Interlobular Veins Research Articles

Arterial constriction, ischemia-reperfusion, and leukocyte adherence in acute pancreatitis

We investigated microcirculatory changes in sodium taurocholate (ST)-induced pancreatitis. Groups of rats received as tracer either fluorescein isothiocyanate-dextran or acridine orange intravenously. The microcirculation of the exposed pancreas was observed by use of a video camera attached to an epi-illumination microscope. Vessel diameters and plaques of adherent leukocytes were measured with a digital image-analyzing system. In contrast to 0.4 ml of saline, intraductal infusion of ST (4%, 0.4 ml) induced a constriction of interlobular pancreatic arteries of 79 +/- 2% (P < 0.01) within 2 min. This constriction could not be antagonized by the leukotriene antagonist CGP-35949B. The radical scavengers superoxide dismutase (SOD) and N-(2-mercaptopropionyl)glycine (MPG) prevented the arterial constriction. Constriction of pancreatic arteries was accompanied by a decrease of erythrocyte velocity in the pancreatic capillaries. Flux in the head of the pancreas measured by laser-Doppler velocimetry decreased from 300 +/- 69 to 74 +/- 23 perfusion units (P < 0.01) after 446 +/- 159 s. Subsequently an increase of perfusion values was observed indicating reperfusion phenomena. ST induced leukocyte adherence to the walls of interlobular veins forming plaques constituting 39% of the observed venular cross section within 6 min. The leukotriene antagonist, SOD, or MPG prevented leukocyte adherence. Arterial constriction followed by ischemia-reperfusion and leukocyte adherence to venular endothelium during the reperfusion period represented the sequence of microcirculatory changes in ST-induced pancreatitis. The radical scavengers SOD and MPG prevented arterial constriction and leukocyte adherence to venular endothelium, indicating the involvement of free radicals in the pathogenesis of ST-induced pancreatitis in the rat.

Lectin binding patterns in normal liver, chronic active hepatitis, liver cirrhosis, and hepatocellular carcinoma. An immunohistochemical and immunoelectron microscopic study.

We studied the binding patterns of 14 lectins in human normal and cirrhotic liver (LC) tissues and hepatocellular carcinomas (HCC) using the ABC method. Lectins were divided into 4 groups according to their binding patterns in normal tissues: (A) PHA, MPA, LcH, RCA-I, and WGA, which bound to hepatocytes and all three types of sinusoidal cells; (B) BPA, GS-I, PNA, and SBA, which bound to Kupffer cells and endothelia of interlobular arteries and veins and bile duct epithelia in the portal tract, but not to hepatocytes; (C) UEA-I, which bound only to endothelia of interlobular arteries and veins and bile duct epithelia in the portal tract; (D) LBA, Lotus, LPA, and SJA, which showed no binding. Thus group B lectins may be useful markers of Kupffer cells. Only electron microscopic examination revealed the precise binding sites of lectins in sinusoidal cells and hepatocytes. Hepatocyte cell surface polarities demonstrated by lectin binding in LC and HCC were different from those in the normal liver. The binding pattern of PHA to LC hepatocytes changed from a membranous to both a membranous and a cytoplasmic pattern, and that of LcH to HCC cells changed to dot-like staining in the cytoplasm. These changes of polarities in LC and HCC might be caused by changes in the distribution of lectin-binding carbohydrates or by the altered glycosylation of glycoconjugates.

Pancreatic microcirculation in the common tree shrew (Tupaia glis) as revealed by scanning electron microscopy of vascular corrosion casts.

Pancreatic vascular casts of the common tree shrew (Tupaia glis) were prepared by infusion of Batson's No. 17 plastic mixture into the blood vessels and examined by scanning electron microscopy (SEM). Routine histological study of the pancreas was also performed. It was found that the A and D cells appeared to occupy the core whereas the B cells were found at the periphery of the islets of Langerhans. With SEM, the insular arteriole, a branch of the interlobular artery, was shown to penetrate deeply into the core of the islets before branching off into the glomerular capillary network supplying the islets. These capillaries reunited at the periphery of the islets to become vasa efferentia and then gave off capillaries to anastomose with those in the exocrine part of the pancreas, the insuloacinar portal system. Such an insuloacinar portal system found in the pancreas of the tree shrew was similar to that found in the horse and monkey. However, there were some intralobular arterioles which did not end in the islets but directly branched into the interacinar capillary network and periductular plexus. The capillaries in the exocrine part not only gathered into intralobular venules which confluently formed the interlobular vein but also supplied the duct system. The periductular plexus also collected blood into the intralobular venule and interlobular vein, respectively.

