Umbilical artery pulsatility index and placental vascular resistance during acute hypoxemia in fetal lambs

The effect of hypoxemia on the pulsatility index (PI) of the umbilical artery flow velocity waveform and placental vascular resistance was studied. Fetal hypoxemia was induced by maternal breathing of a low-oxygen gas mixture. Umbilical venous blood flow was measured with an electromagnetic flowmeter. Placental vascular resistance (PVR) was defined as the ratio perfusion pressure (mean arterial pressure minus umbilical venous pressure) and umbilical blood flow. Umbilical artery velocity waveforms were obtained by a 5-MHz pulsed Doppler device around one umbilical artery in 4 lambs and by a transcutaneous 4-MHz continuous wave Doppler transducer in 3 lambs. Fetal arterial oxygen content was lowered from 2.28 +/- 0.18 to 0.93 +/- 0.15 mM (p less than 0.05), while pCO2 and pH remained unchanged. Control values of the hemodynamic variables were compared with values during deepest hypoxemia. Fetal heart rate, mean arterial and umbilical venous pressure, PVR and the umbilical artery PI did not significantly change, whereas umbilical blood flow increased from 436 +/- 64.7 to 491 +/- 65.9 ml/min (p less than 0.05) during deepest hypoxemia. Individual regression analysis, however, showed a significant inverse correlation of umbilical venous pressure whereas PVR had a positive correlation with actual oxygen content. It is concluded that acute fetal hypoxemia slightly decreases PVR, but does not affect the umbilical artery PI in sheep. Decreasing fetal oxygenation is associated with an increase in pressure in the umbilical vein.     

Assessment of the hepatic arterial and portal venous blood flows during pregnancy with Doppler ultrasonography

Purpose: The aim of this study was to evaluate whether the dual hepatic blood supply is altered in healthy pregnant women compared with that in nonpregnant women. Materials and methods: Flow waveforms in common hepatic artery and portal vein were obtained in 67 healthy pregnant women at 10–40 weeks gestation and 22 nonpregnant women by using Doppler ultrasonography. Results: In the nonpregnant group, the mean (SD) hepatic arterial blood flow, portal venous blood flow, and total liver blood flow were 0.57 (0.31) L/min, 1.25 (0.46) L/min, and 1.82 (0.63) L/min, respectively. In the healthy pregnant group, the portal venous blood flow and total liver blood flow significantly increased after 28 weeks gestation. However, the hepatic arterial blood flow remained unchanged during pregnancy. There was no relationship between the hepatic arterial blood flow and the portal venous blood flow. Conclusion: The results demonstrated that the hepatic perfusion increased during third trimester compared to nonpregnant level. Because the hepatic arterial blood flow remained unchanged during pregnancy, major determinant of the increase in the hepatic perfusion was the portal venous return. The data suggest that the hepatic arterial and portal venous vascular territories have regulatory mechanisms that allow for independent changes during pregnancy. Received: 8 January 2001 / Accepted: 22 February 2001     

Hemodynamic changes after hepatectomy in rats studied with radioactive microspheres

It has been difficult to measure hepatic arterial blood flow and portal venous flow simultaneously, especially in small animals. Radioactive microspheres were used in this experiment to quantitate splanchnic hemodynamics after hepatectomy in rats. With a reference sample technique, a certain amount of radioactive microspheres was injected into the left ventricle. The reference sample was withdrawn from the femoral artery at a constant rate. The animal was killed with a bolus of saturated KCl. The kidneys and splanchnic organs were removed and weighed. The radioactivity of each organ was determined using a gamma scintillation counter. Organ blood flow was calculated by the following formula: [formula: see text] Immediately after partial hepatectomy, a decreased cardiac index from 32.31 +/- 10.12 to 23.44 +/- 3.21 ml/(min x 100g body weight) (p less than 0.05), decreased hepatic arterial blood flow from 0.40 +/- 0.12 to 0.33 +/- 0.03 ml/(min x g liver) (p less than 0.05), increased portal venous inflow from 0.90 +/- 0.30 to 2.20 +/- 0.26 ml/(min x g liver) (p less than 0.05) and increased total hepatic blood flow from 1.30 +/- 0.39 to 2.53 +/- 0.26 ml/(min x g liver) (p less than 0.005) were observed. With an intrasplenic injection of an additional amount of radioactive microspheres, the ratio of lung/(lung + liver) radioactivities indicated the degree of portal systemic shunt (PSS). Though the portal pressure was elevated after hepatectomy (8.80 +/- 0.7 vs 11.9 +/- 1.7 cm H2O, p greater than 0.05), the extent of PSS was negligible (0.02 +/- 0.01% vs 0.03 +/- 0.01%, p greater than 0.05). The radioactive microspheres with the reference sample technique is a simple, rapid, reliable and reproducible method for investigating the hemodynamic changes following partial hepatectomy.     

