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At least 397 records · Page 22Linked to original sources
PubMed2001

A spinal thecal sac constriction model supports the theory that induced pressure gradients in the cord cause edema and cyst formation.

OBJECTIVE: Spinal cord cysts are a devastating condition that occur secondary to obstructions of the spinal canal, which may be caused by congenital malformations, trauma, spinal canal stenosis, tumors, meningitis, or arachnoiditis. A hypothesis that could explain how spinal cord cysts form in these situations has been presented recently. Therefore, a novel spinal thecal sac constriction model was implemented to test various aspects of this hypothesis. METHODS: Thecal sac constriction was achieved by subjecting rats to an extradural silk ligature at the T8 spinal cord level. Rats with complete spinal cord transection served as a second model for comparison. The animals underwent high-resolution magnetic resonance imaging and histological analysis. RESULTS: Thecal sac constriction caused edema cranial and caudal to the ligation within 3 weeks, and cysts developed after 8 to 13 weeks. In contrast, cysts in rats with spinal cord transection were located predominantly in the cranial spinal cord. Histological sections of spinal cords confirmed the magnetic resonance imaging results. CONCLUSION: Magnetic resonance imaging provided the specific advantage of enabling characterization of events as they occurred repeatedly over time in the spinal cords of individual living animals. The spinal thecal sac constriction model proved useful for investigation of features of the cerebrospinal fluid pulse pressure theory. Edema and cyst distributions were in accordance with this theory. We conclude that induced intramedullary pressure gradients originating from the cerebrospinal fluid pulse pressure may underlie cyst formation in the vicinity of spinal canal obstructions and that cysts are preceded by edema.

Animals↗
PubMed1988

Pressure changes following constriction of the cauda equina. An experimental study in situ.

During routine autopsies in 11 cadavers, the intact dural sac, including its nerve roots, was circumferentially constricted by a clamp while the pressure under the clamp among the nerve roots was recorded simultaneously. The first sign of a pressure increase--the critical size--occurred at a cross-sectional area of the cauda equina of 77 +/- 13 mm2. To achieve a pressure increase of 50 mm Hg, the cross-sectional area of the cauda equina had to be further constricted at an average of 19 +/- 8%. The corresponding constriction needed to achieve a pressure of 100 mm Hg was 26 +/- 8%. The results indicated that constriction of the cauda equina to a size less than 75 mm2 probably will affect the normal function of the nerve roots of the cauda.

Aged↗
PubMed2004

Postoperative pressure regulation in glaucoma shunt surgery: focal tube constriction is not the answer.

PURPOSE: To evaluate, in a laboratory setting, the accuracy and the clinical use of focal tube constriction as a means to regulate intraocular pressure after glaucoma drainage implant surgery. MATERIALS AND METHODS: A silicone tube identical to the one used in the Baerveldt and other glaucoma drainage implants was connected to a syringe-pump delivering a continuous flow of demineralized water at a rate of 2.5 microliters per minute. Focal constriction of the tube was obtained by a ring made of a shape-memory metal alloy designed for this purpose. After complete occlusion of the tube lumen by crimping the ring with calibrated pliers, the ring was opened in a stepwise manner by heating it with an argon laser beam. In a second experiment the tube lumen was constricted by placing the tube between the jaws of a micrometer. RESULTS: In both experiments a stepwise lowering of the pressure could be obtained. The resulting pressure levels, however, lacked consistency and predictability to such an extent that clinical application is not feasible. CONCLUSION: It is not possible to regulate pressure in a reliable and predictable way merely by constricting the tube lumen of glaucoma drainage implants.

Aqueous Humor↗
PubMed1988

Pharmacological constriction of the lower oesophageal sphincter: a simple method of arresting variceal haemorrhage.

The effect of pharmacological constriction of the lower oesophageal sphincter (LOS) on oesophageal varices was investigated in an experimental study followed by a controlled clinical trial. In the experimental study intravariceal pressure was measured just above the LOS in 11 patients before and after constricting the LOS by intravenous pentagastrin. Intravariceal pressure fell from a mean of 23 (range 12-36) mmHg to 4 (range 0-7) mmHg (p less than 0.001). This marked pressure drop indicated the considerable compression of varices that occurred within the LOS. A prospective controlled clinical trial examined whether LOS constriction (effected by the longer acting metoclopramide) would compress varices sufficiently to arrest active variceal bleeding originating from the lowest 2 cm oesophagus--the area encircled by the LOS. Of 11 patients who received metoclopramide, 10 stopped bleeding compared with four of the 11 who received placebo (p less than 0.01). Pharmacological constriction of the LOS appears to offer a new and effective approach for arresting active bleeding from oesophageal varices.

