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PubMed1999

Effects of 8-Gy radiation on the microcirculation of muscle flaps in the rat.

Combination of radical excision and radiation has been used as a treatment modality for cancer patients. As a result, in reconstructive surgery there is often a need to harvest flaps in the vicinity of previously irradiated tissues. Radiation has been shown to cause progressive injury to the macrocirculation and microcirculation, often jeopardizing flap survival. The purpose of this study was to examine whether radiation significantly affects the sequence of leukocyte-endothelial interactions or the hemodynamics of the muscle flap in both acute and chronic situations. Male Sprague-Dawley rats (n = 42) were divided into seven groups of six rats each. Rats in group I were not irradiated. Groups II through VII received 8-Gy radiation to the right groin and scrotum. Groups II, III, and IV were examined at 4, 24 and 72 hours, respectively, and groups V, VI, and VII were examined at 1, 2 and 12 weeks. For intravital microscopy, the cremaster muscle was dissected on its neurovascular pedicle. Vessel diameters and red blood cell velocities were measured in the central cremasteric branches and branch arterioles. Capillary perfusion was evaluated in 27 visual fields of each flap. Leukocyte-endothelial interactions were evaluated by numbers of rolling, adhering, and transmigrating leukocytes in post-capillary venules. In the same postcapillary venule, we measured the endothelial edema index (constriction index). The hemodynamics of irradiated flaps did not differ significantly from those of controls. Diameter and red blood cell velocity were increased in the first- and second-order arterioles and were highest at 72 hours and 1 week. After irradiation, third-order arterioles were constricted. Radiation reduced capillary perfusion by 4.3, percent. None of the differences were statistically significant. Neither leukocyte behavior nor the constriction indices differed among the groups. In conclusion, low-dose radiation of 8 Gy does not affect hemodynamics or leukocyte-endothelial interactions of muscle flaps in the rat. Muscle tissue with intact microvasculature can be harvested for reconstructive procedures after low-dose radiation.

Animals↗

PubMed1996

Impact of N-acetylcysteine on the hepatic microcirculation after orthotopic liver transplantation.

Recent observations showed an improvement of hepatic macro- and microhemodynamics as well as survival rates after warm ischemia of the liver following treatment with N-acetylcysteine (NAC). In this study we assessed the influence of NAC on the hepatic microcirculation after orthotopic liver transplantation (OLT) using intravital fluorescence microscopy. OLT with simultaneous arterialization was performed in 16 male Lewis rats following cold storage in University of Wisconsin solution for 24 hr. Within the experimental group (n = 8) donors received NAC (400 mg/kg) 25 min before hepatectomy. In addition, high-dose treatment of recipients with NAC (400 mg/kg) was started with reperfusion. Control animals (n = 8) received an equivalent amount of Ringer's solution. Intravital fluorescence microscopy was performed 30-90 min after reperfusion assessing acinar and sinusoidal perfusion, leukocyte-endothelium interaction, and phagocytic activity. Treatment with NAC reduced the number of nonperfused sinusoid from 52.4 +/- 0.8% to 15.7 +/- 0.5% (p = 0.0001) (mean +/- SEM). Furthermore, we achieved a significant reduction of leukocytes adhering to sinusoidal endothelium (per mm2 liver surface) from 351.9 +/- 13.0 in controls to 83.6 +/- 4.2 in the experimental group (P = 0.0001). In postsinusoidal venules, treatment with NAC decreased the number of sticking leukocytes (per mm2 endothelium) from 1098.5 +/- 59.6 to 425.9 +/- 37.7 (P = 0.0001). Moreover, bile flow was significantly increased after therapy with NAC (4.3 +/- 1.2 vs. 2.2 +/- 0.7 ml/90 min x 100g liver) (P < 0.05). Phagocytic activity was not influenced by application of NAC. We conclude that high-dose therapy with NAC in OLT attenuates manifestations of microvascular perfusion failure early after reperfusion and should be considered as a means to reduce reperfusion injury.

Acetylcysteine↗

PubMed1998

Complement inhibition by soluble complement receptor type 1 improves microcirculation after rat liver transplantation.

