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One of the key goals of haemodynamic resuscitation is to assess the adequacy between oxygen delivery and oxygen requirements. Despite providing important information, clinical examination, lactate, and central or mixed venous oxygen saturation (ScvO2 and \( {\mathrm{S}}_{\dot{\mathrm{v}}}{\mathrm{O}}_2 \), respectively), in this context, all have their limitations, which may be overcome by the carbon dioxide (CO2)-derived variables. In fact, even if it is not an indicator of anaerobic metabolism, the venoarterial difference in CO2 tension (“ΔPCO2” or “PCO2 gap”) reliably indicates whether blood flow is enough to carry CO2 from the peripheral tissue to the lungs, by considering its clearance. Thus, the PCO2 gap reflects the adequacy of cardiac output according to the metabolic condition. In addition, the ratio of the PCO2 gap with the arteriovenous difference of oxygen content (PCO2 gap/Ca-vO2) might be a marker of anaerobiosis. Compared to \( {\mathrm{S}}_{\dot{\mathrm{v}}}{\mathrm{O}}_2 \) and ScvO2, it remains interpretable if the oxygen extraction is impaired, as it is in the case of sepsis. The main advantage when compared to lactate is that PCO2 gap/Ca-vO2 changes without delay and provides real-time monitoring of tissue hypoxia.

Objective To evaluate retinal oxygen metabolism by retinal oximetry for ocular and CNS diseases in a cross-sectional study of sarcoidosis. Methods Overall 201 eyes from 103 biopsy-verified sarcoidosis patients were included and divided into four groups depending on the organ affection: (i) sarcoidosis without ocular or CNS affection, (ii) ocular sarcoidosis, (iii) CNS sarcoidosis, and (iv) combined ocular and CNS sarcoidosis. Retinal oximetry was obtained and analysed, with the mean retinal arteriolar and venular saturation as well as arteriovenous difference as principal outcomes. Comparison between groups was done in a multi linear regression model adjusted for age, sex, duration of sarcoidosis, best corrected visual acuity and retinal oximetry quality. Results Mean (s.d.) age was 50.5 (13.4) (95% CI: 47.9, 53.1) years and 52.2% were males. Eyes of the combined Ocular/CNS group had a higher retinal arteriovenous difference than eyes of the Non-ocular/no-CNS group (42.1% vs 37.7%, P = 0.012) but did not differ between other groups. Eyes in the four groups (Non-ocular/no-CNS, Ocular, CNS and Ocular/CNS) did not differ according to retinal arterial (94.5%, 93.5%, 93.5% and 94.5%, respectively) or venular (57.5%, 56.4%, 55.0% and 52.5%, respectively) oxygen saturation. Conclusions The results of this study suggest that eyes of sarcoidosis patients with combined ocular and CNS affection have an altered oxygen metabolism indicating a subclinical eye affection that is not recognized by conventional screening methods.

The accumulation of abdominal adipose tissue has long been associated with adverse cardiovascular outcomes. Paradoxically, increased gluteofemoral adipose tissue, which is predominantly subcutaneous fat, seems to play a protective role. There has been significant scientific interest in understanding how abdominal and gluteofemoral depots confer opposing metabolic risks. However, the study of regional adipose physiology in vivo remains challenging. We discuss some of the methodologies used. We focus specifically on the arteriovenous difference technique and present some insights into gluteofemoral adipose physiology.

BACKGROUND The present study was designed to assess the underlying mechanism of decline in effort capacity seen with aging. METHODS We analyzed 250 healthy senior patients (≥65 years) with an ejection fraction ≥60% who underwent a stress echocardiogram test. The seniors (aged 65-94) were divided into 3 equal age groups (groups 1, 2, and 3), and their echo characteristics at rest and peak exercise (measured and calculated) were compared. RESULTS Diastolic function at rest declined significantly (E lateral, E septal, E/E', A) with age, while other rest parameters were similar. There was a significant reduction in peak cardiac output (CO) associated with age (time × age group interaction; P