Adult↗
PubMed1996

Collagen network remodelling and left ventricular function in constrictive pericarditis.

OBJECTIVE: To investigate whether patients with constrictive pericarditis have changes in collagen content and architecture that could influence left ventricular function. DESIGN: Cohort study. SETTING: University teaching hospital. PATIENTS: Biopsy specimens of myocardium from 13 patients admitted consecutively for treatment of chronic constrictive pericarditis were compared with normal heart tissue taken at necropsy from 15 patients free of cardiac disease. INTERVENTION: Pericardiectomy through median sternotomy. Biopsy specimens (4 or 5) were taken from the left ventricular free wall. MAIN OUTCOME MEASURES: Biochemical and histological assessment of total collagen content, relative proportion of type I and III collagen, and amount of orthogonal collagen fibre meshwork (crosshatching) in the left ventricular tissue. RESULTS: There was more collagen in the myocardium of patients with constrictive pericarditis than in controls when measured either biochemically by hydroxyproline content (89.4 v 50.4 mg/g dry weight) or by histological measurement of the collagen fraction of the myocardium (2.4% v 7.0%). Neither of these measurements, however, correlated with left ventricular ejection fraction, pulmonary wedge pressure, or right ventricular end diastolic pressure. The thickness of the fibrous trabeculae in the myocardium was, however, inversely related to both left ventricular ejection fraction (r = -0.76) and deceleration time (r = -0.68). Trabecular thickening was also related to NYHA class, with those in class III and IV having the greatest thickening. CONCLUSION: Changes in collagen content and architecture may contribute to impaired ventricular function in patients with chronic constrictive pericarditis.

Adult↗
PubMed1987

Susceptibility to pressure neuropathy distal to a constricting ligature in the guinea-pig.

Silk ligatures were tied round the sciatic nerve in guinea-pigs and left in place in order to produce persistent nerve constriction. Serial nerve conduction studies over the following 9 weeks showed a reduction in motor conduction velocity distal to the ligature. The presence of axonal atrophy in tibial nerve fibres in the leg was subsequently confirmed by histological studies. These changes were not seen in a second group of animals in which similar ligatures were tied but removed after 6 hours. When the ligatures were left in place, the animals developed local plantar nerve lesions in the sole of the foot on the affected side, which were thought to be due to pressure from the floor of the cage. Local pressure changes of varying severity were seen in the foot in all the constricted nerves, but were only occasionally found in control nerves from the opposite foot, or in nerves which had been constricted for a few hours by ligatures which were then removed. These results suggest that atrophic nerve fibres distal to a persistent constriction may be particularly sensitive to local pressure.

Action Potentials↗
PubMed1986

Effects of plasma norepinephrine elevation on the heart's adaptation to chronic aortic constriction in rats.

Chronically elevated plasma norepinephrine has the potential for supporting function of diseased hearts, yet may also initiate harmful biochemical and (or) structural changes in the myocardium. The present study investigated the dosage-related effects of chronic norepinephrine infusion on markers of myocardial damage and then tested the influence of a relatively low norepinephrine infusion rate (0.05 microgram X kg-1 X min-1) on the heart's adaptation to pressure overload in aortic constricted rats. Norepinephrine infusion at 0.50 microgram X kg-1 X min-1 led to significantly increased myocardial hydroxyproline concentration and significant mortality. A rate of 0.25 microgram X kg-1 X min-1 increased myocardial hydroxyproline concentration and mortality in aortic constricted rats but had no such effects on sham-operated rats. The lowest rate tested (0.05 microgram X kg-1 X min-1) significantly increased mean arterial pressure and lung weight of aortic constricted rats, without affecting the degree of left ventricular hypertrophy. This infusion rate and aortic constriction each increased plasma norepinephrine and impaired cardiac performance during rapid preloading, although their combination did not cause further impairment. Thus, it appears that even modest plasma norepinephrine elevation has a negative effect on the heart's adaptation to sustained pressure overload.

Animals↗
PubMed2003

Intrabolus pressure gradient identifies pathological constriction in the upper esophageal sphincter during flow.