Uterine vascular resistance during compression of the umbilical arterial and/or venous circulation in sheep

Total umbilical cord occlusion and selective occlusion of the umbilical arteries and veins is associated with changes in uterine blood flow. In the present study, the resistance to uterine blood flow during selective occlusions of the umbilical arteries and/or veins was analysed in five chronically instrumented pregnant sheep in the last third part of pregnancy. An occluding device which allows separate occlusion of umbilical veins and arteries was applied to the umbilical cord. Median uterine artery blood flow was measured using an electromagnetic flow meter. Maternal pressures were measured in a branch of the uterine artery and vein. Two occlusions of the umbilical veins and/or arteries with a duration of 30-60 s were performed in each animal. Selective occlusion of the umbilical arteries resulted in a small increase in uterine blood flow from 637 +/- 79 ml/min during control toward 664 +/- 77 ml/min at the end of occlusion (p less than 0.05). Uterine perfusion pressure (uterine arterial pressure - uterine venous pressure) did not change. No changes were observed in calculated uterine vascular resistance (Poiseuille equation). Selective occlusion of the umbilical veins on the other hand caused a decrease in uterine blood flow from 617 +/- 75 ml/min during control to 546 +/- 69 ml/min at the end of occlusion (p less than 0.001), and a return to control value at 1 min after occlusion. The uterine perfusion pressure increased from 40.1 +/- 6.8 mmHg during control to 42.8 +/- 7.0 mmHg at the end of occlusion (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Fetal hypertension induced by norepinephrine infusion and umbilical artery flow velocity waveforms in fetal sheep

This study was designed to examine the effects of fetal hypertension on the umbilical artery pulsatility index. Fetal arterial blood pressure and umbilical venous pressure were measured in eight sheep, 3 to 5 days after surgery. Umbilical blood flow was measured with an electromagnetic flowmeter around the common umbilical vein. Umbilical artery flow velocity waveforms were obtained either by an indwelling 5 MHz pulsed Doppler device (n = 4) or transcutaneously by a 4 MHz continuous-wave Doppler device (n = 4). Fetal blood pressure was raised by intravenous infusion of norepinephrine 10 micrograms/min during 5 minutes. Norepinephrine infusion resulted in elevated arterial and umbilical venous pressures, accompanied by a bradycardia during the first 3 minutes. Umbilical blood flow, calculated placental vascular resistance, and umbilical artery pulsatility index did not change. After atropine administration, the norepinephrine-induced elevated arterial and umbilical venous pressures were accompanied by tachycardia, increased umbilical blood flow, and no change in placental vascular resistance and umbilical artery pulsatility index. It is concluded that fetal arterial hypertension provoked by norepinephrine infusion has no effect on placental vascular resistance, umbilical blood flow, and umbilical artery pulsatility index.     

Hepatic hemodynamics after chronic obstruction of the biliary tract in the dog

Hepatic blood flow was measured in 12 dogs before and two weeks after obstruction of the bile duct (BD) or sham operation, using the electromagnetic flowmeter technique. Eight dogs with obstructed BD revealed an 41 per cent decrease in total hepatic blood flow caused by an approximately equal percentage decrease in both hepatic arterial (HA) and portal venous (PV) flow, a decrease in arterial blood pressure, an increase in PV vascular resistance and little change in hepatic oxygen consumption. Four sham operated dogs showed minimal hemodynamic response. A dual mechanism for the hepatic hemodynamic consequences of chronic biliary obstruction is suggested: Decreased HA blood flow associated with diminished blood pressure and reduced PV blood flow resulting from raised intrahepatic PV vascular resistance.     

