PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Microcirculation”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,423 records · Page 79Linked to original sources
PubMed1996

Effect of low-dose dopamine on intestinal villus microcirculation during normotensive endotoxaemia in rats.

Hypoperfusion of the gut mucosa is thought to be a factor in the development of gut barrier failure during sepsis and septic shock. Dopamine stimulates DA-1 receptors which mediate regional vasodilatation in the gut. Therefore, we have investigated the effect of low-dose dopamine (3 micrograms kg-1 min-1) on the intestinal villus microcirculation during endotoxaemia in a rat model of normotensive endotoxaemia, using in vivo videomicroscopy. Blood flow in and the diameters of central villus arterioles were measured before, immediately after and 60 min after a 1-h continuous infusion of endotoxin 1.5 mg/kg body weight. After baseline measurements were obtained, rats received either an infusion of 0.9% saline (group A; n = 7) or a volume-equivalent infusion of dopamine 3 micrograms kg-1 min-1 (group B; n = 7) throughout the study. Control animals (group C; n = 7) received no endotoxin or dopamine. In group A, villus blood flow (mean baseline 8.4 (SEM 0.9) nl min-1) decreased by 29.7 (8.9)% to 5.9 (0.9) nl min-1 immediately after endotoxin challenge and by a total of 43.1 (7.3)% to 4.7 (0.7) nl min-1 after another 60 min. Simultaneously, villus arteriolar diameters decreased from 7.8 (0.2) to 6.9 (0.3) microns and to 6.5 (0.3) microns, respectively. In group B, villus blood flow (baseline 8.7 (0.4) nl min-1) was unchanged immediately after the 1-h infusion of endotoxin (8.3 (0.4) nl min-1). However, another 60 min later blood flow decreased by 28.8 (8.0)% to 6.1 (0.7) nl min-1. In contrast with group A, the diameters of the central villus arterioles were unchanged despite administration of endotoxin (7.9 (0.2) microns; 8.1 (0.4) microns; 8.2 (0.5) microns). In group C, there were no changes in villus blood flow or arteriolar diameters throughout the study. Our results indicated that low-dose dopamine did not prevent, but delayed and attenuated, the decrease in intestinal villus blood during normotensive endotoxaemia.

Animals↗
PubMed2000

Intravenous anaesthesia and the rat microcirculation: the dorsal microcirculatory chamber.

The use of the dorsal microcirculatory chamber in male Wistar rats (n=7) to study the effects of induction and maintenance of anaesthesia on the microcirculation is described. Different patterns of responses were observed. At induction, arteriolar dilation was found following propofol and thiopental but ketamine produced constriction. During maintenance, constriction of arterioles was seen with ketamine and thiopental but dilation persisted with propofol. The dorsal microcirculatory chamber appears to be a useful tool for the study of microcirculatory changes related to anaesthesia.

Anesthetics, Dissociative↗
PubMed1988

Role of red blood cells in the coronary microcirculation during cold blood cardioplegia.

The role of red blood cells during cold blood cardioplegia was studied using an intravital microscope in 13 isolated canine hearts perfused with diluted blood containing potassium chloride. The coronary microcirculation on the left ventricular epicardial surface was observed while the perfusate temperature was varied between 37 degrees C and 10 degrees C. Considerable sludging of red blood cells occurred during hypothermia. The percentage of capillaries perfused by red blood cells (percentage change) significantly decreased as perfusate temperature was reduced (100, 56, and 31% at 37, 20, and 10 degrees C respectively). This was caused by occlusion of microvessels due to sludging and by functional closure due to hypothermia. There was incomplete recovery of perfusion of capillaries at the end of rewarming (60%). The diameters of venules were reduced to 76% of control value at 10 degrees C because of the decrease in the numbers of feeding capillaries, but this value returned to 91% at the end of rewarming. Coronary vascular resistance (mmHg.ml-1.min-1 (kPa.s.litre-1] significantly decreased from 2.0(0.2) at 37 degrees C to 1.2(0.12) at 10 degrees C, but it increased to 2.4(0.24) at the end of rewarming. The finding in this study that sludging occurred which was slow to clear is a definite disadvantage of perfusion with red blood cells during hypothermia.

Animals↗
PubMed1990

Changes in the microcirculation in slow and fast skeletal muscles with long term limitations of blood supply.