Propulsion of a bolus through the upper esophageal sphincter (UES) is driven by a pressure drop in the direction of flow against frictional resisting force. Basic mechanics suggest that the axial rate of drop in intrabolus pressure (IBP), i.e., the intrabolus pressure gradient (IBPG), should be locally sensitive to abnormal constriction. We sought to quantify space-time patterns of IBP and IBPG that correlate with pathological disruption to transsphincteric bolus transport. High-resolution high-fidelity perfused manometry was applied concurrent with videofluoroscopy in 6 healthy controls and 10 patients with restricted UES opening and 4 bolus volumes. Pressures were interpolated spatially and displayed as space-time isocontours with bolus head and tail trajectories superimposed to identify the IBP domain. IBP and IBPG were averaged over an approximately steady period of transsphincteric flow. The axial location and magnitude of maximum IBPG were quantified for each swallow relative to the location of the abnormal restriction. We found that average hypopharyngeal IBP and locally maximal IBPG were significantly higher in the patient group (P < 0.001), whereas the maximum IBPG was insensitive to bolus volume, and the locations of maximum IBPG in the patient group were well correlated with axial locations of maximal UES constriction (r = 0.84, P < 0.01). Space-time structure of IBP and IBPG correlated qualitatively with swallow dysfunction. Because IBPG reflects pressure force driving the bolus against frictional force in the UES, IBPG reflects local changes in frictional resistance from pathological constriction during bolus flow. Consequently, the location and magnitude of IBPG reflect the existence and location of abnormal constriction, and IBP and IBPG structure reflect decompensation of the pharyngeal swallow.

Adult↗
PubMed1984

Heart cyclic nucleotide responses to sustained aortic constriction in neonatal and adult rats.

The present studies examined adenosine and guanosine 3',5'-cyclic monophosphate (cAMP and cGMP) levels in left ventricular tissue of neonatal and adult rats subjected to 3-10 days of abdominal aortic constriction. Left ventricular cAMP levels were elevated after 3 days of pressure overloading in neonatal rats (2,274 +/- 430 pmol/g; mean +/- SE) compared with composite control values (1,280 +/- 124) obtained from sham-operated neonates, sham-operated adults, and aortic-constricted adult groups. cAMP levels declined progressively until, at 10 days after aortic constriction, values were lower (681 +/- 25 pmol/g) than control (1,621 +/- 107). Left ventricular cGMP level was higher in sham-operated neonatal (38 +/- 3 pmol/g) than in sham-operated adult rats (17 +/- 1) at 3 and 10 days postsurgery, but pressure overloading exerted no effect on cGMP measurements. Adenylate cyclase activity in left ventricular tissue homogenate was higher in 3-day sham-operated neonatal (58 +/- 3 pmol X mg protein-1 X min-1) compared with sham-operated adult (10 +/- 1) rats as the result of augmented nonmuscle cell activity. Elevated cAMP values in 3-day, pressure-overloaded neonates occurred despite lower adenylate cyclase activity (44 +/- 2), via degradative modulation (cAMP phosphodiesterase). Guanylate cyclase activity in left ventricular tissue was consistent with prevailing cGMP levels and was not influenced by aortic constriction. The present experiments show that neonatal cardiac enlargement is associated with biphasic alterations in cAMP level which are modulated, at least in part, via degradative reactions.

Adenylyl Cyclases↗
PubMed1982

Hemodynamic responses to methoxamine in exercise-conditioned and aorta-constricted rats.

Hemodynamic responses to methoxamine hydrochloride (Vasoxyl) were determined in rats conditioned by a moderate treadmill exercise program and in rats subjected to 5 wk of abdominal aortic constriction. Rats of comparable age served as controls. Initial hemodynamic values for control rats were as follows: left ventricular pressure, 124 +/- 4 Torr and cardiac index, 145 +/- 8 ml . min-1 . kg-1. Although minor variations were noted, initial hemodynamic values for exercise-conditioned rats were within the normal range, and no left ventricular hypertrophy was present. Aorta-constricted rats exhibited a 50% increase in left ventricular weight and significant differences in left ventricular pressure (173 +/- 9 Torr) and cardiac index (117 +/- 10 ml . min-1 . kg-1). Sequentially increasing doses of methoxamine were infused to elevate myocardial preload and afterload. When compared with control rats, exercise-conditioned animals were better able to maintain cardiac index at comparable increases in either mean arterial or left ventricular end-diastolic pressures. In contrast, aorta-constricted rats demonstrated profound reductions in hemodynamic functions in response to methoxamine infusion. Directionally divergent hemodynamic results occur in exercise-conditioned and aorta-constricted animals when subjected to identical cardiovascular stresses.