Parathyroid hormone reduces acute ischemic injury of the myocardium

Synthetic parathyroid hormone (PTH), particularly the molecular fragment containing amino acids one to 34 (1-34), has been shown to produce coronary vasodilation and systemic vasodilation without tachycardia. On this basis, we tested the hypothesis that PTH(1-34) would favorably affect oxygen balance in acutely ischemic myocardium and reduce the extent of injury after coronary occlusion. Experiments were done upon the left anterior descending coronary artery which was ligated through a thoracotomy in anesthetized dogs subjected to ligation of the left anterior descending coronary artery. After 30 minutes of ischemia, the dogs were randomly assigned to either a group which received an intracoronary infusion of 0.008 nanomoles per kilogram of body weight per minute of PTH (1-34) for ten minutes at intervals of 30 minutes or a control group which received intracoronary saline solution. PTH(1-34) increased circumflex artery blood flow 290 +/- 62 per cent (p less than 0.005) and coronary venous return from the ischemic area 190 +/- 12 per cent (p less than 0.005) while reducing mean arterial pressure 12.5 +/- 1.7 per cent (p less than 0.05) without a change in the heart rate. These hemodynamic changes resulted in a 54.3 +/- 3.7 per cent (p less than 0.005) decrease in ischemic myocardial oxygen extraction and a reduction of infarct size (25 +/- 5 per cent of myocardium at risk in treated versus 75 +/- 10 per cent in the control group). It is concluded that PTH given after coronary artery occlusion increases collateral blood flow and oxygen supply to the ischemic myocardium while reducing oxygen requirements. Thus, PTH may offer significant protection for the acutely ischemic myocardium.     

Behavior of the portal vein system in man after laparotomy.

At the end of an abdominal operation, a Teflon catheter was inserted into the portal vein, where it remained for nine days. Thus, blood samples could be withdrawn for analyses, and pressures could be recorded. The investigations were carried out in 41 patients who had a gastric or intestinal operation and had an uncomplicated postoperative course. The pressures in the portal vein and the arterioportal oxygen content difference were constant with 7 to 8 millimeters of mercury and by 2 volume per cent, respectively, during the period of all nine postoperative days. The pressure gradient between portal and central veins was about 6 millimeters of mercury. By infusing 350 to 500 milliliters of dextran 60 on day one or two postoperatively, the cardiac output was elevated about one-third, the central venous pressure increased from 0.9 to 4.9 millimeters of mercury and the portal venous pressure increased from 7.8 to 9.7 millimeters of mercury. This means that the pressure difference between the portal and central veins diminished. Simultaneously, the oxygen content difference between the systemic and pulmonary artery decreased from 4.7 to 3.3 volume per cent and between the systemic artery and portal vein, from 1.8 to 1.3 volume per cent. By assuming a constancy of the oxygen consumption in the region of the mesenteric circulation during infusion, it can be calculated from the behavior of the arterioportal oxygen content difference that the flow increase in the portal vein nearly equals that of cardiac output. The physical transhepatic resistance decreased about 50 per cent.     

Effects of amrinone and dopamine on uterine blood flow and vascular responses in the gravid baboon

Amrinone is a bipyridine derivative with positive inotropic and vasodilator properties. We investigated its effects on uterine and iliac artery blood flow, blood pressure, and heart rate in 10 acutely instrumented gravid baboons. Amrinone was compared with dopamine, infused systemically or regionally via the common iliac artery. When given intravenously at a constant rate of 40 micrograms/kg/min, amrinone produced a slight increase in iliac artery blood flow but did not significantly alter mean arterial pressure, heart rate, or uterine artery blood flow. Dopamine at an intravenous dose of 40 micrograms/kg/min produced a mean (+/- SD) 49.2% +/- 18.7% increase in mean arterial pressure (p less than 0.01) and a 84.2% +/- 56.1% increase in uterine vascular resistance (p less than 0.01), but caused no changes in heart rate, uterine artery blood flow, or iliac artery blood flow. Regional infusion of amrinone at the rate of 25 micrograms/kg/min produced a significant increase in iliac artery blood flow (p less than 0.01) without changing uterine artery blood flow, heart rate, or mean arterial pressure. Regional infusion of dopamine at concentrations of 2.5 to 25 micrograms/kg/min produced decreases in flow (p less than 0.01) and increases in resistance (p less than 0.01) in the uterine and iliac vascular beds. We conclude that amrinone dilates the vascular bed of the external iliac artery, but has no remarkable effect on the uterine vascular bed. Dopamine increases uterine vascular resistance and may impair uteroplacental perfusion.     