STUDY OBJECTIVE: Long term limitation of blood flow leads to decreased muscle performance and to damage, particularly in predominantly oxidative muscles. This study was performed to assess to what extent such damage can be explained by changes in microcirculation in capillaries supplying glycolytic or oxidative muscle fibres. DESIGN: Velocity and intermittency of flow, capillary diameters and proportion of adhering leucocytes were measured in capillaries in the epi-illuminated superficial glycolytic layer of rat tibialis anterior and in oxidative soleus muscles five weeks after ligation of the common iliac artery. EXPERIMENTAL MATERIAL: Male Sprague Dawley rats (approximately 350 g) were used, under sodium pentobarbitone anaesthesia. MEASUREMENTS AND RESULTS: Pressure in the saphenous artery, distal to the ligation site, recovered to 61% of carotid mean pressure. In tibialis anterior with limited blood supply, capillary diameters were narrower, red blood cell velocity was greater and intermittency of flow was reduced, resulting in a calculated volume flow per capillary which was only marginally reduced compared with controls. In soleus with limited blood supply, the time spent stationary by red blood cells was increased and there was a greater adhesion of white blood cells to venular walls. In neither muscle did limitation of blood supply result in a change in capillarity. CONCLUSIONS: Long term limitation of blood supply does not diminish the capillary density or capillary to fibre ratio of anatomically present capillaries in oxidative or glycolytic muscles and does not affect blood flow in capillaries supplying glycolytic fibres appreciably; circulation in capillaries supplying oxidative fibres is impaired.

Animals↗
PubMed1987

Effects of AQA-39 on granulocytes in the microcirculation of rat mesentery.

Recent evidence suggests that granulocytes play a key role in perfusion of the microcirculation. In this regard two phenomena are of specific importance: pseudopod formation and adhesion to the endothelium. Thus we studied the influence of AQA-39 on leukocyte adhesion to the endothelium in rat mesentery venules and on pseudopod formation in human granulocytes. Direct intravital estimates of granulocyte fracture stress were obtained by measurement of the ratio of leukocyte and midstream velocity. The marginating and circulating cell flux and the areal density of stationary granulocytes on the intraluminal side of the endothelium were measured simultaneously in the same venular segments. During administration of 10 mg kg-1 AQA-39 the fracture stress is significantly reduced resulting in decreased areal density of marginating cells and also washout of strongly adhering stationary leukocytes found frequently on the endothelium of such vessels. Furthermore it was observed on single granulocytes that AQA-39 leads to transient obliteration of pseudopod formation. These results suggest that the effect of AQA-39 on flow may be mediated in part by reduction in granulocyte adhesion to the endothelium and suppression of pseudopod formation.

Animals↗
PubMed1992

Copper deficiency alters vasodilation in the rat cremaster muscle microcirculation.

The effects of copper deficiency on smooth muscle relaxation were studied in the cremaster muscle microcirculation. Male Sprague-Dawley rats were fed either a copper-adequate diet (CuA, 5 micrograms copper/g diet) or copper-deficient diet (CuD, no added copper) for 17-27 d before experimentation. In vivo television microscopy was used to quantify agonist-induced diameter changes in third-order arterioles. Endothelium-dependent relaxation, which is hypothesized to be mediated by nitric oxide, was attenuated by copper deficiency. Both receptor (acetylcholine, 10(-7) to 10(-4) mol/L) and nonreceptor (calcium ionophore A23187, 10(-8) to 10(-7) mol/L) relaxation was decreased. Nitric oxide-mediated dilation, which was endothelium-independent (10(-7) to 10(-5) mol/L sodium nitroprusside), was also attenuated by copper deficiency. Maximal responses were as follows: for acetylcholine, 136 +/- 16% CuA vs. 45 +/- 15% CuD; for A23187, 104 +/- 16% CuA vs. 21 +/- 11% CuD; and for nitroprusside, 125 +/- 12% CuA vs. 46 +/- 13% CuD. There was no difference in microvascular dilation between groups treated with 10(-6) to 10(-4) mol/L of the phosphodiesterase inhibitor papaverine (e.g., CuA 109 +/- 11% vs. CuD 133 +/- 21% with 10(-4) mol/L). These results suggest that copper deficiency inhibits the nitric oxide-mediated mechanism of vascular smooth muscle relaxation without altering the capacity of the smooth muscle to relax. We suggest that copper deficiency either decreases nitric oxide radical availability or disrupts the nitric oxide-guanylate cyclase interaction.

Acetylcholine↗
PubMed1994

Platelet thrombus formation and hemostasis are delayed in the microcirculation of copper-deficient rats.

