Terminal Veins Research Articles

Quality control of perfusion: Monitoring venous blood oxygen tension to prevent hypoxic acidosis

The long-held belief that venous oxygen tension mirrored tissue oxygen tension became suspect in the 1960s when new instrumentation consistently showed that tissue oxygen tension was 10 to 30 torr less than venous oxygen tension. Moreover, a countercurrent of oxygen exchange between terminal arteries and veins was shown to exist. Despite this conflict in scientific theory, however, monitoring venous oxygen tension as a means to control hypothermic cardiopulmonary bypass has been repeatedly urged, since myocardial acidosis is clearly extremely detrimental. This study of the relationship between venous oxygen tension during hypothermic bypass and a concurrent increment in lactacidemia yields strong objective evidence to support the use of on-line venous oxygen tension monitoring to guide perfusion. In a random series of 36 patients, venous blood samples were drawn at five preselected intervals during operation and were analyzed for pH, carbon dioxide tension, oxygen tension, lactic acid, hematocrit, and base excess. Analysis of the data revealed that venous pH and base excess showed no correlation to venous oxygen tension. However, lactic acid showed a strong correlation with venous oxygen tension, with a correlation coefficient of 0.4338 at a confidence level of p less than 0.0001. If the patients were divided into three clinically pertinent groups based on the lowest venous oxygen tension recorded, a strong relationship between venous oxygen tension and lactic acid emerged. If the lowest measurement of venous oxygen tension was greater than 35 mm Hg (group A), the mean rise in lactic acid was only 0.12 microns/ml. If the lowest measurement was between 30 and 34 mm Hg (group B), the mean rise was 0.64 microns/ml. Whereas, if any venous oxygen tension value fell below 30 mm Hg (group C), the mean rise in lactic acid was 2.56 microns/ml. Analysis of variance showed that group C values were significantly different from groups A and B values (p less than 0.0002). A scientific hypothesis relating venous oxygen tension to adequate tissue oxygenation is proposed. Use of venous oxygen tension monitoring with the goal to maintain the level above 35 mm Hg is strongly supported by this study.

Subcutaneous transposition of the spleen enhances the survival rate following 90% hepatectomy in rats.

The effects of subcutaneous transposition of the spleen (STS) on the survival rate following 90% hepatectomy were investigated in rats. The survival rate was significantly higher in the STS group than in the non-STS group. Light microscopy enabled us to note that congestion in the terminal portal veins and sinusoids occurred either slightly earlier or to a higher degree in the non-STS group.

Venoocclusive Disease of the Liver and Phlebectatic Peliosis in the Golden Hamster Exposed to Dimethylnitrosamine

The liver of Syrian hamsters was studied after exposure to dimethylnitrosamine (DMN) in drinking water for, respectively, 8, 12 and 16 weeks. One additional group of animals was offered DMN for 8 weeks, but maintained for further 8 weeks after removal of the compound. The changes consisted of a narrowing portal venopathy, probably arising, initially, from toxic pylephlebitis, being followed by widespread subendothelial prolapse of hepatocytes encroaching upon the lumen of terminal hepatic veins, which generally were free of inflammatory fibrosing lesions. The venous lesions were unrelated to malignant processes in the biliary duct system, which occurred after 16 weeks. Dilatation of sinusoids and small venules was associated with the presence of prolapsed hepatocytes around their openings into involved larger veins. At the end of 12 and 16 weeks of continuous ingestion of DMN, but also where the agent was withdrawn already at 8 weeks, phlebectasis and transitional stages in the formation of teleangiactatic type of peliosis were demonstrated, probably resulting from progressively impeded blood flow due to partial occlusion by prolapsed hepatocytes in terminal veins. The mechanism enabling hepatocytes to penetrate the venous wall was not clarified. There was no indication of invasive malignancy. Hepatocyte prolapse appeared more likely to result from some unknown mechanism of benign infiltration, promoted by regenerative stimulation. This may have been initiated by mild persistent ischemia due to the demonstrated portal venopathy. No endothelial hyperplasia was seen at any stage of the experiments thus eliminating the probability of peliosis being a source of vascular neoplasia, which has previously been described following more prolonged exposure to DMN. Certain parallelisms of the experimental results with hepatic vascular lesions in man subjected to drug therapy are discussed.