BACKGROUND: Recent observations provide evidence that complement is involved in the pathophysiology of ischemia/reperfusion injury. In this study, we assessed the impact of complement inhibition on hepatic microcirculation and graft function using a rat model of liver transplantation. METHODS: Arterialized orthotopic liver transplantation was performed in Lewis rats after cold preservation (University of Wisconsin solution, 4 degrees C, 24 h). Eight animals received the physiological complement regulator soluble complement receptor type 1 (sCR1) intravenously 1 min before reperfusion. Controls received Ringer's solution (n=8). Microvascular perfusion, leukocyte adhesion, and Kupffer cell phagocytic activity were studied 30-100 min after reperfusion by in vivo microscopy. RESULTS: Microvascular perfusion in hepatic sinusoids was improved in the sCR1 group (87+/-0.7% vs. 50+/-1%; P < 0.001). The number of adherent leukocytes was reduced in sinusoids (68.3+/-4.7 vs. 334.1+/-15.8 [adherent leukocytes per mm < or = liver surface]; P < 0.001) and in postsinusoidal venules after sCR1 treatment (306.6+/-21.8 vs. 931.6+/-55.9 [adherent leukocytes per mm < or = endothelial surface]; P < 0.001). Kupffer cell phagocytic activity was decreased in the sCR1 group compared to controls. Postischemic bile production reflecting hepatocellular function was increased by almost 200% (P = 0.004) after complement inhibition. Plasmatic liver enzyme activity was decreased significantly upon sCR1 treatment, indicating reduced parenchymal cell injury. CONCLUSIONS: Our results provide further evidence that the complement system plays a decisive role in hepatic ischemia/reperfusion injury. We conclude that complement inhibition by sCR1 represents an effective treatment to prevent reperfusion injury in liver transplantation.

Animals↗

PubMed2001

Effects of FK409 on intestinal ischemia-reperfusion injury and ischemia-induced changes in the rat mucosal villus microcirculation.

BACKGROUND: The small intestine is extremely sensitive to ischemia-reperfusion (I/R) injury and a range of microcirculatory disturbances contribute to tissue damage. Nitric oxide (NO) seems to be involved in tissue protection after I/R injury. This study therefore assessed the effects of the NO donor, FK409, on intestinal I/R injury and changes induced in intestinal microcirculation. METHODS: PVG rats were subjected to 30-min intestinal ischemia with a subgroup of animals receiving FK409 (10 mg/kg i.v.) 30 min before ischemia and 30 min postreperfusion. Controls underwent sham surgery. The mucosal surface was visualized via an incision made in an exteriorized ileal segment and FITC-BSA or acridine orange was used to quantitate macromolecular leak (MML) and leukocyte adhesion, respectively. MML from, and numbers of adherent leukocytes within, individual villi were determined every 15 min for 2 hr after removal of the vessel clamp. Heart rate and mean blood pressure (mBP) were monitored throughout the experiment. RESULTS: Eleven of 12 untreated animals subjected to intestinal I/R injury failed to survive the 2 hr reperfusion period, whereas all 12 FK409-treated animals survived. MML and leukocyte adhesion were increased in untreated animals (P<0.001), and blood flow stasis eventually ensued. Although FK409 decreased mBP (P<0.001), MML and leukocyte adhesion were significantly (P<0.001) reduced, and villus blood flow was maintained throughout the observation period. CONCLUSIONS: FK409 prevented mortality after intestinal I/R, significantly reduced leukocyte adhesion, and maintained blood flow after intestinal ischemia and may therefore be of value in reducing tissue damage and improving outcome after small bowel transplantation.

Animals↗

PubMed1997

Acute effects of 17 beta-estradiol on the coronary microcirculation: observations in sedated, closed-chest domestic swine.

OBJECTIVES: To test the hypotheses: that acute administration of 17 beta-estradiol dilates normal coronary microvessels in vivo; that coronary microvascular responses to acute estrogen stimulation exhibit sexual dimorphism; and that nitric oxide has a role in mediating these effects. METHODS: Measurements of hemodynamics, coronary flow velocity (Doppler), myocardial blood flow (microspheres) and oxygen consumption were made in closed-chest swine: group 1 consisted of castrated juvenile males, groups 2 and 3 of estrogen pretreated, castrated juvenile males, and group 4 of sexually mature females. 17 beta-Estradiol (2, 20 or 200 ng/kg) was given by intracoronary injection and data obtained 20-30 min later; additional measurements were made 1 h after the 200 ng/kg dose. The effect of L-NG-monomethylarginine (L-NMMA) on 17 beta-estradiol responses was also tested. Tissue and blood concentrations of 17 beta-estradiol, and concentrations of estrogen receptor in myocardium and coronary vessels were obtained. RESULTS: In estrogen-naive castrated males, 17 beta-estradiol had no effect on coronary flow velocity or myocardial blood flow, but 1 h after the 200 ng/kg dose there was an increase in diastolic coronary resistance compared with baseline (48 +/- 20 versus 41 +/- 17 mmHg/mkHz; P < 0.05). Estrogen pretreated castrated males also showed no change in myocardial blood flow after 17 beta-estradiol, but coronary flow velocity decreased (P < 0.05) compared with baseline 1 h after the 200 ng/kg dose (from 1.69 +/- 0.61 to 1.41 +/- 0.42 kHz) and diastolic coronary resistance increased significantly (P < 0.01) compared with control at this time (51 +/- 15 compared with 39 +/- 14 mmHg/mkHz). In sexually mature females, 17 beta-estradiol had no effect on myocardial blood flow but did cause a significant (P < 0.05) decrease in diastolic coronary vascular resistance compared with baseline (51 +/- 9 mmHg/mkHz) at both the 20 ng/kg and the 200 ng/kg doses (both 43 +/- 11 mmHg/mkHz). Coronary flow velocity also increased (P < 0.06) compared with baseline (1.34 +/- 0.26 mmHg/mkHz) after the 200 ng/kg dose (1.69 +/- 0.61 mmHg/mkHz). L-NMMA had no effect on flow responses to 17 beta-estradiol in any group. Classical estrogen receptors were not present in myocardium or coronary arteries from male or female swine. CONCLUSIONS: These results demonstrate that 17 beta-estradiol exerts a mild constrictor effect on the coronary microvessels of normal castrated, juvenile males whether estrogen-naive or estrogen-pretreated. In contrast, sexually mature normal females exhibit mild dilatation of the coronary microcirculation in response to acute estrogen stimulation. Nitric oxide does not appear to have a role in mediating the dilator response in females, and classical estrogen receptors are not involved. A direct membrane effect of the hormone (perhaps via alteration in potassium conductance) seems likely, and demonstrates sexual dimorphism.