The blood vascular bed of the human pancreas, with special reference to the insulo-acinar portal system. Scanning electron microscopy of corrosion casts.

Microdissection and scanning electron microscopy of corrosion casts showed the structures of the vascular bed of the human pancreas to consist mainly of the capillary plexuses of the exocrine lobules, extralobular ducts and endocrine islets. A considerable number of the exocrine lobules were found to contain one to four marked endocrine islets larger than 30 microns in diameter. These intralobular islets received one or more arterioles (afferent vessels) and emitted conspicuous insulo-acinar portal vessels which continued into the lobular capillaries, suggesting insular control over the functions of the exocrine acini of the pancreas. Direct drainage of the intralobular islets into the veins was never reproduced. Not excluding the possibility that some lobules might contain smaller, unidentifiable islets, there nonetheless were many lobules which directly received arterioles. These lobules are free of control by an islet. Rarely, an islet was located in the interlobular tissue space or along an extralobular duct. Such an extralobular islet issued no portal vessels, and drained into the interlobular or periductal veins. The surface of this type of islet comprised a thin network of fine capillaries. A possibility was suggested that this cortical network might be homologous with the lobular capillaries. No portal route was observed between the islets and extralobular ducts. Few connections were noted between the capillary plexuses of the lobules and ducts.

Microcirculation of the rat pancreas, with special reference to the insulo-acinar portal and insulo-venous drainage systems: a further scanning electron microscope study of corrosion casts.

Microcirculation in rat pancreas was studied by scanning electron microscopy of resin vascular casts and by light microscopy of India ink-injected and sectioned tissue samples. In the scanning survey of the casts, islets larger than 30 microns in diameter counted no less than 400 in the adult rat pancreas. They were located either in the exocrine lobules (intralobular islets, counting 210 or more), or in the interlobular tissue spaces and along the secretory ducts (extralobular islets, 190 or more). Every islet received arterial blood via one or more proper arterioles. These afferent vessels first divided in the peripheral zone of the islet consisting of A and D cells and later extended deeper to form a capillary network in the islet core consisting of B cells. Blood originating from this capillary network left the islet via efferent vessels. This microvascular pattern may favor the regulation by A and D cells over the secretory activity of B cells. The intralobular islets gave their efferent vessels to the capillary bed of the exocrine tissue of the lobule, thus forming an insulo-acinar portal system. When the lobule was relatively small in size, superfluent blood was led directly to veins via insulo-venous drainage vessels. The intralobular islets sometimes issued one or more long translobular portal vessels reaching adjacent lobules. The extralobular islets issued either insulovenous vessels draining to interlobular veins, or extralobular insulo-acinar portal vessels supplying adjacent lobules.

Light and electron microscopy of neuropeptide Y-containing nerves in human liver, gallbladder, and pancreas

Neuropeptide Y-containing nerve fibers were identified by light and electron microscopic immunocytochemistry in the human liver, gallbladder, and pancreas. In the liver, neuropeptide Y-containing nerve fibers were distributed richly in Glisson's sheath and were prominent around the walls of the interlobular vein, interlobular hepatic artery, and hepatic bile duct. The fibers also formed a dense network surrounding the hepatocytes. The nerve terminals were found close to the endothelial cells of blood vessels, as well as being distributed in Disse's space, where they appeared to terminate. Occasionally these terminals contacted directly the membrane of a hepatocyte. In the gallbladder, neuropeptide Y fibers were found in each layer, with an especially dense network in the lamina propria. The fibers also ran close to the epithelium and parallel to the muscle bundles. Blood vessels throughout the gallbladder were well supplied with such nerve fibers. In the pancreas, neuropeptide Y fibers were found mainly near blood vessels and partly in gaps between exocrine glands, seeming to terminate on certain endocrine cells. Nerve terminals were located in the vascular walls and adjacent to the surface of exocrine acinar cells. These studies provide a basis for correlating the neuropeptide Y distribution with pharmacological and physiological studies in humans.