Gestational changes in the germinal matrix of the normal rhesus monkey fetus.

To explain the reported predisposition to germinal matrix hemorrhage in premature infants, pathogenetically important morphological features of the germinal matrix should be present in the 3rd trimester and rapidly change near term. Such features were sought in this study of the germinal matrix and its vasculature in normal rhesus monkey fetuses. The matrix cells, glia, ependyma, and capillaries showed no important structural changes during the 3rd trimester. The terminal vein tributaries were greatly enlarged by 148 days, but cellular and collagen support in their walls was minimal at this time. The latter features developed by the final days of gestation. These findings do not support a structural immaturity or specialization of the germinal matrix predisposing to germinal matrix hemorrhage. Our results, therefore, support the recent emphasis on physiological parameters in the pathogenesis and prevention of germinal matrix hemorrhage.

Functional Anatomy of the Calcium-Excreting System of Gleditsia triacanthos L.

Very young, growing leaflets of Gleditsia triacanthos L. (honey locust) contain a few druse-shaped calcium oxalate crystals (DC) in the phloem parenchyma of the midvein and in the mesophyll near veins. During leaf expansion and maturation, prismatic crystals (PC) form in abaxial bundle sheath cells (BSC) associated with sclerenchymatous fibers of the major veins, while terminal veins remain free of PC. BSC without PC are elongate, but most PC-containing BSC are isodiametric, suggesting that cell division precedes the formation of PC. Large numbers of very small, irregular crystals form in the walls of the epidermis cells, but not in the stomatal apparatus. In mature, fully expanded and differentiated leaflets, large PC develop in virtually all BSC of major and minor veins, and DC form in the mesophyll, particularly in the palisade parenchyma; as the cells of the latter differentiate into crystal idioblasts, they divide, increase in diameter, and undergo structural changes. In Gleditsia stems, PC are depos...

Primary portal venopathy in the golden hamster treated with low doses of dimethylnitrosamine.

Ingestion of dimethylnitrosamine in a low dose and for a limited period by hamsters resulted in primary intrahepatic pylephlebitis. The process began at 24 h and progressed within 2-4 weeks to narrowing and, eventually, to partial obstruction of the portal bed. The lesions were characterized by endothelial necrosis followed by infiltrations of lymphoid cells extending into the portal tracts. Superficial lesions of terminal hepatic veins and parenchymal changes occurred only after a lapse of, respectively, 2 and 4 weeks when restrictions of portal blood had been assumed. The parenchymal changes consisted of regional regenerative hyperplasia accompanied by subendothelial prolapse of hepatocytes into the wall of terminal veins. The lesions of the portal veins persisted for a prolonged period of time after the exposure to dimethylnitrosamine had ceased. These findings, associated with characteristic histological aspects, suggested secondary immune reaction following the initial toxic pylephlebitis. The possible relevance of the experimental results to understanding the nature of endemic portal venopathy in man is discussed with regard to pathogenesis and etiology.

Peritoneoscopy of the liver stained by intravenous injection of indocyanine green-experimental and clinical studies.

Liver surface patterns were observed by peritoneoscopy after intravenous injection of indocyanine green (ICG). The normal rat liver was diffusely stained dark greenish-brown 5 minutes after the injection of ICG 25 mg/kg body weight into the tail vein. Green spots persisted longer in the centrolobular area, clearly revealing lobular markings. This regional difference in hepatocyte staining suggested differing abilities of hepatocytes to take up or excrete ICG. This dyeing technique was applied to liver disease patients. The liver was diffusely stained light greenish-brown 5 minutes after the injection of ICG 5 mg/kg body weight. In patients, especially those with obscure lobular markings before ICG injection, lobules were clearly demarcated by reddish terminal portal veins against a green background. This simplified detection of lobular distortions. Prenodular patches (Kalk's Bunteflecke) on the liver surface were stained green more intensely than surrounding areas, which supports the hypothesis that patches are composed of active hepatocytes.