PURPOSE To investigate changes in retinal oximetry and the diameter of retinal vasculature in patients with chronic kidney disease (CKD) and relationships between retinal vasculature and the estimated glomerular filtration rate (eGFR), provide a scientific basis for the early detection and diagnosis of CKD. METHODS Eighty-three patients with CKD and 103 healthy individuals were included after providing informed consent. All participants were examined using a noninvasive technology (Oxymap Inc., Reykjavik, Iceland) for measuring the arterial (SaO2 ) and venous (SvO2 ) oxygen saturation and the arteriovenous difference in oxygen saturation (Sa-vO2 ). The corresponding retinal vessel diameters of these arterioles (D-A) and venules (D-V) were measured. The eGFR of patients with CKD was calculated from the serum creatinine concentration. RESULTS In general, patients with CKD had higher mean SaO2 values than healthy individuals (100.15 ± 4.68% versus 97.14 ± 4.22%; p

Purpose This study aimed to elucidate the relationship between visual field defects in the upper and lower hemifields and the corresponding oxygen saturation of the retinal vessels in patients with glaucoma. Methods Patients with glaucoma (n = 44) exhibiting more than a 10 dB difference between the upper and lower total deviation (TD) were enrolled in the study. After measuring the retinal vessel oxygen saturation by a non-invasive spectrophotometric retinal oximeter, the hemifields in one eye of each patient were divided into worse (worse TD) and better (better TD) hemifield areas. We additionally evaluated a separate group of 40 patients with glaucoma who exhibited less than a 5 dB difference between the upper and lower TD. Statistical analysis was performed using a Student's t-test. Results A higher mean venous saturation of oxygen (SaO2) was observed in the worse (59.0 ± 8.0%) hemifield compared to the better (55.4 ± 7.2%) hemifield (p

Based on the stoichiometry and thermochemical characteristics of the biosynthesis description it was calculated the energy expenditure necessary for the final stages of biosynthesis of the major milk constituents (lactose, protein and fat). The theoretical analysis indicated that the energy expended for the biosynthesis of fatty acids of milk triglycerides depends on the used precursors’ spectrum. It was supposed that the similar mechanism explains the decrease of the energy efficiency in the milk components synthesis, while milk productivity increases. Another supposition was that simultaneously, there is an increase of the energy expenditure for the homeostatic maintenance.

Purpose To determine normal retinal oxygen saturation (SO2) values measured with retinal oximetry in a multiethnic group of healthy subjects and to evaluate the association of retinal SO2 with demographic and clinical parameters. Methods Retinal oximetry was performed in both eyes of 61 normal healthy subjects. Global and quadrant venous (SvO2) and arterial oxygen saturation (SaO2), arteriovenous difference in SO2, and venular and arteriolar width were measured. The association of SO2 parameters with age, gender, ethnicity, refraction, iris color, history of controlled systemic hypertension, and smoking was analyzed. Results Average SvO2 and SaO2 were 55.3 ± 7.1% and 90.4 ± 4.3%, respectively. All average measurements were comparable in both eyes, both genders, and among ethnic groups. Inferonasal quadrant SaO2 was higher in Asians. Age was associated with decreased SvO2 (β = -0.19; P = 0.001) and SaO2 (β = -0.11; P = 0.003). History of controlled systemic hypertension was associated with an increase in arteriovenous difference in SO2 (β = 3.99; P = 0.013). Conclusion This is the first description of retinal SO2 in healthy, multiethnic subjects. Aging decreases SvO2 and SaO2 and should be accounted for when interpreting retinal oximetry measurements. Other demographic and clinical parameters studied did not seem to significantly influence retinal SO2 measurements.