3D visualisation and quantification by microcomputed tomography of late gestational changes in the arterial and venous feto-placental vasculature of the mouse

This study evaluates microcomputed tomography (micro-CT) as a method to obtain quantitative three-dimensional (3D) information on the arterial and venous vasculature of the mouse placenta. Surface renderings at embryonic days (E) 13.5, 15.5, and 18.5 (full term) revealed that the arterial and venous vasculature branched within the chorionic plate whereas only the arterial vasculature deeply penetrated the placenta. Umbilical vessel diameters measured by micro-CT did not significantly differ from those measured non-invasively in vivo by ultrasound biomicroscopy. Variability in umbilical diameters, and surface area and volume measurements of arterial and venous vascular trees due to experimental error was low relative to biological variability, and significant inter-litter differences within gestational ages were detected. Furthermore, umbilical vessel diameter increased significantly and incrementally to an arterial diameter of 0.631+/-0.009 mm and a venous diameter of 0.690+/-0.018 mm at E18.5. Umbilical vein diameter was 3-9% greater than the artery, and both were significantly correlated with embryonic body weight (R> or =0.96). Surface area and volume were determined for vessels greater than the minimum resolvable diameter of 0.03 mm which therefore excluded capillaries. Arterial surface area and volume were unchanged from E13.5-15.5 but then more than doubled at E18.5 (to 170+/-13 mm(2) and 7.2+/-0.8mm(3), respectively). Venous surface areas and volumes changed similarly with development although surface areas were lower than their arterial counterparts. We conclude that micro-CT has sufficient accuracy and precision to quantify late gestational changes in the 3D structure of the arterial and venous vasculature of the mouse placenta.     

Agonal hepatic arterial vasospasm

The effect of donor pretreatment with Dibenzyline (phenoxybenzamine) on hepatic arterial vasospasm was studied in a porcine asphyxia model. Nine pigs underwent hepatectomy without pretreatment, while six were given 2 milligrams per kilogram of Dibenzyline prior to hepatic dissection. Hepatic arterial blood flow was monitored with an electromagnetic flow probe, and after cardiac arrest, arteriograms of the hepatic circulation were obtained. Hepatic arterial vasospasm occurred in seven of the pigs in group 1 and in only one of group 2 (p less than 0.05). Agonal hepatic arterial blood flow remained constant (415 +/- 30 milliliters per minute) in pretreated pigs during asphyxia, but was markedly reduced (98.6 +/- 63.3 milliliters per minute) in nonpretreated pigs (p less than 0.05). Results of this study demonstrate the agonal occurrence of hepatic arterial vasospasm and its prevention with Dibenzyline. Donor pretreatment with alpha-adrenergic antagonists may be indicated in clinical organ procurement to prevent agonal arterial vasospasm and its potentially adverse effect on early hepatic allograft function.     

Insulin, glucagon and glucose in the regeneration response of the liver

The effects of intraduodenal glucose load on the hepatic uptake of insulin, glucagon and glucose after a 70 per cent hepatectomy were studies in anesthetized dogs. Dogs without a hepatectomy served as the control study. Data were derived from plasma concentrations in the portal vein, aorta and hepatic vein with simultaneous portal vein and hepatic artery plasma flow measurements. The concentrations of glucose in the arterial blood of dogs after a hepatectomy were less than those for the controls throughout the study, while insulin and glucagon concentrations showed no differences between the groups. Hepatic uptakes of insulin, glucagon and glucose per gram of liver perfused were significantly greater in the hepatectomy group and occurred because the amounts of these substances reaching the liver remnant were the same as those for the controls. The increased uptake of insulin and glucagon after partial hepatectomy may reflect increased binding of these hormones to the liver cell receptors, by which hepatic regeneration is induced. Increased glucose uptake could serve as the substrate for the accelerated anabolic processes.     

Quantification of the capacity of the liver to remove ammonia from the circulation of dogs with portacaval transposition.