Animals↗
PubMed1982

Contralateral renal function following unilateral renal artery constriction.

The acute (0.5-3.0 h) response of the contralateral kidney to unilateral renal artery constriction was studied in 7 pentobarbital-anesthetized dogs. Within 30 min after unilateral renal artery constriction to a pressure of about 60 mm Hg, contralateral vascular resistance, sodium excretion and filtration fraction increased significantly while glomerular filtration rate, blood flow and plasma flow did not change. Renin secretion decreased dramatically within 30 min, demonstrating a negative venous minus arterial plasma renin activity in some dogs. Unilateral renal artery constriction did not change the rate of angiotensin II extraction across the contralateral kidney or the urinary renin activity (measured in 4 dogs). These results indicate that the acute response of the contralateral kidney to unilateral renal artery constriction is somewhat different from that seen in the chronic state.

Angiotensin II↗
PubMed2004

Novel model of constrictive pericarditis associated with autoimmune heart disease in interferon-gamma-knockout mice.

BACKGROUND: Constrictive pericarditis represents a serious hemodynamic syndrome that may lead to heart failure. Studies of its pathophysiological mechanisms have been impeded by the lack of an animal model. METHODS AND RESULTS: Cardiac myosin-induced experimental autoimmune myocarditis in interferon (IFN)-gamma-knockout (KO) mice results in increased cardiac inflammation and development of severe grossly detectable pericarditis. Using in vivo pressure-volume studies, we found that the acute phase of experimental autoimmune myocarditis in IFN-gamma-KO mice was characterized by reduced left ventricular (LV) volumes compared with wild-type mice. The KO mice exhibited a classic restrictive/constrictive phenotype with decreased cardiac output, increased chamber stiffness, preserved ejection fraction, and impaired diastolic filling, characterized by reduced deceleration time and pressure tracings showing the square root sign similar to that observed in clinical cases of constrictive pericarditis. This phenotype was not associated with the severity of myocarditis but correlated with the presence of grossly detectable adhesive pericarditis present only in the KO group and characterized by increased pericardial inflammation and fibrosis. Comparison of IFN-gamma-KO and wild-type mice matched for the severity of myocardial disease further confirmed that pericarditis, and not myocarditis, was responsible for smaller LV volumes, reduced cardiac output, increased cardiac stiffness, and increased peak filling rate adjusted for end-diastolic volumes in KO mice. CONCLUSIONS: Autoimmune heart disease in IFN-gamma-KO mice results in increased pericardial inflammation and fibrosis, leading to constrictive phenotype during the acute phase of disease. It represents a novel animal model of constrictive pericarditis.

Animals↗
PubMed1999

Endothelial dysfunction and collagen accumulation: two independent factors for restenosis and constrictive remodeling after experimental angioplasty.

BACKGROUND: Constrictive remodeling plays a prominent role in restenosis after balloon angioplasty, but its regulation remains unclear. Because endothelial dysfunction and changes in extracellular matrix have been reported after angioplasty, this study was designed to simultaneously evaluate endothelial function and collagen and elastin changes after restenosis and arterial remodeling. METHODS AND RESULTS: Atherosclerosis was induced in femoral arteries of 22 New Zealand White rabbits by air-desiccation and a high-cholesterol diet. One month later, angioplasty was performed. Histomorphometry and in vitro assessment of endothelial function were performed 4 weeks after angioplasty. Restenosis correlated with constrictive remodeling (r=0.60, P=0.01) but not with neointimal growth (r=-0.06, P=0.79). Restenosis correlated with an impaired relaxation to acetylcholine (ACh; r=0.61, P=0.02) but not with the response to the endothelium-independent vasodilator sodium nitroprusside (r=-0.25, P=0.40). Restenosis correlated positively with collagen accumulation (r=0.69, P=0.004) and inversely with elastin density (r=-0.48, P=0.05). Relaxations to ACh were significantly more decreased in arteries with constrictive remodeling than in those with enlargement remodeling (3.7+/-7.9% versus 35.5+/-15.0%, P=0.04). Neointimal collagen density was significantly higher in arteries with constrictive remodeling than in those with enlargement remodeling (34.5+/-4.5% versus 18.2+/-4.7%, P=0.03). Endothelial function and collagen and elastin density were independent predictors of restenosis in the study. CONCLUSIONS: These results demonstrate that the severity of restenosis after angioplasty correlated with both defective endothelium-dependent relaxation and increased collagen density.