Purpose. To evaluate the retinal vessel oxygen saturation in central serous chorioretinopathy (CSC) cases among the Chinese. Methods. Relative oxygen saturation of retinal blood vessels was measured in 33 Chinese patients with single-eye CSC using the Oxymap T1 retinal oximeter. The contralateral eyes were the control. The mean saturation of the retinal arteriole (AS) and venule (VS), arteriovenous difference (AVS), and arteriole and venule diameters (AD, VD) was analyzed in the optic disc area and macular region. Results. In the optic disc area, the inferotemporal quadrant (TI) AS (93.2 ± 10.2%) and inferonasal quadrant (NI) VS (61.3 ± 7.3%) were higher in the affected eyes than in the contralateral eyes (88.7 ± 7.7% and 56.9 ± 6.5%) and AVS in NI (36.7 ± 10.4%) decreased compared to the contralateral eyes (41.5 ± 11.2%). The VD in TI was expanded (19.9 ± 2.5 pixels versus 18.1 ± 3.4 pixels). Around the macular region, AS was 93.6 ± 7.6%, higher than in the contralateral eyes (89.5 ± 6.3%). No other significant changes were found. Conclusions. AS increased in the TI, and VS decreased in the NI in the eyes with CSC. In addition, AS also increased around the macular region, suggesting that these are contributors to CSC pathophysiology.

There are several methods for measuring the rate of myofibrillar protein degradation using 3-methylhistidine (3-MeHis) levels in urine, plasma and isolated muscle. However, these methods lack the accuracy of rate measurements. Therefore, it is necessary to develop a new method for determining the rate of myofibrillar protein degradation. We characterized an arteriovenous difference method using 3-MeHis plasma concentration. Rats were fasted overnight and subsequently administered leucine (135 mg/100 g BW) or fed a 20% casein diet. The rate of myofibrillar protein degradation was calculated by multiplying the femoral artery blood flow rate by the arteriovenous difference in 3-MeHis concentrations (vein−artery). The blood was collected from the femoral vein and abdominal aorta. The release of 3-MeHis from hindlimb muscle was significantly suppressed (p

Resume Objectif Evaluer la concordance de l’index cardiaque (IC), du sang veineux mele (SvO 2 ) et de la difference arterioveineuse de contenu en O 2 – C(a–v)O 2 – en chirurgie cardiaque. SvO 2 et IC devraient induire une quantite d’incertitude croissante par rapport a C(a–v)O 2 dans la mesure ou ils ne prennent en compte que partiellement ou pas du tout la composante metabolique. Type d’etude Analyse de variables collectees en routine. Patients Quatre-vingts patients anesthesies et ventiles, en postoperatoire de chirurgie cardiaque. Methodes Realisation simultanee d’un point hemodynamique par Swan-Ganz (SG) a debit continu et un gaz du sang arteriel et veineux mele, en situation stable. Resultats Par deux regressions lineaires : SvO 2 versus C(a–v)O 2 (Reg 1) et IC versus C(a–v)O 2 (Reg 2), nous montrons qu’un IC = 2,2 l/min/m 2 et une SvO 2 = 70 % correspondaient a une C(a–v)O 2 = 5 ml/100 ml. La dispersion, identifiee par la distribution verticale des points autour de la ligne de regression, une fois normalisee, etait 3,2 fois plus grande dans Reg 2 que dans Reg 1. Conclusions La correspondance des valeurs d’IC, de SvO 2 et de C(a–v)O 2 en chirurgie cardiaque est identique a celles presentees dans la litterature chez les patients de reanimation polyvalente. SvO 2 et surtout IC induisent une dispersion tangible des valeurs diminuant leur capacite a evaluer le ratio debit/metabolisme qui est au mieux apprecie par C(a–v)O 2 .