Renal morphology of the hook‐lipped african rhinoceros, Diceros bicornis, linnaeus

The kidney of Diceros bicornis has about 60 lobes, all appearing peripherally. These are separated by interlobar septa, except for small septal defects through which tubules pass. Renal capsule and interlobar septa are fibromuscular and contain small blood vessels. The kidney is about 65% cortex. It contains about 12.5 x 10(6) glomeruli, which form about 7% of the cortical mass and 4.6% of the renal mass. Diameter of a glomerular capsule is about 244 microns, there being no difference in size across the cortex in these adults. The ureter bifurcates into a cephalic and a caudal, fibromuscular, urothelial-lined conduit, into which open about 23 urothelial-lined infundibula. The common large collecting duct, or tubus maximus, of every lobe opens at the apex of its infundibulum. Two tubi may join into one infundibulum. The tubi and their terminal collecting ducts (of Bellini) are part of the inner medulla. Musculature of conduits and infundibula is largely longitudinal. The calyx may be represented by a circular muscle bundle near the apex of every infundibulum. The large intralobar veins are partly adherent to their infundibulum and calyx and receive arcuate veins via valved orifices. Most branches of the renal artery enter via the interlobar septa. Within a septum they branch again and also supply numerous perforators, which thence enter the cortex. Remaining branches of the renal artery enter cortex directly from without. A fibromuscular scaffolding lies deep to arcuate veins where they contact medulla. Where these veins contact cortical tubules; however, their walls become merely endothelium, like the walls of the interlobular veins.

Microvasculature of the Thyroid Gland in the Common Tree Shrew (&lt;i&gt;Tupaia glis&lt;/i&gt;): Microvascular Corrosion Cast/Scanning Electron Microscopy Study

A thyroid vascular cast of the common tree shrew (Tupaia glis) was obtained by injection of Batson's No. 17 plastic mixture into the ascending aorta. The cast was studied under the scanning electron microscope. It was found that each half of the gland is supplied by a large superior and a rather small inferior thyroid artery. After plunging into the gland, the arteries divide into smaller branches that are the interlobular, intralobular and follicular arteries (afferent vessels). The basket-like capillaries arising from the follicular arteries and encapsulating thyroid follicles are of large diameter and are arranged in a single layer. The follicular side of the capillary casts was observed to contain numerous small and some large projecting knobs compatible with the presence of fenestrations in the endothelial cells. On the other hand, endothelial nuclear imprints were found mainly on the stromal surface of the follicular capillary casts. Transfollicular capillaries connecting the adjacent follicular capillary networks were also observed. Blood from the follicular capillaries either drains into the follicular veins (efferent vessels) or abruptly drains into the intralobular veins before proceeding to intralobular and interlobular veins, respectively. The interlobular veins are collected into a few small superior, a few larger middle and a few even larger inferior thyroid veins. These veins drain directly into the laryngeal vein lying adjacent to the deep surface of the thyroid gland before joining the jugular vein. Venous valves were identified outside the thyroid gland. In addition, the glomerular capillary island of the parathyroid gland was often seen at the cranioanterolateral and sometimes at the cranioposterolateral aspect of the thyroid gland.

