Change In Arteriovenous Difference Research Articles

Dependence of diameters and oxygen saturation of retinal vessels on visual field damage and age in primary open-angle glaucoma.

To investigate the interrelationship between the oxygen supply of the retina and its regulation with the severity of primary open-angle glaucoma (POAG). Central retinal artery (CRAE) and vein (CRVE) diameters and oxygen saturation of peripapillary retinal vessels in 41 patients suffering from POAG (64.1 ± 12.9 years) and 40 healthy volunteers (63.6 ± 14.1 years) were measured using the retinal vessel analyzer. All measures were taken before and during flicker light stimulation. The mean retinal nerve fiber layer thickness (RNFLT) was determined by OCT and the visual field mean defect (MD) was identified using perimetry. In glaucoma patients, CRAE (r = -0.48 p = 0.002) and CRVE (r = -0.394 p = 0.014) at baseline were inversely related to MD, while arterial and venous oxygen saturation showed no significant dependence on the severity of the damage. However, the flicker light-induced change in arterio-venous difference in oxygen saturation was correlated with the MD (r = 0.358 p = 0.027). The diameters of arteries and veins at baseline decreased with reduction of the mean RNFLT (arteries: r = 0.718 p < 0.001; veins: r = 0.685 p < 0.001). Vessel diameters showed a strong correlation with RNFLT and MD. This, as well as the reduction of stimulation-induced change in arterio-venous oxygen saturation difference with visual field loss, may be explained by a reduction of the retinal metabolic demand with progressive loss of neuronal tissue in glaucoma.

Etude méthodologique sur la mesure des différences artério-veineuses mammaires chez la vache laitière

The effects of feeding frequency and diet composition on mammary arteriovenous (AV) differences were observed in lactating dairy cows. Two diets with 30 or 70 p. 100 concentrate (table 1) were offered 2 or 8 times daily in limited amounts. Circadian patterns of mammary AV differences in the main blood metabolites and in milk production (table 2) were studied in two cows with an exteriorized carotid. Diet digestibility and ruminal fermentation profiles were studied in two other cows fitted with a rumen cannula (tables 3, 4). 1. Circadian patterns of arterial levels and AV differences in acetate and beta-hydroxybutyrate depended on feeding frequency (fig. 2). With two feedings per day, the arterial levels reached a maximum 4 or 5 hrs after feeding, and the circadian patterns of AV differences were strongly related to those of the arterial levels. With 8 feedings per day, the circadian changes in AV differences were smaller (fig. 2), and their coefficients of variation decreased from 13 to 9 p. 100. On the other hand, packed cell volume and arterial glucose did not show any noticeable circadian changes, even with 2 feedings per day. 2. The mean arterial levels and AV differences in acetate, beta-hydroxybutyrate and most of the essential amino acids (EAA) decreased (-16, -8 and -10 p. 100) (table 5) when the feeding times were increased from 2 to 8 per day. The EAA decreased more with the high concentrate (-19 p. 100) than with the low concentrate (-8 p. 100) diet (table 6). 3. With the "high concentrate" diet, the arterial levels and AV differences in acetate were lower (-25 p. 100), while those of beta-hydroxybutyrate were higher (+13 p. 100), although the ruminal fermentations were not very different. "Continuous feeding" stabilized the AV differences, thus permitting the number of blood samples required to be reduced (50 p. 100). But this technique caused some physiological modifications, and the results obtained are not applicable to the standard practice of two feedings per day.

Myocardial nucleoside and carbohydrate metabolism and hemodynamics during partial occlusion and reperfusion of pig coronary artery

The effect of local ischemia on myocardial metabolism and hemodynamics was studied in open-chested pigs. Coronary artery flow was reduced by 74% with a screw clamp for one hour, after which period the clamp was released. Arterial and local coronary venous samples were taken repeatedly during control, occlusion and reperfusion. During control, the myocardium extracted lactate (20%) and inosine (24%). No or minor arteriovenous differences were measured for glucose, potassium, inorganic phosphate and hypoxanthine. During ischemia, the heart consumed glucose (about 25%); lactate and inosine extraction decreased to minimal values of −126% and −642%, respectively. Hypoxanthine, potassium and inorganic phosphate showed relatively small changes in arteriovenous difference. Extraction patterns approached control values during release. Myocardial oxygen uptake decreased by 68% after occlusion. Immediately following release, uptake returned to control value, but subsequently it fell again by 20 to 30%. Extensive and long-lasting reactive hyperemia was observed during reperfusion. However, flow debt was only partially repaid. Throughout the experiment heart rate increased, and cardiac output and mean aortic pressure decreased. During occlusion, the peak derivative of left ventricular pressure decreased about 24%; peripheral resistance and left ventricular end-diastolic pressure increased 20 to 30%. These changes were only partially reversed during reperfusion. It is concluded that, in addition to changes in lactatemetabolism, myocardial inosine production is a good marker for myocardial ischemia in the pig, because it correlates well with carbohydrate extraction and ventricular function, and the occlusion-induced changes are relatively large.