Thirty-three paired indicator/nutrient dilution curves across the mammary glands of four cows were obtained after rapid injection of para-aminohippuric acid (PAH) plus glucose into the external iliac artery. For the measurement of extracellular volume and kinetics of nutrient uptake from indicator dilution curves, several models of solute dispersion and disappearance have been proposed. The Crone-Renkin models of exchange in a single capillary assume negligible washout of solutes from the extracellular space and do not describe entire dilution curves. The Goresky models include a distribution of capillary transit times to generate whole system outflow profiles but require two indicators to parametize extracellular behavior. A compartmental capillary, convolution integration model is proposed that uses one indicator to account for the extracellular behavior of the nutrient after a paired indicator/nutrient injection. With the use of an iterative approach to least squares, unique solutions for nonexchanging vessel transit time μ and its variance σ were obtained from all 33 PAH curves. The average of heterogeneous vascular transit times was approximated as 2σ = 8.5 s. The remainder of indicator dispersion was considered to be due to washout from a well-mixed compartment representing extracellular space that had an estimated volume of 5.5 liters or 24% of mammary gland weight. More than 99% of the variation in the time course of venous PAH concentration after rapid injection into the arterial supply of the mammary glands was explained in an unbiased manner by partitioning the organ into a heterogeneous nonexchanging vessel subsystem and a well-mixed compartmental capillary subsystem.

The objective of this study was to deter- mine whether the porcine mammary gland responds to increasing dietary CP concentration through changes in AA arteriovenous difference (a-v). Sixteen Landrace × Yorkshire lactating sows were provided ad libitum access to one of four isocaloric diets varying in CP con- centration (7.8, 13.0, 18.2, and 23.5 %; as-fed basis). Litters were adjusted to 11 pigs within 48 h of birth. Sows were fitted with catheters in the carotid artery and main mammary vein on d 4. On d 10, 14, 18, and 22 of lactation, arterial and venous blood samples were obtained every 30 min over 6 h. Milk yield was esti- mated on d 11 and 21 using the D2O dilution technique. Final litter sizes on d 21 were 10.3, 11, 9.5, and 11 piglets for sows fed the 7.8, 13.0, 18.2, and 23.5% CP diets, respectively. Piglet ADG tended (P = 0.088) to increase with increasing dietary CP concentration and were 186, 221, 220, and 202 g for sows fed the 7.8, 13.0, 18.2, and 23.5% CP diet, respectively. Daily total milk yield on d 21 (kg milk/d) tended (P = 0.099) to increase, and average milk yield per nursed piglet (kg of milk pig −1 d −1 ) increased (P < 0.05) with increasing CP con- centration and were, on a per-piglet basis, 0.95, 1.19

Maximal O2consumption (V˙o2 max) is lower in individuals with Type 2 diabetes than in sedentary nondiabetic individuals. This study aimed to determine whether the lowerV˙o2 maxin diabetic patients was due to a reduction in maximal cardiac output (Q˙max) and/or peripheral O2extraction. After 11 Type 2 diabetic patients and 12 nondiabetic subjects, matched for age and body composition, who had not exercised for 2 yr, performed a bicycle ergometer exercise test to determine V˙o2 max, submaximal cardiac output, Q˙max, and arterial-mixed venous O2(a-v̄ O2) difference were assessed. Maximal workload, V˙o2 max, and maximal a-v̄ O2difference were lower in Type 2 diabetic patients ( P < 0.05). Q˙maxwas low in both groups but not significantly different: 11.2 and 10.0 l/min for controls and diabetic patients, respectively ( P > 0.05). Submaximal O2uptake and heart rate were lower at several workloads in diabetic patients; respiratory exchange ratio was similar between groups at all workloads.V˙o2 maxwas linearly correlated with a-v̄ O2difference, but not Q˙maxin diabetic patients. These data suggest that a reduction in maximal a-v̄ O2difference contributes to a decreasedV˙o2 maxin Type 2 diabetic patients.

The determination of O2consumption by using arteriovenous O2content differences is dependent on accurate oxyhemoglobin saturation measurements. Because swine are a common experimental species, we describe the validation of CO-oximeter for porcine-specific oxyhemoglobin saturation. After developing a nonlinear mathematical model of the porcine oxyhemoglobin saturation curve, we made 366 porcine oxyhemoglobin saturation determinations with a calibrated blood-gas analyzer and a porcine-specific CO-oximeter. There was a high degree of correlation with minimal variability ( r2= 0.99, SE of the estimate = 5.2%) between the mathematical model and the porcine-specific CO-oximeter measurements. Bland-Altman comparison showed that the CO-oximeter measurements were biased slightly lower (−0.4 vol%), and the limits of agreement (±2 SD) were 0.7 and −1.5 vol%. This is in contrast to a 10–20 vol% error if human-specific methods were used. The results show excellent agreement between the nonlinear model and CO-oximeter for porcine-specific oxyhemoglobin saturation measurements. In contrast, comparison of the porcine-specific oxyhemoglobin saturations with saturations obtained by using human methods highlights the necessity of species-specific measurement methodology.