The role of dietary copper in platelet thrombus formation and hemostasis was studied in the cremaster muscle microcirculation. Male weanling Sprague-Dawley rats were fed purified diets that were either copper-adequate (94 mumol Cu/kg diet) or copper-deficient (0 mumol Cu/kg diet) for 1, 3 or 5 wk. The rats were anesthetized with pentobarbital, and the cremaster was spread in a Krebs-filled tissue bath. Fluorescein isothiocyanate tagged to bovine serum albumin (FITC-BSA) was injected intra-arterially. After a 20-min equilibration, blue light (1.8 W/cm2, 450-490 nm) was used to activate the FITC-BSA and induced platelet thrombus formation within the vasculature. In vivo television microscopy was used to quantify the thrombus formation. In rats fed the copper-deficient diet for 3 or 5 wk, platelet thrombus formation induced by photoactivation was significantly (P < 0.05) delayed and prothrombin time was significantly longer but the number of circulating platelets was significantly greater than in age-matched rats fed the copper-adequate diet. Bleeding time, measured after micropuncture of a second-order venule, was significantly longer but hematocrit was significantly lower in rats fed the copper-deficient diet than in those fed the copper-adequate diet. The results demonstrate that platelet-mediated hemostasis is depressed in dietary copper deficiency and that this may be due to a decrease in hematocrit, a decrease in the activity of a coagulation factor and/or an alteration of platelet function.

Animals↗
PubMed1991

Preferential localization of human adherent lymphokine-activated killer cells in tumor microcirculation.

The efficacy of adoptive immunotherapy for solid tumors with lymphokine-activated effector cells presumably depends on the ability of these cells to localize adequately in tumor tissues. We present here the first quantitative study of the in vivo movement of fluorescently labeled adherent lymphokine-activated killer (A-LAK) cells. These cells were injected intra-arterially along with low-dose interleukin-2 into normal (mature granulation) tissue and an implant of VX2 carcinoma grown in the rabbit ear chamber. A small proportion of A-LAK cells accumulated preferentially in the tumor microcirculation in vivo because of an increased frequency of long-term adhesive interactions with the tumor vasculature. Stasis of blood flow in the tumor vasculature was observed 1 to 2 days after injection. Subsequent necrosis of the tumors was observed, along with diffuse infiltrates of lymphocytes, monocytes, and granulocytes in the interstitial space within the tumor. Development of necrosis despite low ratios of effector cells to target cells suggests that in addition to direct cytotoxicity, the response to adoptive immunotherapy is mediated via the tumor vasculature. This novel mechanism for adoptive immunotherapy must be taken into account in the development of improved strategies for cancer treatment.

Animals↗
PubMed1998

Acute effects of haemodialysis on cutaneous microcirculation in patients with peripheral arterial occlusive disease.

BACKGROUND: Peripheral arterial occlusive disease (PAOD) is an increasing problem in patients on maintenance haemodialysis. Alterations in microvascular perfusion accompany and complicate arteriosclerosis of large vessels and might contribute to the disease process. The aim of the study was to investigate the acute effects of haemodialysis on the cutaneous microcirculation in 26 patients with and without intermittent claudication. METHODS: Cutaneous perfusion was assessed by measuring transcutaneous oxygen pressure (tcPO2) and skin temperature at the dorsum of the foot. After standardized cooling to 15 degrees C of a 2cm2 skin area, the time to reach baseline skin temperature was evaluated as an indirect parameter of reactive hyperaemia. RESULTS: During haemodialysis, tcPO2 dropped significantly in both groups. The decrease in tcPO2 was more pronounced in patients with PAOD (20% vs 15% n.s.). The reactive hyperaemia response was reduced significantly in patients with intermittent claudication indicated by a prolonged time to reach baseline skin temperature after cooling. Values of tcPO2 and reactive hyperaemia did not reach baseline values at the end of haemodialysis in either group. CONCLUSIONS: Nutritive skin perfusion is impaired during haemodialysis. These changes are more pronounced in patients with PAOD and persist after dialysis. These findings are relevant for the treatment of patients with vascular disease on maintenance haemodialysis.

Adult↗
PubMed2005

Beneficial effects of aminoguanidine on peritoneal microcirculation and tissue remodelling in a rat model of PD.