Normoglycemia after reflux of islet-containing pancreatic fragments into the splenic vascular bed in dogs.

Canine pancreata obtained at total pancreatectomy were cannulated via the ducts and perfused with collagenase to prepare a tissue suspension that was isografted into the spleen (preparation congruent to 2 h, mean graft vol = 10 +/- 1 ml containing 24% of the B-cell mass/pancreas). In 13 dogs the tissue was implanted by reflux into terminal splenic veins: two died postoperatively, and in two the intrasplenic vein wall was inadvertently punctured during cannulation. In the remaining nine, mean fasting blood glucose (BG) was less than or equal to 150 mg/dl initially; one was killed at 2 wk (distemper) and one at 6 wk (sepsis, diabetes), and one died at 9 wk (intestinal obstruction). Mean BG was 94 +/- 4 mg/dl at 1 mo and remained in this range until the dogs were killed at 5 mo (91 +/- 13 mg/dl). During glucose-tolerance testing 1 wk preimplantation and 1 mo and 2-3 mo postimplant, mean values were: K (decline in glucose concentration, %/min), 3.4 +/- 0.2, 1.4 +/- 0.1, and 1.5 +/- 0.1; peak insulin (microU/ml), 50 +/- 5, 12 +/- 1, and 11 +/- 2; fasting serum glucagon (pg/ml), 33 +/- 3, 59 +/- 12, and 53 +/- 9, with no change in the glucagon response. Histologically, the spleens contained prominent islets. In five other dogs, the tissue was injected into the splenic pulp: mean BG rose to greater than or equal to 250 mg/dl at 2 wk (compared with initial series, P less than 0.001) and remained elevated until death at 6 wk, when histologic examination of the spleens showed severe fibrosis and no islets. Apancreatic controls (N = 4) survived 10 +/- 3 days; BG was 343 +/- 11 mg/dl terminally. We conclude that this modified method for collagenase perfusion of a single large-mammal pancreas via the ducts provides sufficient viable islets to induce prolonged normoglycemia (5 mo) and preserve the response to glucose challenge. Reflux of pancreatic fragments into splenic veins appears more efficient than intrapulp implantation.

Gastric Infarction

We describe a 62-year-old man with diabetes mellitus and peripheral vascular insufficiency, with an ulcer on his foot which led to staphylococcal septicemia, endocarditis, and disseminated intravascular coagulation. All these factors contributed to thromboembolic occlusion of the terminal arteries and veins supplying the stomach, causing gastric infarction.

Intrahepatic vascular lesions in experimental and natural ovine fascioliasis.

Using acrylic resin casts prepared from the liver vasculature and histology, subdivisions of the portal and hepatic systems stenosed as a result of experimental and natural infections of F. hepatica were identified as terminal, secondary and tertiary portal veins and central and sublobular hepatic veins; primary portal veins were also involved in the experimentally infected livers. Fewer veins tended to be involved in livers naturally-infected and they were more evenly distributed among liver lobes than in the experimental disease where most were found in the ventral lobe. Casts of both types of infection also demonstrated enlargement and tortuosity of arteries in ventral lobes and those forming the peribiliary arterial plexus, as well as showing that multiple anastomotic channels had formed. The arterial changes and anastomoses were suggested as developing to compensate for the effects of vascular stenosis. Portal vein stenosis induced experimentally was the outcome of replacement of eosinophils and oedema-like fluid present in veins around fluke tracks and of the organisation of fluke tracts impinging upon veins. During the post-migratory period of infection, stenosis became more marked, for which no adequate cause was identified. In livers naturally-infected, in addition to stenosed portal and hepatic veins, vascular channels in collagen septa in sinusoids and a slight convolution of arteries were seen.

Origin of intraventricular haemorrhage in the preterm infant.