Purpose.To evaluate the effects of long-term tamponade with silicone oil on retinal saturation.Methods.A total of 49 eyes that received tamponade with silicone oil were included. The patients were divided into 3 groups (3–6 months, 6–9 months, and >9 months) according to the duration of silicone oil tamponade. Retinal oximetry was performed using the Oxymap system before and 2 months after silicone oil removal.Results.The mean retinal oxygen saturation before silicone oil removal was 107% ± 12% in the arterioles and 60% ± 10% in the venules, with an overall arteriovenous difference (AVD) of 47% ± 14%. The AVD in the >9-month group was significantly higher than that in the 3–6-month group (54% ± 16% versus 44% ± 11%,P=0.042). After silicone oil removal, the AVD in the >9-month group was significantly decreased (45% ± 9% versus 54% ± 16%,P=0.009); additionally, the arterioles were significantly wider than before surgery (10.8 ± 0.7 pixels versus 10.4 ± 0.9 pixels,P=0.015).Conclusions.The tamponade with silicone oil for more than 9 months will cause the alterations of retinal saturation and the narrowing of retinal arterioles, which may further interfere with the oxygen metabolism in the retina.

Objectives To investigate the effect of water immersion on oxygen uptake \( V ˙ O 2 \) and central hemodynamic responses during incremental maximal exercise at the same external power output ( P ext ) and recovery on an immersible ergocycle vs. a dryland ergocycle. Design Cross-over design study. Methods Twenty healthy participants (32±7 years; 173±6cm; 71.7±9.7kg) performed maximal incremental exercise tests while pedalling either immersed on immersible ergocycle (Hydrorider ® ) or on dryland ergocycle (Ergoline 800S; Bitz, Germany). Initial P ext of dryland ergocycle protocol was set at 25W and increased by 25W every minute until exhaustion. P ext on immersible ergocycle was controlled by pedalling rate (rpm). Initial rpm was set at 40rpm and was increased by 10rpm until 70rpm and thereafter by 5rpm until exhaustion. Gas exchange and central hemodynamic parameters were measured continuously during exercise and a 5-min recovery period. Reported V ˙ O 2 , stroke volume, cardiac output ( Q ˙ ) and arteriovenous difference (C(a-v)O 2 ) were compared. Results During exercise on immersible ergocycle, V ˙ O 2 and C(a-v)O 2 were lower ( P Q ˙ were higher ( P P ext . Conclusions During exercise and recovery in immersion, \( V ˙ O 2 \) and arteriovenous difference were reduced in healthy young participants, while stroke volume and cardiac output were increased for the same P ext . During the recovery, central hemodynamics responses remained higher in immersible ergocycle.

To test the role of blood flow in tissue hypoxia-related increased veno-arterial Pco 2difference (ΔPco 2), we decreased O2 delivery (D˙o 2) by either decreasing flow [ischemic hypoxia (IH)] or arterial Po 2 [hypoxic hypoxia (HH)] in an in situ, vascularly isolated, innervated dog hindlimb perfused with a pump-membrane oxygenator system. Twelve anesthetized and ventilated dogs were studied, with systemic hemodynamics maintained within normal range. In the IH group ( n = 6), hindlimbD˙o 2 was progressively lowered every 15 min by decreasing pump-controlled flow from 60 to 10 ml · kg−1 · min−1, with arterial Po 2 constant at 100 Torr. In the HH group ( n = 6), hindlimbD˙o 2 was progressively lowered every 15 min by decreasing Po 2 from 100 to 15 Torr, when flow was constant at 60 ml · kg−1 · min−1. LimbD˙o 2, O2 uptake (V˙o 2), and ΔPco 2 were obtained every 15 min. Below the criticalD˙o 2,V˙o 2 decreased, indicating dysoxia, and O2 extraction ratio (V˙o 2/D˙o 2) rose continuously and similarly in both groups, reaching a maximal value of ∼90%. ΔPco 2 significantly increased in IH but never differed from baseline in HH. We conclude that absence of increased ΔPco 2 does not preclude the presence of tissue dysoxia and that decreased flow is a major determinant in increased ΔPco 2.