BACKGROUND: The formation of glucose degradation products (GDPs) and accumulation of advanced glycation end products (AGEs) partly contribute to the bioincompatibility of peritoneal dialysis fluids (PDF). Aminoguanidine (AG) scavenges GDPs and prevents the formation of AGEs. METHODS: In a peritoneal dialysis (PD) rat model, we evaluated the effects of the addition of AG to the PDF on microcirculation and morphology of the peritoneum, by intravital microscopy and quantitative morphometric analysis. RESULTS: AG-bicarbonate effectively scavenged different GDPs from PDF. Daily exposure to PDF for 5 weeks resulted in a significant increase in leucocyte rolling in mesenteric venules, which could be reduced for approximately 50% by addition of AG-bicarbonate (P<0.02). Vascular leakage was found in rats treated with PDF/AG-bicarbonate, but not with PDF alone. Evaluation of visceral and parietal peritoneum showed the induction of angiogenesis and fibrosis after PDF instillation. PDF/AG-bicarbonate significantly reduced vessel density in omentum and parietal peritoneum (P<0.04), but not in mesentery. PDF-induced fibrosis was significantly reduced by AG (P<0.02). PDF instillation led to AGE accumulation in mesentery, which was inhibited by supplementation of AG. Since addition of AG-bicarbonate to PDF raised pH from 5.2 to 8.5, a similar experiment was performed with AG-hydrochloride that did not change the fluid acidity. We could reproduce most of the results obtained with AG-bicarbonate; however, AG-hydrochloride induced no microvascular leakage and had a minor effect on angiogenesis. CONCLUSION: The supplementation of either AG reduced a number of PDF-induced alterations in our model, emphasizing the involvement of GDPs and/or AGEs in the PDF-induced peritoneal injury.

Animals↗
PubMed1998

Visualization of chronic neck-shoulder pain: impaired microcirculation in the upper trapezius muscle in chronic cervico-brachial pain.

This study pertains to the 71 patients who had received a diagnosis of cervico-brachial pain syndrome after thorough clinical examination of a total series of 300 patients, who had been referred to the National Insurance Hospital in Tranås because of chronic neck pain that interfered with their ability to work. Changes in trapezius muscle blood flow and EMG were examined and related to the anamnesis and physical findings. The microcirculation in the upper part of the right and left trapezius muscles was examined simultaneously by using optical laser-Doppler single-fibres after insertion into the muscle directly via the skin. Continuous recordings were made during stepwise increased static contraction determined electro-myographically. Signal processing was performed on-line by computer. MRT of the cervical spine was performed in 12 patients. None showed nerve root affliction. Ten showed a bulging intervertebral disc and two, a narrowed nerve hole (lateral stenosis). The muscle blood flow (LDF) was significantly lower in the most painful side compared with the opposite side in the group of 41 patients with predominantly unilateral pain (21 women and 20 men). A lowered blood flow was also found when the 21 females in this group was compared with a normal control group of 20 healthy women. The patients had lower rms-EMG and EMG mean power frequency (MPF) in the painful side compared with the opposite side. A further lowering of the MPF was observed with induced fatigue. It was concluded that the chronic neck pain in cervico-brachial syndrome can become visualized by the finding of lowered blood flow of the trapezius muscle which seems to be an expression of the chronic neck pain.

Adult↗
PubMed1997

Effect of high-voltage pulsed current and alternating current on macromolecular leakage in hamster cheek pouch microcirculation.

BACKGROUND AND PURPOSE: Electrical stimulation (ES) is supposed to affect edema formation by inhibiting macromolecular leakage from microvessels. The purpose of the study was to determine the effects of various forms of ES on macromolecular leakage from microvessels. SUBJECTS: Fifty-three hamsters were randomly assigned to one of seven groups: a control group (histamine only); groups that received histamine with cathodal high-voltage pulsed current (HVPC) at intensities of 90%, 50%, and 10% of visible motor threshold (VMT); groups that received anodal HVPC at intensities of 90% and 50% of VMT; and a group that received alternating current (AC) at 90% of VMT. METHODS: Anesthetized animals were injected with fluorescein-labeled dextran. Macromolecular leakage was determined by computer analysis of fluorescence microscopy images for 5 minutes after treatment. RESULTS: When compared with controls, leakage was less in groups treated with cathodal HVPC at 90% and 50% of VMT and anodal HVPC at 90% of VMT. CONCLUSION AND DISCUSSION: Cathodal and anodal HVPC, but not AC, curb macromolecular leakage from the microvessels of histamine-treated hamsters. [Taylor K, Mendel FC, Fish DR, et al. Effect of high-voltage pulsed current and alternating current on macromolecular leakage in hamster cheek pouch microcirculation.