The buffering behaviour of blood during hypoxaemia and respiratory exchange: Theory

The buffering of the blood during hypoxaemia and during respiratory exchange in the lungs and in the tissues is considered in the presence of factors known to influence the in vivo buffering of CO 2 alone. It is argued that during systemic hypoxaemia or asphyxia the Haldane effect in the circulating blood has a smaller value than it has in vitro, but during respiratory exchange in the lungs and in the tissues, the Haldane effect retains its full in vitro value. Changes in arteriovenous differences can be shown to appear to alter the acid-base characteristics of the arterial blood. It is concluded that the in vivo CO 2 dissociation curve is the dissociation curve of mixed venous blood and that the arterial blood is related to the mixed venous blood through the in vitro dissociation curve.

Gestational changes in arteriovenous differences of oxygen across the uterus of the rhesus monkey

Data on arteriovenous differences of oxygen and pH across the placenta of the rhesus monkey, Macula mulatta, throughout pregnancy are presented. The coefficient of oxygen utilization increased with gestation. The oxygen saturation, oxygen tension, and pH of the uterine venous drainage decreased with increasing gestation.

Studies of Coagulation and Fibrinolysis of Arterial and Venous Blood in Normal Subjects and Patients with Atherosclerosis

In studies of coagulation of the arterial and venous blood of relatively young normal subjects, there were statistically significant arteriovenous differences in some of the tests employed. These differences, however, were not all in the same direction, in that some indicated increased and some decreased coagulation activity of the arterial blood. In patients with coronary heart disease, these arteriovenous differences were absent or less marked. It was suggested that this change in arteriovenous difference in such patients could possibly be attributed to the surface effect of the diseased arterial wall on the coagulation mechanism. It was recognized, however, that a number of other factors could contribute to, or entirely account for, this phenomenon. There was some evidence of increased coagulation activity in the venous blood of patients with coronary heart disease as compared to matched controls. This was indicated by a more rapid generation of thromboplastin with the addition of inosithin (platelet s...

Studies of coagulation and fibrinolysis of the arterial and venous blood in normal subjects and patients with atherosclerosis.

In studies of coagulation of the arterial and venous blood of relatively young normal subjects, there were statistically significant arteriovenous differences in some of the tests employed. These differences, however, were not all in the same direction, in that some indicated increased and some decreased coagulation activity of the arterial blood. In patients with coronary heart disease, these arteriovenous differences were absent or less marked. It was suggested that this change in arteriovenous difference in such patients could possibly be attributed to the surface effect of the diseased arterial wall on the coagulation mechanism. It was recognized, however, that a number of other factors could contribute to, or entirely account for, this phenomenon. There was some evidence of increased coagulation activity in the venous blood of patients with coronary heart disease as compared to matched controls. This was indicated by a more rapid generation of thromboplastin with the addition of inosithin (platelet substitute), and a more rapid generation as well as a greater yield of thromboplastin without the addition of inosithin. Fibrinolytic activity was significantly lower in the arterial blood compared to the venous in both the normal subjects and patients with atherosclerosis. This arteriovenous difference was greater in the atherosclerotic group and it was widely variable. Because of this variability, venous fibrinolysis determinations could not be taken as an indicator of the level of fibrinolytic activity in the arterial blood. Hence, it was suggested that in studies of fibrinolysis as related to atherosclerosis, arterial blood samples should be routinely used. Fibrinolytic activity of the blood in the atherosclerotic group as a whole was lower than that in the normal group on both the arterial and the venous sides. The difference between the two groups was greater in the arterial than the venous blood. In the group with atherosclerosis, the subgroup with coronary heart disease and that with occlusive disease of the peripheral arteries were separately analyzed. The subgroup with coronary heart disease exhibited a significantly lower fibrinolytic activity compared to normal subjects only in the arterial blood, whereas the subgroup with occlusive disease of the peripheral arteries showed a lower fibrinolytic activity in both the arterial and the venous blood. In the subgroup with occlusive disease of the peripheral arteries, it was particularly note-worthy that the younger patients had a very low fibrinolytic activity. It was thought that one could only speculate as to whether this low fibrinolytic activity in such young patients is in any way causally related to the disease process. It appeared that in patients with coronary heart disease the delicate balance of coagulation and fibrinolysis was tipped in the direction of clot formation. It was not clear, however, whether the changes in blood coagulation and fibrinolysis observed in such patients were etiologic in the pathogenesis of the disease process, associated with it, or simply a secondary phenomenon. Moreover, it was recognized that in vitro demonstration of such changes in blood coagulation and fibrinolysis does not necessarily imply in vivo hypercoagulability. No correlation was found between the level of serum cholesterol and plasma fibrinolytic activity.