Error estimates for arteriovenous difference were calculated by two models, a lag time model and a compartmental model, using Tc99m-diethylenetriaminepentaacetic acid (DTPA) plasma clearance curves from 40 subjects and Tc99m-MAG3 (mercaptoacetyltriglycine) curves from 18 subjects. It was found that correcting for the effect of the initial bolus largely cancelled the conventional arteriovenous difference, so that the net error was negligible.

We investigated whether a negative arterial-portal venous (a-pv) glucose gradient, or “portal signal,” can increase net hepatic glucose uptake (NHGU) and decrease muscle glucose uptake at euglycemia as it does at hyperglycemia. Twenty 42-h fasted dogs were studied during a basal and two 120-min euglycemic periods ( period I and period II). Glucagon was maintained at basal levels, and insulin was raised 3-fold (3×Ins, n = 10) or 15-fold (15×Ins, n = 10). During period I, dogs received glucose only peripherally. During period II, one-half of the dogs continued the peripheral infusion; the other one-half received glucose intraportally (4 mg ⋅ kg−1⋅ min−1and reduced peripheral glucose infusion). A negative a-pv glucose gradient was present during intraportal glucose infusion. All 3×Ins and 15×Ins dogs had similar NHGU in period I. In period II, it was 2.1 ± 0.3 (3×Ins) and 2.5 (15×Ins) mg ⋅ kg−1⋅ min−1greater in the presence than in the absence of the portal signal ( P < 0.001). The net glucose fractional extraction data paralleled NHGU. In 3×Ins, but not in 15×Ins, whole body nonhepatic glucose uptake was lower in the presence of the portal signal than in its absence. In conclusion, in hyperinsulinemic, but not hyperglycemic conditions, the portal signal is effective in activating NHGU. The inhibition of nonhepatic glucose uptake, on the other hand, is minimal under euglycemic as opposed to hyperglycemic conditions.

Aims To demonstrate that the linear coefficient of the Q.c-V.O2 relationship is an indice of the tissular oxygen extraction capacity (d(a-v-)O2) in children.

In the clinical setting it has been shown that activation will increase cerebral glucose uptake in excess of cerebral oxygen uptake. To study this phenomenon further, this study presents an experimental setup that enables precise determination of the ratio between cerebral uptake of glucose and oxygen in the awake rat. Global CBF was measured by the Kety-Schmidt technique, and the ratio between cerebral uptake rates for oxygen, glucose, and lactate was calculated from cerebral arterial—venous differences. During baseline conditions, rats were kept in a closed box designed to minimize interference. During baseline conditions CBF was 1.08 ± 0.25 mL·g−1·minute−1, and the cerebral oxygen to glucose uptake ratio was 5.5. Activation was induced by opening the sheltering box for 6 minutes. Activation increased CBF to 1.81 mL·g−1·minute−1. During activation cerebral glucose uptake increased disproportionately to cerebral oxygen uptake, and the cerebral oxygen to glucose uptake ratio was 4.2. The accumulated excess glucose uptake during 6 minutes of activation amounted to 2.4 μmol/g. Activation was terminated by closure of the sheltering box. In the postactivation period, the cerebral oxygen to glucose uptake ratio rose to a maximum of 6.4. This response is exactly opposite to the excess cerebral glucose uptake observed during activation.