Angioplasty, Balloon↗
PubMed1991

Pathogenesis of edema in constrictive pericarditis. Studies of body water and sodium, renal function, hemodynamics, and plasma hormones before and after pericardiectomy.

BACKGROUND: The pathogenesis of sodium and water accumulation in chronic constrictive pericarditis is not well understood and may differ from that in patients with chronic congestive heart failure due to myocardial disease. This study was undertaken to investigate some of the mechanisms. METHODS AND RESULTS: Using standard techniques, the hemodynamics, water and electrolyte spaces, renal function, and plasma concentrations of hormones were measured in 16 patients with untreated constrictive pericarditis and were measured again in eight patients after pericardiectomy. The average hemodynamic measurements were as follows: cardiac output, 1.98 l/min/m2; right atrial pressure, 22.9 mm Hg; pulmonary wedge pressure, 24.2 mm Hg; and mean pulmonary artery pressure 30.2 mm Hg. The systemic and pulmonary vascular resistances (36.3 +/- 2.5 and 3.2 +/- 0.3 mm Hg.min.m2/l, respectively) were increased. Significant increases occurred in total body water (36%), extracellular volume (81%), plasma volume (53%), and exchangeable sodium (63%). The renal plasma flow was only moderately decreased (49%), and the glomerular filtration rate was normal. Significant increases also occurred in plasma concentrations of norepinephrine (3.6 times normal), renin activity (7.2 time normal), aldosterone (3.4 times normal), cortisol (1.4 times normal), growth hormone (21.8 times normal), and atrial natriuretic peptide (5 times normal). The ratio of left atrial to aortic diameter measured by echocardiography was only minimally increased (1.29 +/- 0.04), indicating that in constrictive pericarditis the atria are prevented from expanding. The studies repeated after pericardiectomy in the eight patients showed that all measurements returned toward normal. CONCLUSIONS: The restricted distensibility of the atria, in constrictive pericarditis, limits the secretion of atrial natriuretic factor and, thus, reduces its natriuretic and diuretic effects. This results in retention of water and sodium greater than that occurring in patients with edema from myocardial disease. The arterial pressure is maintained more by the expansion of the blood volume than by an increase in the peripheral vascular resistance.

Adult↗
PubMed1997

Preload reduction to unmask the characteristic Doppler features of constrictive pericarditis. A new observation.

BACKGROUND: Respiratory variation of > or = 25% in mitral E velocity is a characteristic Doppler echocardiographic feature in constrictive pericarditis. However, a subset of patients with constriction do not exhibit the typical respiratory change, most likely because of marked increase in the left atrial pressure, and preload reduction may unmask the respiratory variation. METHODS AND RESULTS: In 12 patients with surgically confirmed constrictive pericarditis who had < 25% respiratory variation in mitral E velocity during an initial preoperative examination, the Doppler study was repeated after an attempt to decrease left ventricular filling pressure. At baseline, mean mitral E velocity was similar after inspiration and expiration (0.81 +/- 0.24 and 0.84 +/- 0.21 m/s, respectively). On repeat Doppler examination, with the patient in a head-up tilt or sitting position the decrease in mitral E velocity with inspiration (0.61 +/- 0.13 m/s) was significant (P < .004), whereas it did not change significantly with expiration. The mean percent respiratory change in E velocity was 5 +/- 7% at baseline and 32 +/- 28% with preload reduction. Eight (75%) of the 12 patients developed respiratory variation of > or = 25%. CONCLUSIONS: When the respiratory variation in Doppler mitral E velocity is blunted or absent during the evaluation of suspected constrictive pericarditis, repeat Doppler recording of mitral flow velocities after maneuvers to decrease preload is recommended to unmask the characteristic respiratory variation in mitral E velocity.

Echocardiography↗
PubMed1995

Restenosis after experimental angioplasty. Intimal, medial, and adventitial changes associated with constrictive remodeling.