Leaky intra-acinar arteries in rat lungs perfused with hydrogen peroxide

We have investigated the effects of H2O2 (150 or 300 microM) on the ultrastructure and permeability of the pulmonary endothelium in rat lungs perfused for 60 min with buffered Hanks' bovine serum albumin medium. In one group of experiments, we examined the effect of H2O2 on the uptake and transport of cationized ferritin (CF) by endothelial cells in intra-acinar arteries, alveolar capillaries, and interlobular veins. The influence of the oxidant on endothelial adsorptive endocytic processes was assessed by measuring the density of ferritin particles in luminal vesicles, multivesicular bodies, and basal lamina. In a second group of experiments, we examined the effects of H2O2 on the fine structure and permeability to electron-dense macromolecules of arterial, microvascular, and venous endothelium. For this purpose, at the end of the 60-min perfusion with H2O2, CF was perfused to identify leaky vessels. We found that H2O2 caused a dose-dependent inhibition of transcytosis of CF in all vascular segments. At the lower dose of H2O2, inhibition of transcytotic activity was not associated with structural injury to the vascular endothelium or with elevation of wet-to-dry ratios. At the higher oxidant dose, inhibition of transcytosis was associated with leaky arterial endothelium and elevation of wet-to-dry ratios (6.44 +/- 0.12 vs. 5.64 +/- 0.16, P less than 0.02). The effects of H2)2 were prevented by adding catalase to the perfusate. The selective loss of structural integrity and leakiness of the arterial endothelium were diminished but not completely abolished by perfusing the oxidant retrograde from the venous side.(ABSTRACT TRUNCATED AT 250 WORDS)

Islet Vasculature in Atrophic Pancreas

Islet vasculature was studied in rats rendered dietarily copper-deficient, a regimen that effects progressive acinar atrophy while leaving islets and ducts intact. Scanning electron microscopy of corrosion casts produced from Mercox injected rats was used to analyze islet angioarchitecture in the atrophied gland. The results indicate that with the onset of acinar atrophy, the vasculature of islets remained intact despite loss of insuloacinar interconnectivity. With atrophy of the dense acinar vascular matrix, three populations of islets could be distinguished according to their size and vascular structures: (a) All small islets (40-150 microns in diameter) were found to have exclusively serial vasculature since no postcapillary collecting venules were found directly continuous with parallel efferent veins. (b) A second population of intermediate size islets (160-250 microns) was found to have serial vessels in addition to postcapillary collecting venules that were directly continuous with larger interlobular veins indicative of a parallel mode of microcirculation. (c) All larger islets (260-700 microns) were also found to have both serial as well as parallel microcirculatory patterns based upon the coexistence of both types of postcapillary venules within the same islet. In all cases, postcapillary venules, which normally link islet capillaries to peri-insular acinar plexuses, were continuous with veins that extended through lipomatous lobules devoid of acini to link with branches of interlobular veins. It is proposed that the functional integrity of islet blood flow remains in the atrophied pancreas because of preservation of both serial and parallel microcirculation that facilitate normal glucose-stimulated insulin secretion in the atrophied pancreas, as demonstrated in an earlier study. Furthermore, it is suggested that analysis of the atrophied state of the gland provides a valid comparative model with which to study islet angioarchitecture and microcirculation in the normal gland.

The blood vascular architecture of the rat thyroid gland: A scanning electron microscope study of corrosion casts.

The blood vascular bed of the rat thyroid gland was reproduced by injection of a methacrylate casting medium and observed with a scanning electron microscope. The rat thyroid gland received the superior and inferior thyroid arteries and emitted the superior and inferior thyroid veins. Anastomosis between the interlobular arteries or between the interlobular veins was frequently observed in the thyroid gland. The arteriovenous anastomosis was rarely observed between the terminal branches of the lobular arteries and veins. The thyroid blood vascular bed was divided into lobular units which consisted of basket-like capillary networks surrounding the thyroid follicles; a small lobular unit consisted of a few networks, whereas a large one of fifty or more networks. Sizes and forms of the networks varied widely in each case. However, the networks in the superficial layers of the lateral parts of the thyroid gland were typically most developed. Regardless of its size and form, each network always received a proper efferent vessel continuous with the lobular vein, though it was sometimes provided with an accessory afferent or efferent vessel. Only occasionally were the adjacent networks fused with each other or connected by transfollicular capillaries. Thus, the present data suggest that each follicular capillary network is a fairly independent functional-unit in the thyroid microcirculation. The capillaries of the network were sinusoidal in nature and sometimes protruded fine projections which indicated the neogenesis of capillaries. The blood vascular bed of the newborn rat thyroid gland was not always differentiated into basket-like capillary networks.