Animals↗
PubMed1997

Comparative effects of hypotension due to isoflurane, nitroglycerin, and adenosine on subendocardial microcirculation: observation of the in situ beating swine heart under critical stenosis.

BACKGROUND: Although isoflurane may cause subendocardial hypoperfusion in the presence of coronary stenosis because of its coronary arteriolar dilatory effects, it is not known how the subendocardial microcirculation is affected. The authors examined the effects of isoflurane on poststenotic subendocardial microvessels with coronary stenosis. METHODS: The authors observed subendocardial microvessels in in situ beating swine hearts with or without critical stenosis of the left anterior descending coronary artery (LAD) with a needle-type videomicroscope during isoflurane- (ISO-H), adenosine- (ADE-H), and nitroglycerin- (NTG-H) induced hypotension (mean arterial pressure, 55 mmHg). Regional myocardial function, oxygen balance, and lactate metabolism in the region perfused by the LAD also were determined. RESULTS: In swine with stenosis, there were no differences in heart rate, cardiac output, and LAD blood flow among the three types of hypotension. Regional lactate production and anterior interventricular venous pO2 were similar during ISO-H and NTG-H but higher during ADE-H. With videomicroscopy, about half as many subendocardial microvessels could be visualized during ADE-H as with ISO-H and NTG-H. The average decrease in the systolic diameter of subendocardial microvessels of greater than 100 microm was 9 +/- 6% during ISO-H and 12 +/- 5% during NTG-H, but no consistent phasic diameter changes were observed during ADE-H. In swine without stenosis, a systolic diameter decrease was observed during all three types of hypotension. CONCLUSIONS: These findings suggest that hypotension induced by isoflurane or nitroglycerin preserves phasic diameter changes in subendocardial microvessels in the presence of critical coronary stenosis, whereas that induced by adenosine does not.

Adenosine↗
PubMed1997

Leukocyte-endothelium interaction in the rat mesenteric microcirculation during halothane or sevoflurane anesthesia .

BACKGROUND: The effects of inhalational anesthetics on the microcirculation, including leukocyte dynamics, remain to be clarified. The authors investigated halothane and sevoflurane anesthesia to determine if these agents evoked leukocyte adhesion through endothelial cell-dependent mechanisms involving such adhesion molecules. METHODS: Rats were anesthetized with halothane or sevoflurane in 100% oxygen and the lungs were mechanically ventilated. Leukocyte behavior in mesenteric venules was recorded through intravital video microscopy under monitoring microvascular hemodynamics. To examine the mechanisms for leukocyte rolling and adhesion, these studies were repeated after animals were pretreated with a monoclonal antibody against P-selectin (MAb PB1.3) or against intracellular adhesion molecule-1 (ICAM-1; MAb 1A29): P-selectin required for rolling of circulating leukocytes and ICAM-1 for firm adhesive interactions with leukocyte integrins. RESULTS: Under baseline anesthetic conditions (1 minimum alveolar concentration [MAC]), venular wall shear rates, an index of the disperse force on marginating leukocytes, in the sevoflurane-treated rats were about two times higher than those with halothane. At 2 MAC, halothane caused a marked arteriolar constriction and decreasing shear rates concurrent with an increasing density of venular leukocyte adhesion. Sevoflurane at 2 MAC induced leukocyte rolling and adhesion, which were attenuated by PB1.3 and 1A29, without alterations in the wall shear rates. Halothane-induced leukocyte adhesion was not prevented by PB1.3 but it was by 1A29. CONCLUSIONS: Halothane or sevoflurane anesthesia induces venular leukocyte rolling and adhesion: P-selectin upregulation plays a crucial role in leukocyte rolling and adhesion during sevoflurane anesthesia, whereas low-flow perfusion is likely to evoke ICAM-1-dependent leukocyte adhesion during halothane anesthesia.

Anesthetics, Inhalation↗
PubMed1999

Interferon-gamma improves muscle flap microcirculation in double-strand RNA-induced inflammation.

