesia. Perfusion of the parenchymal cell mass was assessed by comparing the hepatic elimination of indocyanine green (ICG) administered via the two vascular routes. The ICG uptake was assessed by measuring relative areas under the hepatic venous outflow curve obtained following bolus injections of ICG into the artery and portal vein. In a separate series, using different methods, the hepatic venous levels reached early (2 min) and later (5 min) during a constant infusion were compared during administration via the two routes and found to be equal. Parenchymal cell functions (ICG extraction, bile salt stimulation of bile flow) indicate that blood from the artery and portal vein supplies the hepatic parenchymal cells equally well. This suggests a well-mixed blood supply prior to exposure of either blood stream to parenchymal cells. Substances being processed by the liver are thus equally well handled if reaching the liver via either the arterial or portal blood stream. This has significance in validating the use of some isolated liver perfusion methods that perfuse only via the portal vein. Access of vasoactive compounds in the two blood streams to hepatic arterial resistance vessels was assessed using electromagnetic flow probes.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of acute and chronic ethanol consumption on hepatic tissue oxygen tension in rats

In vivo hepatic tissue oxygenation was investigated in chronically ethanol-treated rats using micro oxygen electrode and reflectance spectrophotometry. Effect of acute ethanol administration was also studied. Hepatic oxygen tension of rats treated with ethanol chronically (daily ethanol intake, 9∼12 g/kg for 9 months) was very low as compared with that of normal rats, the decrease being comparable to that of rats treated with carbon tetrachloride. The hepatic oxygen tension in normal controls shortly after ethanol ingestion increased from basal level (median, 23 mmHg) to 40∼70 mmHg, while in chronically ethanol-treated rats, the hepatic oxygen tension decreased transiently, followed by a gradual increase, but it still remained low. In CCl 4-treated rats, the hepatic oxygen tension decreased further after the ethanol ingestion. It is concluded that chronic ethanol consumption in rats resulted in hepatic hypoxia with decreased liver blood flow and volume. Also acute ethanol administration does not induce hepatic hypoxia in normal rats, while in rats with injured liver it induces hypoxia.

Contributions of blood drainage from the liver, spleen and intestines to cardiac effects of aortic occlusion in the dog.

By occluding the descending thoracic aorta, blood transferred from the lower to the upper part of the body increases left ventricular end-diastolic volume and maintains stroke volume despite a rise in systolic left ventricular pressure (LVP) of about 60 mmHg. Seventy percent of the blood drained stems from the splanchnic circulation. To examine which splanchnic organs contribute to the cardiac effects, selective occlusions were performed during ultrasonic measurements of spleen and liver dimensions and left ventricular myocardial chord length (MCL) in atropinized, open-chest dogs. Drainage of 15 +/- 2 ml from the spleen accounted for 18 +/- 4% of the increase in end-diastolic MCL, whereas liver dimensions remained unaltered. Similar results were obtained during aortic occlusion at high inotropy (isoproterenol infusion). It was ascertained by occlusion of the coeliac and mesenteric arteries that about 50% of the cardiac response to aortic occlusion was due to drainage from the intestines and the aorta. Liver blood volume could be reduced by combined occlusion of the aorta and portal vein or coeliac and mesenteric arteries and was sensitive to changes in pressure in the inferior vena cava, did not contribute to the cardiac response to aortic occlusion.

Change in liver blood flow and blood content in dogs during direct and reflex alteration of hepatic sympathetic nerve activity.

A mean decrease of 60% in liver blood volume was recorded by a plethysmographic technique during electrical stimulation of the hepatic nerves in anesthetized, vagotomized dogs. A decrease in pressure in the vascularly isolated carotid sinus to 40 mm Hg, from a mean control of 144 mm Hg, decreased liver blood volume by a mean of 16%; arterial blood pressure increased by a mean of 77 mm Hg. Carotid sinus hypotension was accompanied by respective mean increases of 16% and 1.4% in hepatic arterial and portal venous blood flows, and of 45% and 22% in arterial and portal resistances. Increase in sinus pressure to 240 mm Hg increased liver blood volume by a mean of 20%; arterial blood pressure decreased by 90 mm Hg. Sinus hypertension was accompanied by respective mean decreased of 10% and 1.5% in hepatic arterial and portal venous blood flows, and of 44% and 18% in arterial and portal resistances. Interruption of afferent vagal traffic from cardiopulmonary receptors was maximally effective in decreasing liver blood volume at a carotid sinus pressure of 40 mm Hg and was ineffective at carotid sinus pressures greater than 160 mm Hg. Combined withdrawal of carotid and cardiopulmonary vasomotor inhibition decreased liver blood volume by 42%; of this 37% was due to the cardiopulmonary and 63% to the carotid baroreflex. The study showed the canine liver to function as a blood reservoir by active mobilization of a portion of its blood volume.

Liver blood flow and blood volume following chronic phenobarbitone administration.

Mlae rats were ra&ndomly divided into 2 groups one of which received 30 mg/kh phenobarbitone for 4 days i.p. and the other sodium chloride. Liver blood flow was measured 24 hr following the last injection of phenobarbitone or sodium chloride using the radioactive colloidal gold clearance technique. In addition, blood volume, liver weight and extraction of radioactive gold were estimated. Following 4 daily infections of phenobarbitone the body weight and the blood volume of both groups were not significantly different. The liver weight in the phenobarbitone treated groups was 27% higher than that found in the control group. Liver blood flow increased from 22.7 ml/min (92,8 ml/min/kg body weight) to 30.1 ml/min (123.7 ml/min/kg body weight). This increase of 33% was highly significant (p less than 0.005). In contrast, the extraction of radioactive gold was 11% lower in the phenobarbitone treated groups than in the controls. The earlier, semiquanititative finding of increased blood flow using a chronic implanted thermocouple could thus be quantified by the present study.

Liver Volume Estimated by Ultrasonic Scanning before and after Portal Decompression Surgery

In 12 patients with cirrhosis of the liver, determination of the liver volume by ultrasonic scanning and of the galactose elimination capacity (GE) were made before and after portal decompression surgery. The liver volume decreased significantly, with a median decrease of 402 ml (psmaller than 0.01). Also the GE decreased, but relatively less than the liver volume, so that the calculated GE per unit liver volume increased, with a median increase of 5 mg per minute times 100 ml liver volume (psmaller than 0.005). The decrease in liver volume following portal decompression is assumed to be due in part to reduction of liver blood volume, in part to loss of tissue water and fat, and probably to some loss of parenchyma, accounting for a reduction of the GE.

Erythrocyte production in mice infected by the polycythaemia-inducing Friend virus or by the anaemia-inducing Friedn virus.

Summary. The changes induced by infection with the anaemia‐inducing (FVA) or the polycythaemia‐inducing (FVP) strain of Friend virus on PCV, RBC, reticulocyte counts, red‐cell and plasma volume and reticulocyte maturation time were studied in Swiss mice for 7 weeks after viral infection. The data indicated that the increase in total blood volume is mainly due to the augmentation of the spleen and liver blood volume in FVA‐disease, whereas it results from the large numbers of red cells produced by the spleen in FVP‐disease.The daily output of reticulocytes was increased four‐fold in FVA infected mice, and thirty‐fold in FVP infected mice by the 50th day post‐infection. The total redcell production for the duration of the experiment was 3 times normal for the FVA group and 13 times normal for the FVP group. A theoretical estimate of the mean red‐cell lifespan in infected mice gave 8 1/2 days for the FVP‐disease and 22 days for the FVA‐disease as opposed to 40 days for the normal mouse.