A technique has been developed for the injection and stereomicroscopic examination of blood vessels in the preterm newborn brain. Using this technique it can be seen that in the immature brain there is a rich capillary bed in the germinal layer region supplied mainly by Heubner's artery. Capillary channels drain directly into the terminal vein and its main branches. Study of 19 cases with spontaneous germinal layer haemorrhage (GLH) with or without intraventricular haemorrhage (IVH) failed to show rupture of the terminal vein or germinal layer infarction. In babies of up to 28 weeks' gestation GLH developed most frequently over the body of the caudate nucleus, whereas in babies of 29 weeks' gestation or more the haemorrhages were usually over the head of the caudate nucleus. Histological study of 10 cases of GLH failed to show rupture either of arteries or veins, though evidence of rupture at a capillary-vein junction was seen in one case and masses of fibrin adjacent to the vein wall in 2 others. Injection through the carotid artery caused prominent leaks of injection mass within the germinal layer capillary bed, often adjacent to the veins. Injection through the jugular veins in 2 cases failed to rupture the terminal vein but caused multiple vein ruptures at the junction of deep and cortical venous systems. Additional small ruptures in the germinal layer occurred in one of the cases only. It is suggested that the capillaries within the germinal layer may be ruptured by a rise in arterial pressure, particularly in conditions of hypercapnia and hypoxia.

Fluorescein angiography and its prognostic significance in central retinal vein occlusion.

To determine the prognostic value of fluorescein angiograms in central retinal occlusion 75 patients presenting within the first three months of their initial visual symptoms were studied prospectively. The prognosis was found to be best (complete or partial resolution) in eyes with good capillary perfusion, an intact perifoveal capillary arcade, and leakage only from terminal venules and veins. A broken perifoveal capillary arcade and much capillary leakage, even in the absence of obvious capillary closure, were precursors of permanent macular oedema. All eyes with extensive capillary closure developed severe complications such as thrombotic glaucoma and neovascularization (pre-retinal fibrosis), and all became blind. Macular transit time and leakage from arteries and veins were not used as prognostic features. Fluorescein angiography during the first month of the initial visual symptoms was of prognostic value only in those cases with poor prognosis. The three-month angiogram was an accurate indicator of the visual outcome in all cases.

Pathogenesis of intraventricular haemorrhage in newborn infants.

The ventricular CSF of a group of preterm infants dying in the newborn period contained a large excess of protein which appeared to be a plasma filtrate. This excess was found whether or not an intraventricular haemorrhage (IVH) was also present. After consideration of the clinical features of the infants, their coagulation status, and the findings at necropsy, we suggest that increased cerebral venous and capillary pressure, usually caused by heart failure resulting from hypoxia and acidosis, was responsible both for the IVH, by rupturing the terminal veins, and for promoting the filtration of plasma proteins into the CSF. Abnormalities of haemostasis, though very common, did not seem to provide an adequate explanation for the initiation of intraventricular bleeding, though they may have exacerbated it.

Angiographic Findings in Patients with Choledocholithiasis and Obstructive Jaundice

Hepatic angiograms of ten patients with impacted common duct stones were studied to determine the effects of obstructive jaundice. Angiographic evidence of increased hepatic artery blood flow was present in all patients. Seven patients had nonhomogeneous hepatograms (patchy, mottled appearance throughout the liver). In two cases rounded lucencies were misdiagnosed as hepatic metastases; this delayed surgery. Alterations in hepatic blood flow are caused by increased resistance to blood flow in terminal portal vein radicles compressed by distended bile ducts.

A Mathematical Model Of Intracranial PressureAnd Cerebral Hemodynamics ResponseTo CO2 Changes