Whole-body hyperthermia-induced renal atrophy of mice as evinced by obstruction and degeneration of renal tubules caused by acute ischemia.

Effects of microwave-induced whole-body hyperthermia (WBH) on the mouse kidney were examined histologically for acute and late effects up to 150 days after WBH treatment at 43.5 degrees C (rectal temperature) for 20 min or 42 degrees C for 40 min. As a whole the damage could be divided into two types. One was the damage to distorted epithelial cells in the subcapsular region. This lesion was common in most animals, possibly caused by direct hyperthermic effect of microwave. The other was general renal atrophy accompanied with aqueous or protein-rich cysts due to a chain of physiological reactions of the whole body to WBH. The first reaction was characterized by general stasis of the blood stream in all parts of the kidney, which resulted in acute ischemia of some tissues. This was seen immediately by dilatation of the renal and interlobular veins as well as the bundles of capillaries in the medulla region. The subsequent event was rather specific cell necrosis of distal and collecting tubular epithelium as compared to proximal tubules. The cell destruction induced cell proliferation of the proximal tubular epithelia after two days. Later on, in accord with the recovery of the blood circulation, the proliferated cells were carried away into the lumen, these processes then resulting in obstruction of tubules through formation of protein casts in the lumen. The block incidentally led to the destruction of nephrons. The degenerated area sometimes consisted of aqueous or protein-rich cysts of various sizes after 7 to 30 days. Thereafter these cysts degenerated, decreasing in both number and size. Thus irreversible atrophy of the kidney developed after WBH.

Analysis of PCO2 variations in the renal cortex. II. Countercurrent exchange.

In an effort to explain the relatively high values of CO2 partial pressure (PCO2) that have been measured in the superficial renal cortex of the rat, we developed a mathematical model based on the concept of countercurrent exchange between blood vessels. The model includes the possibility of exchange of CO2 between interlobular arteries and veins throughout the cortex, and between "terminal" arterioles and venules (those associated with the most superficial nephrons). The effect of countercurrent exchange is to amplify the increases in PCO2 that occur in the microcirculation of individual nephrons, which are due to the addition of metabolic CO2 and reabsorbed HCO3- and CO2 to peritubular capillaries. The model is formulated in terms of correlations that describe blood buffering equilibria in peritubular capillaries and in interlobular arteries and veins, and steady-state mass balances for the interlobular vessels. By use of physically reasonable vascular permeability values, simulations for the normal euvolemic Munich-Wistar rat yielded values of the surface-to-arterial PCO2 difference (delta PCO2) comparable to previously measured values. Predicted variations in delta PCO2 with afferent arteriolar blood flow rate and systemic arterial PCO2 were also in accord with available data. These results suggest that the amplifying effect of countercurrent exchange is in fact adequate to explain the high values of PCO2 measured in surface structures. The solutions to the mass balance equations are in closed analytical form and can be readily adapted to describe countercurrent exchange in the renal cortex of solutes other than CO2.

Immunohistochemical localization of metallothionein in the liver and kidney of cadmium- or zinc-treated rats.

The localization of metallothionein (MT), a small molecular weight heavy-metal binding protein, in the liver and kidney of rats treated with either cadmium (Cd) chloride or zinc (Zn) sulfate was investigated by the indirect immunofluorescent technique. Male Wistar rats were subcutaneously injected with CdCl2 at a single dose of 3.0 mg Cd/kg body weight or 50 mg Zn/kg body weight, followed by sacrifice at 3, 6, 12 and 24 hr. For comparison, tissues were also obtained from rats treated with 1.5 mg Cd/kg body weight, 4 times a week for 6 weeks. In control rats from both short- and long-term studies the MT antigenicity was detected in the cytoplasm of hepatocytes and proximal tubular cells. A major difference in the localization of MT between the two studies was found only in the liver. The immunoreactive stain was limited to the hepatocytes around both central and interlobular veins in the long-term study compared to rather uniform localization throughout the liver in the short-term study. The intensity of immunostain of MT in both organs upon Cd or Zn treatment tended to increase with tissue concent-rations of the protein, as determined by a radioimmunoassay. Cd and Zn treatment resulted in the localization of MT in a similar manner. In particular, the number of proximal tubules with immunofluorescence increased upon an injection of Cd or Zn, and once a renal Cd level considerably increased by the repeated injections of Cd, intense stain of MT was observed not only in the proximal tubule but also the distal tubule and collecting duct. No specific immunostain was observed in the glomerulus, vascular endothelial cells and connective tissues. Although not only the cytoplasm but also the nucleus of the hepatocytes and proximal tubular cells often showed immunofluorescence, no significant change in the induction of MT between these subcellular compartments with time was found.