We have measured skin and muscle protein kinetics and amino acid (AA) transport in anesthetized rabbits during 1) 64-h fast, 2) AA infusion, 3) AA plus fat emulsion infusion, and 4) AA plus hyperinsulinemia.l-[ ring-13C6]phenylalanine was infused as the tracer, and the ear and hindlimb were used as arteriovenous units to reflect skin and muscle protein kinetics, respectively. Skin protein net balance was not different from zero in all groups, indicating a maintenance of protein mass. In contrast, the muscle net balance differed over a range from −1.6 ± 0.6 after fasting to 0.2 ± 0.2 μmol ⋅ 100 g−1⋅ h−1during hyperinsulinemia. In the skin, 59–66% of intracellular free phenylalanine came from proteolysis, and phenylalanine availability from proteolysis was positively correlated to the protein synthesis rate. In conclusion, normal skin maintains its constant protein mass by efficient reutilization of AAs from proteolysis. In contrast to muscle, skin protein is relatively insensitive to control by nutritional and hormonal factors. Because of the metabolic differences, when limb models are used for muscle protein metabolism, the potential contribution by limb skin should be considered.

We have previously shown that a selective increase of 84 pmol/l in either arterial or portal vein insulin (independent of a change in insulin in the other vessel) can suppress tracer-determined glucose production (TDGP) and net hepatic glucose output (NHGO) by ∼50%. In the present study we investigated the interaction between equal increments in arterial and portal vein insulin in the suppression of TDGP and NHGO. Isotopic ([3-3H]glucose) and arteriovenous difference methods were used in conscious overnight fasted dogs. A pancreatic clamp was used to control the endocrine pancreas. A 40-min basal period was followed by a 180-min test period, during which arterial and portal vein insulin levels were simultaneously and equally increased 102 pmol/l. Hepatic sinusoidal glucagon levels remained unchanged, and euglycemia was maintained by peripheral glucose infusion. TDGP was suppressed ∼60% by the last 30 min of the experimental period. In contrast, NHGO was suppressed 100% by that time. Coincidentally, hepatic glucose uptake (net hepatic [3H]glucose balance) increased significantly (∼4 μmol ⋅ kg−1⋅ min−1). The effects of simultaneous equal increases in peripheral and portal venous insulin were not additive in the suppression of TDGP. However, they were additive in decreasing NHGO as a result of an increase in the uptake of glucose by the liver.

Maeda, Seiji, Takashi Miyauchi, Michiko Sakane, Makoto Saito, Shinichi Maki, Katsutoshi Goto, and Mitsuo Matsuda. Does endothelin-1 participate in the exercise-induced changes of blood flow distribution of muscles in humans? J. Appl. Physiol. 82(4): 1107–1111, 1997.—Endothelin-1 (ET-1) is an endothelium-derived potent vasoconstrictor peptide that potentiates contractions to norepinephrine in human vessels. We previously reported that the circulating plasma concentration of ET-1 is significantly increased after exercise (S. Maeda, T. Miyauchi, K. Goto, and M. Matsuda. J. Appl. Physiol. 77: 1399–1402, 1994). To study the roles of ET-1 during and after exercise, we investigated whether endurance exercise affects the production of ET-1 in the circulation of working muscles and nonworking muscles. Male athletes performed one-leg cycle ergometer exercise of 30-min duration at intensity of 110% of their individual ventilatory threshold. Plasma concentrations of ET-1 in both sides of femoral veins (veins in the working leg and nonworking leg) and in the femoral artery (artery in the nonworking leg) were measured before and after exercise. The plasma ET-1 concentration in the femoral vein in the nonworking leg was significantly increased after exercise, whereas that in femoral vein in the working leg was not changed. The arteriovenous difference in ET-1 concentration was significantly increased after exercise in the circulation of the nonworking leg but not of the working leg, which suggests that the production of ET-1 was increased in the circulation of the nonworking leg by exercise. The present study also demonstrated that the plasma norepinephrine concentrations were elevated by exercise in the femoral veins of both the working and nonworking legs, suggesting that the sympathetic nerve activity was augmented in both legs during exercise. Therefore, the present study demonstrates the possibility that the increase in production of ET-1 in nonworking muscles may cause vasoconstriction and hence decrease blood flow in nonworking muscles through its direct vasoconstrictive action or through an indirect effect of ET-1 to enhance vasoconstrictions to norepinephrine and that these responses may be helpful in increasing blood flow in working muscles. We propose that endogenous ET-1 contributes to the exercise-induced redistribution of blood flow in muscles.