Alterations in blood CO] tension (paco) are frequently used in neurosurgical Intensive Care Units to manage patients with severe brain diseases and to test the status of mechanisms regulating cerebral blood flow. In this work, the complex relationships between Pacc>2> cerebral blood volume, cerebral blood flow and intracranial pressure (ICP) are investigated by means of an original mathematical model. The model incorporates the intracranial compliance, the cerebrospinal fluid production and reabsorption processes, the collapse of the terminal cerebral veins, and the active response of large and small cerebral arteries to perfusion pressure changes (autoregulation) and to changes inpaCO; (chemical regulation). Two different kinds of simulations have been performed to validate the model and to test its possible clinical usefulness. In a first stage, ICP was maintained constant to mimic experiments with the open skull and the ccrebrovascular response to changes in systemic arterial pressure and in Paco^ was reproduced. The results of the model show that agreement with the experimental curves of various authors is quite good. In the second stage, conditions occurring with a closed skull were simulated. These are characterized by acute changes in ICP, induced by active changes in cerebral blood volume. In these conditions, the model was used to reproduce the time pattern of ICP and blood flow velocity at the level of the middle cerebral artery observed in patients during alterations in systemic arterial pressure and Paco^A comparison between simulation results and real tracings is presented and discussed. The model may represent a valid tool to interpret the complex relationships between cerebral hemodynamic quantities in neurosurgical Intensive Care Units. Transactions on Biomedicine and Health vol 4, © 1997 WIT Press, www.witpress.com, ISSN 1743-3525

Experimental study on hemorrhage in the brain stem induced by an intracranial space occupyting lesion.

Summary Increased intracranial pressure was experimentally produced in dogs by inserting a rubber balloon epidurally in the left temporal region and then inflating the balloon with water. The animals were killed after a set interval and the hemorrhagic lesion in the brain stem examined in detail. 1. The hemorrhagic lesions in the brain stem could be microscopically classified into three types; arterial, venous and capillary. Massive hemorrhagic lesion was also observed in some animals. 2. Arterial hemorrhage was distributed mostly in the area supplied by the thalamo-perforating artery in the diencephalon and in the area supplied by the paramedian branches of the basilar artery in the lower brain stem. Venous hemorrhage was found mostly in the region of the terminal vein and basal vein in the diencephalon and in the region of the basilar vein in the lower brain stem. Capillary hemorrhage was extensive and the distribution corresponded approximately with that of venous hemorrhage but also in part with that of arterial lesions. 3. A relation was apparent between the hemorrhagic lesion in the brain stem and the amount of water instilled into the rubber balloon, which could be correlated to intracranial pressure. Capillary hemorrhage was observed in most cases in which over 3.5 ml of water was instilled. With instillation of 4.0 ml of water, all types of hemorrhage were observed profusely but venos hemorrhage predominated. With instillation of more than 4.5 ml of water, arterial hemorrhage was dominant. 4. The relation between the hemorrhagic lesions and the survival time after procedure was studied in the animals which had died naturally. Capillary hemorrhage was observed in almost all the animals irregardless of the survival time. Both arterial and venous hemorrhage were observed abundantly in animals which survived for over 10 hours. Arterial hemorrhage, in particular, was dominant in the cases which died within 12 hours and the venous type was dominant in the case surviving over 12 hours.

Subependymal cerebral hemorrhage in infancy.

SUBEPENDYMAL cerebral hemorrhage with intraventricular inundation, occurring almost exclusively in premature infants, 1-9 has been encountered in approximately 15% of premature babies autopsied in the neonatal period. 10 A series of sporadic reports suggested the frequent occurrence of subependymal bleeding in premature infants was due to possible developmental factors such as: (1) thin-walled veins with large diameters that lack adequate supporting fibers in the subependymal matrix, 6,11 (2) congenital vascular defects or early vascular injuries, 12 or (3) thin-walled terminal veins that are unusually susceptible to venous congestion. 6,8,13 The most prevalent theory is that asphyxia produces generalized venous congestion and damage to the cerebral blood vessels which is sufficient to rupture the terminal veins. The purpose of this report is to present a comprehensive description of the clinicopathological findings of 30 infants who had subependymal bleeding at autopsy and to elucidate further the possible existence of a special predisposition

Evidence of the Atrial Location of Receptors Influencing Urine Flow

Receptors believed responsible for the diuresis of negative pressure breathing have been located by observing the effect on urine flow of a stepwise engorgement of the intrathoracic vascular bed. Distension of the pulmonary arterial tree (injection of plastic beads) and of the entire pulmonary circulation (snares on the pulmonary veins) were without effect. A diuresis was however elicited by expansion of a balloon in the left atrium. It is concluded that stretch receptors in the left atrium and terminal pulmonary veins are instrumental in a mechanism linking changes in the actively circulating blood volume with homeostatic responses of the kidney.