Biological effects of shock waves: Kidney damage by shock waves in dogs—Dose dependence

The effect of shock waves on normal canine kidneys was examined in three groups of dogs whose right kidneys were exposed to 500, 1500, or 3000 shock waves. Autopsy was performed 24-30 h later. The kidneys were enlarged with haemorrhages in the outer and inner renal capsule and intraparenchymally. Macroscopically intraparenchymal haemorrhages were restricted to the high pressure field of the shock wave and consisted of haematomas up to 18 mm diameter (most frequently 6 mm or less) and diffuse haemorrhages. Histologically, haemorrhages were shown to originate from interlobular and arcuate veins. Venous thrombosis, tubular dilatation, and diffuse interstitial haemorrhage occurred in the same area. The number of haematomas was larger, and diffuse haemorrhages were more extended after the application of 1500 and 3000 than after 500 shock waves. No difference was seen between 1500 and 3000 shock waves.

Preferential localization of calcium-activated neutral protease in epithelial tissues

Immunohistochemical localization of calcium-activated neutral protease (CANP) in rabbit organs was determined using a monoclonal antibody against CANP. In most organs, epithelial tissues reacted intensely: these tissues include great alveolar and squamous alveolar cells in lung; interlobular artery, vein, and bile duct in liver; small vessels in skeletal muscle; glomeruli, juxtanglomerular cells, distal and collecting tubules in kidney; mucous epithelium in gallbladder; interstitial cells in testis; and cuboidal epithelial cells in brain choroid plexus. On the other hand, hepatocytes, epithelial cells which have ill defined basal lamina, were stained very faintly. These observations suggest that the physiological function of CANP is involved with transport systems in epithelial tissues through basal lamina.

The intrarenal and pericapsular venous systems of kidneys of the ringed seal, Phoca hispida.

The kidneys of Phoca hispida are comprised of many closely adherent renculi, each of which is a small kidney, functionally independent of its neighbours except with respect to venous drainage. Venous blood from the rencular parenchyma drains to the periphery through interlobular veins. These interlobular veins empty into a perirencular plexus comprised of subcapsular veins on the free surface of the renculus, interrencular veins on adjoined surfaces, and marginal subcapsular veins lying in the furrows between adjoined renculi. A pericapsular plexus of large veins overlies the marginal subcapsular veins and has frequent connections with them. Blood drains from the pericapsular plexus into large superficial collecting veins that converge over the surface of the kidney toward the divided hilum and connect directly to the paired trunks of the posterior vena cava. There are also connections to other major venous systems of the region. There is no arcuate venous system, no major vein at the rencular hilum, and no vein of consequence emerging from the renal hilum. Venous outflow is virtually entirely directed to the peripheral plexuses. The venous pattern differs from that of most mammals in which blood drains from the renal parenchyma to arcuate veins and leaves the kidney through a renal vein, or veins, emerging from the hilum. The walls of veins in the kidney are remarkably thin in comparison to their size. Subcapsular veins up to 0.5 mm wide have walls on the parenchymal side that in places consist only of a thin, fenestrated endothelium and a basal lamina.

Functional differences between sinusoidal endothelial cells and interlobular or central vein endothelium in rat liver.