Endothelial cell (EC) activation and subsequent expression of leukocyte adhesion molecules are initial events in multiple pathological processes. Viral double-strand ribonucleic acid (dsRNA) induces EC adhesion protein expression and leukocyte adhesion in vitro. Interferon-gamma (IFN-gamma) has been demonstrated to modulate the expression of certain adhesion proteins. The purpose of this study was to measure the inflammatory response to a viral mimetic--a synthetic dsRNA, polyinosinic-polycytidylic acid (poly-I:C)-on the microcirculation of a muscle flap in a rat model and to determine whether IFN-gamma attenuated the response. Two-stage surgery to create a cremaster muscle end-organ tube flap was performed on 18 male Sprague-Dawley rats in three groups. After intra-arterial injection into the abdominal aorta, the reagents (phosphate-buffered saline-bovine serum albumin [PBS-BSA] in groups I and II, and IFN-gamma in group III) were kept for 1 hour in this end-organ system. During the second stage at 16 hours, after injection into the penile vein (PBS-BSA in group I, poly-I:C in groups II and III), the flap was prepared for intravital microscopic measurement. The following parameters were measured: red blood cell velocity; vessel diameter; number of functional capillaries; and number of rolling, sticking, and transmigrating neutrophils and lymphocytes. Wilcoxon's rank sum test was used for statistical comparison. Poly-I:C caused a 70% increase in the main artery diameter and a 7% increase in velocity. But as a consequence of dynamic activation of leukocyte interaction, a 30% drop in functional capillary perfusion was observed. Injury to the entire vascular endothelium was confirmed by a 160% increase in transmigrating leukocytes. Treatment with IFN-gamma inhibited the poly-I:C-induced inflammation, as shown by 88%, 63%, and 85% decreases in rolling, sticking, and transmigrating leukocytes respectively, and by a 28% increase in capillary perfusion. Treating the system with IFN-gamma in advance, inhibited poly-I:C-induced inflammation, shown by marked decreases in rolling, adhering, and transmigrating leukocytes, and a notable increase in perfused capillaries. These observations reflect an inhibitory effect of IFN-gamma on leukocyte adhesion molecule expression in vascular endothelium in response to dsRNA in a muscle flap at the microcirculatory level.

Animals↗
PubMed1975

Microcirculation of the normal and inflamed canine pancreas.

Pancreas of normal dogs and the inflamed gland of experimental pancreatitis were studied by intra-arterial injection of Microfil, a silicone-rubber compound especially suited for study of the microcirculation. Duodenal vasculature and lobular vessels of the pancreas were studied as were those supplying the duct. Inter-lobular vessels were well visualized in the normal pancreas and intralobular vessels formed a fine reticular pattern throughout the cleared lobules. A complex network of vessels in the pancreatic duct was observed using this technique, apparently derived from the interlobular vessels. The blood supply of each layer of the duodenum was evaluated. Intraductal trypsin injection produced focal areas of pancreatitis associated with edema, poor vascular filling and spastic changes of the lobular vessels. Extravasation of Microfil, although not apparent on normal specimens, was prominent in inflamed specimens and suggested vascular weakness and disruption. Pancreatic lobules adjacent to inflammatory areas showed definite evidence of dilatation. The inflamed pancreatic ducts were markedly edematous, thickned, and showed incomplete vascular filling. When the duodenum adjacent to pancreatitis was injected with Microfil, edema and vasoconstriction were especially prominent in the duodenal muscular layer.

Animals↗
PubMed1993

Red-cell trapping in the rat renal microcirculation induced by low-osmolar contrast media and mannitol.

RATIONALE AND OBJECTIVES: In acute renal failure after ischemia, intravascular obstruction by trapped red blood cells in the microvasculature of the renal outer medulla is a consistent finding. The influence of intravenously injected contrast media (CM) on such obstruction was investigated. METHODS: Anesthetized rats were subjected to 45 minutes of unilateral renal ischemia. Red-cell trapping in ischemically injured kidneys and in the contralateral uninjured kidneys was estimated from the intrarenal distribution of 51Cr-labelled erythrocytes after injection of ioxaglate or iopamidol in a dose of 1,600 mg I/kg body weight. As an osmolar control substance, mannitol (950 mOsm/kg) was given to a third group and isotonic Ringer's solution was administered to a fourth group. RESULTS: In the uninjured kidneys, treatment with ioxaglate or mannitol resulted in no red-cell trapping, while the iopamidol-treated group showed red-cell trapping in the inner stripe of the outer medulla in a dose-dependent manner. In the ischemically injured kidneys, both CM and mannitol enhanced the red-cell trapping in the inner stripe of the renal medulla. CONCLUSION: The results indicate that intravenously administered ioxaglate and iopamidol enhance the microvascular obstructions evoked by ischemic injury and that iopamidol may induce local impairment in renal medullary microcirculation in a normal kidney.

Animals↗