Predicting and preventing arterial restenosis after angioplasty has failed despite considerable research into mechanisms and techniques. We examined the roles of chronic constriction, neointimal-medial growth, and adventitial changes in restenosis in atherosclerotic rabbits. Angioplasty was performed on femoral artery lesions 4 weeks after lesion induction by air drying and cholesterol-supplemented diet. Angiographic and histological evaluation was conducted 3 to 4 weeks after angioplasty. The angiographic minimum luminal diameter (MLD) increased from 1.31 +/- 0.21 to 1.73 +/- 0.41 mm after angioplasty. Loss in MLD by 3 to 4 weeks was 0.95 +/- 0.64 mm. Initial gain and late loss correlated (P = .008). Late residual stenosis, defined histologically as the difference between the luminal areas of a proximal reference site and lesion site normalized by the luminal area of the reference site, was 52 +/- 32%. Histological indices of chronic constriction, neointimal-medial growth, and adventitial growth were defined on the basis of the areas of these arterial wall layers at the lesion site relative to the reference site. Another parameter defined as the ratio of adventitial area to the area of intima+media at the lesion site allowed evaluation of the relative importance of these layers. Surprisingly, late residual stenosis correlated with chronic constriction (P = .0003) but not with neointimal-medial growth or adventitial growth. The ratio of adventitial area to the area of intima+media at the lesion site also correlated with chronic constriction (P = .01). These findings suggest that factors related to arterial remodeling rather than neointimal-medial growth may dominate the response to angioplasty.

Angiography↗
PubMed2001

Eplerenone suppresses constrictive remodeling and collagen accumulation after angioplasty in porcine coronary arteries.

BACKGROUND: Coronary artery angioplasty triggers healing that causes constrictive remodeling. Because collagen accumulation correlates with constrictive remodeling and aldosterone has been implicated in collagen accumulation, we examined how aldosterone and the mineralocorticoid receptor antagonists spironolactone and eplerenone affect remodeling and collagen in porcine coronary and iliac arteries after angioplasty. METHODS AND RESULTS: Twenty-four pigs were allocated into 4 treatment groups: oral eplerenone (100 mg/d), oral spironolactone (200 mg/d), subcutaneous aldosterone (400 microgram/d), or no treatment. Twenty-eight days after angioplasty of the coronary arteries, eplerenone increased total vessel area by 30% (P<0.05) and luminal area by nearly 60% (P<0.05) compared with the no-treatment group, without affecting neointima size. These effects were accompanied by a 65% reduction in neointimal and medial collagen density (both P<0.05). Spironolactone was less effective, and aldosterone tended to exert opposite effects on coronary artery structure after angioplasty. These effects were not observed in angioplastied iliac arteries. CONCLUSIONS: Eplerenone attenuates constrictive remodeling after coronary artery angioplasty by mechanisms involving reduction in collagen accumulation, which thus appears to be an important contributor to constrictive remodeling of angioplastied coronary arteries.

Aldosterone↗
PubMed1971

A microperfusion study of sucrose movement across the rat proximal tubule during renal vein constriction.

Constriction of the renal vein has been shown to inhibit net sodium and water reabsorption by the rat proximal tubule. The mechanism is unknown but might be the result of inhibition of the active sodium pump induced by changes in the interstitial fluid compartment of the kidney, or to enhanced passive backflux of sodium and water into the cell or directly into the tubular lumen. Since passive movement of solutes across epithelial membranes is determined in part by the permeability characteristics of the epithelium, an increase in the permeability of the proximal tubule during venous constriction would suggest that enhanced passive flux is involved in the inhibition of reabsorption. In the present experiments, isolated segments of rat proximal convoluted tubules were microperfused in vivo with saline while the animals were receiving (14)C-labeled sucrose intravenously. In normal control animals, no sucrose was detected in the majority of the collected tubular perfusates. In rats with renal vein constriction (RVC), however, sucrose consistently appeared in the tubular perfusates. The rate of inflow of sucrose correlated with the length of the perfused segment, estimated by fractional water reabsorption. In another group of animals with renal vein constriction, inulin-(14)C was given intravenously and the proximal tubules similarly microperfused. Inulin did not appear in the majority of collected perfusates in these animals. These observations indicate that a physiological alteration in the permeability of the proximal tubule occurs during RVC. Such an increase in permeability is consistent with the view that enhanced passive extracellular back-flux plays a role in the reduction of net sodium and water reabsorption in this experimental condition.

Animals↗