To quantitate the ammonia that the liver removes from the circulation and to investigate the distribution of this substance during and after an exogenous ammonia load, ten dogs with portacaval transposition were studied by placing catheters in the hepatic and portal veins through the external jugular vein, in the portal vein going to the liver and in the infrarenal vena cava through the femoral vein. A catheter also was inserted into the femoral artery. Blood ammonia levels were measured in each catheter, then an infusion of ammonium sulfate, 0.7 milligram per minute per kilogram for 45 minutes through the infrarenal vena cava, was given continuously. All other catheters were simultaneously sampled at 15 minute intervals during the infusion and for a 45 minute period after it was stopped. By using a continuous infusion of indocyanine green and Fick's formula, the total hepatic blood flow was estimated in five of the ten dogs. Thus, knowing the amounts of ammonia in the hepatic inflow and outflow tracts and relating them to the estimated hepatic blood flow, the hepatic extraction ratios of ammonia were calculated. The estimated hepatic blood flow changed minimally before and after portacaval transposition. The blood ammonia levels in all sites where samples were obtained, except for the hepatic vein, followed uniform patterns. In the femoral artery, the portal vein and liver-portal vein now anastomosed to the infrahepatic infrarenal vana cava-the blood ammonia levels during the period of infusion increased by at least 90 per cent. When the infusion was discontinued, the blood ammonia levels decreased but remained elevated, from 30 to 60 per cent of the preinfusion blood ammonia levels. Blood ammonia levels in the hepatic veins increased some but never exceeded 56 micrograms per 100 milliliters. It also was found that the liver removes 80 to 87 per cent of the ammonia reaching it by means of the urea cycle; the other 13 to 19 per cent of the ammonia returns to the circulation through the hepatic veins and is distributed into the circulation, causing the blood ammonia levels to remain higher for at least 45 minutes after the ammonia infusion load was discontinued than the preinfusion control levels in all the sites where samples were obtained.     

Human umbilical arterial and venous progesterone concentrations: effect of fetal sex, weight, and mode of delivery

Umbilical venous and umbilical arterial progesterone concentrations were determined in 99 pregnancies by radioimmunoassay. The mean +/- SE plasma progesterone in the umbilical vein was 1295 +/- 73 ng/ml, and in the umbilical artery it was 520 +/- 38 ng/ml with an arterio-venous difference of 775 +/- 58 ng/ml and a vein:artery progesterone ratio of 3.6 +/- 0.3. The secretion rate of progesterone into the fetal compartment was calculated to be 84 mg/24 hr. There was no significant difference in these parameters between male and female fetuses, fetal weight, mode of delivery, Apgar score, and duration of labor. It was therefore concluded that the fetal genotype and stress on the fetus did not appear to significantly affect fetal extraction and utilization of progesterone.     

Management of portal venous thrombosis in hepatic transplant recipients

Portal venous thrombosis in hepatic transplant candidates is considered a relative contraindication to transplantation. In addition to thrombectomy, which is often technically impossible, donor portal venous arterialization or extra-anatomic venous bypass have been described. Two patients who underwent portal venous resection and subsequent anatomic reconstruction are presented herein. In the first patient, a graft with donor common iliac vein was interposed, and in the second, the donor portal vein was long enough to be anastomosed to the mesentericosplenic venous confluens. One patient is well 12 months after transplantation with patent portal vein and the other died of fungal sepsis after rejection treatment (the portal vein being open and unobstructed at autopsy).     

Blood flow velocity waveforms in large maternal and uterine vessels throughout pregnancy and postpartum: a longitudinal study using Duplex sonography

Summary. Blood flow velocity waveforms in large maternal and uterine vessels were measured longitudinally from 16 weeks gestation onwards until 12 weeks postpartum in 21 singleton pregnancies by duplex sonography. In the maternal carotid artery, time average mean velocity (TAVmean) did not show significant changes. In both the femoral artery and vein, however, significant changes were observed. In the femoral artery, TAVmean and systolic maximum velocities decreased with advancing gestation. In the femoral vein, TAVmean remained constant throughout pregnancy and was lower than postpartum. The resistance index in the uterine arteries decreased with advancing gestation and increased after delivery. Among many factors contributing to femoral arterial blood flow velocity changes in pregnancy, we suggest that a major one is the increase in uterine blood flow. Reduction in venous femoral blood flow velocity and increase in the femoral vein diameter might be associated with the common occurrence of venous disorders in pregnancy.     