OBJECTIVE To review the findings and discuss the implications of jugular venous bulb oxygenation monitoring in children with severe traumatic brain injury. DESIGN A critical appraisal of Perez et al, Jugular venous oxygen saturation or arteriovenous difference of lactate content and outcome in children with severe traumatic brain injury. FINDINGS Two episodes of jugular venous bulb desaturation and abnormal values of arteriovenous difference in lactate content are associated with poor neurologic outcome in children with severe traumatic brain injury-risk ratio 6.6 (95% confidence interval, 1.5-29.7) and risk ratio 17.6 (95% confidence interval, 2.5-122.5), respectively. This confirms the findings of previously reported adult studies. CONCLUSIONS This study is the first to demonstrate that jugular venous monitoring may aid in predicting the neurologic outcome of children with severe traumatic brain injury. More studies need to be performed (particularly on safety) before adopting jugular venous bulb oxygenation monitoring as a prediction tool or, ultimately, as a therapeutic intervention to help manage and improve outcome for children with severe traumatic brain injury.

The normal rate of blood lactate accumulation during exercise is increased by hypoxia and decreased by hyperoxia. It is not known whether these changes are primarily determined by the lactate release in locomotory muscles or other tissues. Eleven men performed cycle exercise at 20, 35, 50, 92, and 100% of maximal power output while breathing 12, 21, and 100% O2. Leg lactate release was calculated at each stage of exercise as the product of femoral venous blood flow (thermodilution method) and femoral arteriovenous difference in blood lactate concentrations. Regression analysis showed that leg lactate release accounted for 90% of the variability in mean arterial lactate concentration at 20-92% maximal power output. This relationship was described by a regression line with a slope of 0.28 +/- 0.02 min/l and a y-intercept of 1.06 +/- 0.38 mmol/l (r2 = 0.90). There was no effect of inspired O2 concentration on this relationship (P > 0.05). We conclude that during continuous incremental exercise to fatigue the effect of inspired O2 concentration on blood lactate accumulation is principally determined by the rate of net lactate release in blood vessels of the locomotory muscles.

1. Previous evidence has suggested that fluid is extracted from the blood during its passage through the splenic circulation. In order to further investigate this phenomenon, flow probes were placed around the splenic artery and vein of rats. Splenic blood flow and mean arterial blood pressure were measured immediately after surgery, while the rats were still anaesthetized. Five days later, the measurements were repeated first in conscious rats, and then after administering sodium pentobarbitone. Final measurements were made in the conscious animals at day 10 post surgery. 2. Splenic arterial blood flow was lowest at the time of surgery. It had doubled by day 5, and remained stable thereafter at about 8 ml min-1. Splenic venous blood flow also increased after surgery, but less so than the arterial flow, so that the arteriovenous difference had increased to 2.0 +/- 0.4 ml min-1 by day 5. 3. In response to sodium pentobarbitone (20 mg I.V.), there was a transient fall in splenic arterial blood flow from 6.7 +/- 0.9 to 4.9 +/- 0.7 ml min-1. There was no significant change in the arteriovenous difference of blood flow. 4. In conclusion, we have shown that splenic blood flow is considerably higher than previously reported. We have also revealed a significant new path for fluid efflux from the intravascular space; at least 25% of fluid volume flowing into the splen is removed from the circulating blood. 5. Although anaesthesia modulates splenic blood flow, the changes are not as pronounced as those observed in the acute surgically prepared animal.