The fine topological relationship between sinus-lining endothelial cells (SLE) and vessel-lining endothelial cells (VLE) at the opening portion of sinusoids into central or interlobular veins of rat liver was studied by a comparison of morphological and functional properties of both types of cells. Three minutes after intravenous injection of formalin-denatured albumin conjugated with horseradish peroxidase (HRP-FDA), liver was perfused with fixative. Chopped sections of the liver (50 micron thick) were incubated in diaminobenzidine-H2O2 medium, followed by processing for electron microscopy. The HRP-FDA was localized in endocytotic vesicles and vacuoles of the SLE and Kupffer cells but not of the VLE lining interlobular or central veins or interlobular arteries. In the opening portion of the sinusoids into these veins, the attenuated cytoplasmic extensions of the SLE containing positive vesicles were in direct contact with squamous process of the VLE having no positive vesicles. The contact was mediated by overlapping junctions. No intermediate cell type between the SLE and VLE in this region or other portions was noted. The results indicate that the habitat of the SLE is exactly isolated from that of the VLE in rat liver and at the transitional portion from sinusoids to veins or arteries they are directly connected with each other by overlapping junctions.

Countercurrent diffusion in the renal cortex of the rabbit.

Evidence was obtained for countercurrent diffusion of 14C-n-butanol in the rabbit renal cortex. After injection into the renal artery of perfused, isolated rabbit kidneys, concentrations of both 14C-butanol and tritiated water in the initial samples collected from the renal venous outflow exceeded those of 125I-albumin when the rate of perfusion was low. When flow was increased, the 125I-albumin curve was shifted to earlier times relative to the other labels. These observations confirm the existence of arteriovenous diffusion of 14C-butanol and tritiated water in the kidney. In a second set of experiments, 14C-butanol and tritiated water were infused for 10 or 60 seconds into the renal arteries of anesthetized rabbits, and the kidneys were then removed and frozen in liquid nitrogen. Cores were cut from the kidney surface and sectioned in a cryostat, and the ratio of 14C-butanol to tritiated water was calculated at increasing depths in the cortex. This ratio rose from 0.54 +/- 0.03 (SEM) at the surface to 0.98 +/- 0.07 at 3 mm beneath the surface in kidneys perfused for 10 seconds. This gradient was less steep after 60 seconds of perfusion. The early appearance of 14C-butanol relative to tritiated water in the renal venous outflow and delayed equilibration of 14C-butanol in the outer renal cortical tissue are consistent with counter-current diffusion. It is suggested that this exchange may occur between adjoining interlobular arteries and veins in the cortex and may contribute to high carbon dioxide tensions found near the renal surface.

Ultrastructural evidence for a reabsorptive role by intrarenal veins.

Intrarenal veins, although known to have thin walls, are considered to be simple conducting vessels. Using light- and electron microscopy, the distribution and structure of named intrarenal veins was examined qualitatively and quantitatively in rat kidneys fixed by retrograde arterial perfusion. Although the venous system follows the pattern of arterial branching in general, a class of intracortical veins similar in appearance to interlobular veins but without a companion artery was found in the present study. It is suggested that these vessels be designated intralobular veins. Structurally, we have found intrarenal veins to be surprisingly similar to peritubular capillaries both in respect to their spatial relations to renal tubules as well as ultrastructurally. Like peritubular capillaries, the majority of the wall of intrarenal veins is intimately apposed to renal tubules. This fraction decreases centrally, values of 0.83 being obtained in intralobular veins, 0.69 in interlobular veins, and 0.56 in arcuate veins. The walls of intrarenal veins are comprised of little more than an endothelium, which, like peritubular capillaries, is remarkable for its thinness, high density of fenestrae, and lack of extraintimal elements. Endothelial thickness was not significantly greater in either interlobular or arcuate veins than in peritubular capillaries; the fenestrae were, however, about twice as frequent in peritubular capillaries as in interlobular or arcuate veins and 35 times more frequent than in interlobar veins. The size and numerical and volume densities of uncoated endocytotic vesicles did not differ significantly between peritubular capillaries and any of the intrarenal veins. Based on their marked qualitative and quantitative similarities to peritubular capillaries, we conclude that, like the latter, intrarenal veins are capable of sustaining passive transport between plasma and interstitium.