Blood flow velocity waveforms in large maternal and uterine vessels throughout pregnancy and postpartum: a longitudinal study using Duplex sonography

Blood flow velocity waveforms in large maternal and uterine vessels were measured longitudinally from 16 weeks gestation onwards until 12 weeks postpartum in 21 singleton pregnancies by duplex sonography. In the maternal carotid artery, time average mean velocity (TAVmean) did not show significant changes. In both the femoral artery and vein, however, significant changes were observed. In the femoral artery, TAVmean and systolic maximum velocities decreased with advancing gestation. In the femoral vein, TAVmean remained constant throughout pregnancy and was lower than postpartum. The resistance index in the uterine arteries decreased with advancing gestation and increased after delivery. Among many factors contributing to femoral arterial blood flow velocity changes in pregnancy, we suggest that a major one is the increase in uterine blood flow. Reduction in venous femoral blood flow velocity and increase in the femoral vein diameter might be associated with the common occurrence of venous disorders in pregnancy.     

Pulsatility index and its relationship to placental vascular resistance during partial umbilical venous occlusion: a study in fetal lambs

To study the effect of partial occlusion of the umbilical vein upon umbilical artery velocity waveforms, 4 chronically instrumented pregnant sheep have been subjected to measurement of the relevant haemodynamic parameters, i.e. the arterial inflow pressure, placental venous outflow pressure (Pv), venous blood flow (Quv) and arterial blood velocity waveform. The pulsatility index (PI) of the velocity waveform increases significantly for a Quv reduction of 40% or more (p less than 0.05). The Quv correlates well with the PI (r = 0.61) and the Pv (r = 0.71). The correlation between fetal heart rate (FHR) and Quv, FHR and PI is 0.75 and 0.64, respectively. The placental vascular resistance (R) can be calculated using the Poiseuille equation. There is not significant correlation between R and PI. It can be concluded that the increase in PI in the umbilical artery during partial venous occlusion is very likely caused by an increased Pv rather than a change in R.     

Application of rat in situ single-pass intestinal perfusion in the evaluation of presystemic extraction of indinavir under different perfusion rates

BACKGROUND/PURPOSE: First-pass effect has been an important concern for oral pharmaceuticals. An in vivo system was developed for measuring different concentrations of pharmaceuticals in the portal vein and hepatic vein (via the inferior vena cava) for delineating presystemic metabolism under different perfusion rates by using indinavir as an exemplary agent. METHODS: An in situ single-pass intestinal perfusion technique was modified from previous studies to concomitantly obtain portal and hepatic venous bloods. Portal and hepatic venous samples were simultaneously taken from rats at appropriate time points using the perfusion model of 1 mg/mL indinavir at flow rates of 0.05, 0.1, 0.5 and 1.0 mL/min. The indinavir concentrations were assayed by binary-gradient high-pressure liquid chromatography with UV detection. RESULTS: The mean indinavir concentrations in portal vein concentration-time profiles at different perfusion times under various flow rates were all higher than those obtained for hepatic veins. At flow rates of 0.5 and 1.0 mL/min, in particular, the area under the curve (AUC) and maximal concentration (Cmax) of indinavir absorption were significantly different between portal veins and hepatic veins (p < 0.05), indicating considerable hepatic involvement in the presystemic extraction of indinavir. The system also has potential for use when estimating the hepatic extraction ratio (E(H)) and hepatic clearance (Cl(H)). CONCLUSION: This in vivo approach could provide another useful tool for improving our basic understanding of the absorption kinetics and hepatic metabolism of pharmaceuticals under development and facilitating the clinical application of such.     

Deleterious effects of testicular venous occlusion in young rats

To determine the differences between testicular arterial and venous obstruction, the spermatic artery or vein, or both, were occluded for varying periods of time in young rats. Two months later, at the conclusion of the study, the testes were examined. Histologic degeneration after vascular obstruction was graded by a modified Johnsen's tubular biopsy score (TBS). The testicular concentrations of enzymes (lactic dehydrogenase and sorbitol dehydrogenase), known to decrease with testicular injury, were measured. TBS and seminiferous tubule diameter (STD) were found to decrease significantly after two hours of vascular occlusion and were similar regardless of whether the obstruction was produced by occlusion of arterial inflow or venous drainage, or both. Testicular concentration of enzymes decreased significantly after permanent ligation of the spermatic artery and vein, but decreased minimally when the vascular obstruction lasted less than 120 minutes. Testicular injury produced by venous occlusion was equally severe and occurred as rapidly as injury produced by arterial or combined arteriovenous occlusion. No significant injury was noted in the contralateral testes in any group.