Animals↗

PubMed1994

Role of nitric oxide in the small intestinal microcirculation during bacteremia.

Nitric oxide (NO) is an important mediator of the hemodynamic effects of sepsis; however, its microcirculatory effects are unknown. To determine the role of NO in the small intestinal (SI) microcirculation, an intact SI loop was exteriorized from decerebrate rats into a controlled Krebs' bath. Bacteremic rats received 10(9) Escherichia coli intravenously. Videomicroscopy was used to measure arteriolar diameters (A1, A3) and optical Doppler velocimetry to quantitate flow. In controls, topical NO synthase (NO-S) substrate L-arginine (L-ARG; 10(-4) M) did not affect diameters or flow. Inhibition of NO-S by N omega-nitro-L-arginine methyl ester (L-NAME; 10(-4) M) caused constriction (A1 = -18%; A3 = -24% from baseline diameter) and reduced A1 flow by 62%. These alterations were similar to bacteremic controls (A1 = -20%; A3 = -18%; A1 flow = -42%), despite the increased cardiac output (+21%). L-NAME treatment of bacteremic rats resulted in further constriction (A1 = -31%; A3 = -32%) and decreased A1 flow (-75%). Topical L-ARG (10(-4) M) ameliorated constriction (A1 = -6%; A3 = +7%) and improved blood flow (-5%) during bacteremia. We conclude that: 1) NO is important for basal SI microvascular tone; 2) bacteremia causes SI arteriolar constriction and hypoperfusion; 3) NO-S inhibition during sepsis may exacerbate SI vasoconstriction and hypoperfusion.

Amino Acid Oxidoreductases↗

PubMed1994

Heat shock attenuates endothelium-dependent vasodilation in skeletal muscle microcirculation.

Endothelium-derived relaxing factors (EDRFs) mediate vasodilation of small arterioles in skeletal muscle under various (patho)physiological conditions: Escherichia coli sepsis, systemic hypoxia, and topical acetylcholine (ACH) application. To test if heat shock changes EDRF-dependent reactivity of arterioles to ACH, we used closed-circuit videomicroscopy in the in vivo cremaster muscle of rats whose systemic temperatures had been slowly raised to and maintained at 41 degrees C. We also tested for ACH responses after increasing cremaster muscle temperatures and maintaining those at 40 degrees C. The experiments showed that EDRF-dependent vasodilation of small arterioles to acetylcholine was substantially attenuated in response to systemic and local heat treatment. In two other animal groups, concentration-dependent vasodilation of small arterioles to sodium-nitroprusside was not as much attenuated in the response to local tissue temperature elevation. This suggests that locally elevated tissue or systemically elevated body temperatures can change generation or efficacy of EDRFs in the post-hyperthermia phase in the skeletal muscle microcirculation.

Acetylcholine↗

PubMed2004

Arginine vasopressin compromises gut mucosal microcirculation in septic rats.

OBJECTIVE: Arginine vasopressin (AVP) is increasingly used in the therapy of septic patients with hypotension. However, its effects on the microvascular networks have not been studied in detail. This study was designed to determine the effects of AVP infusion on the villus microcirculation of the septic rat ileum. DESIGN: Prospective, placebo-controlled, randomized, single-blinded trial. SETTING: University research laboratory. SUBJECTS: Fifteen male Sprague-Dawley rats. INTERVENTIONS: Twenty-four hours after cecal ligation and perforation to create sepsis (M1), rats (n = 8) received a continuous AVP infusion to increase mean arterial pressure by 20 mm Hg (M2) and 40 mm Hg (M3) from M1. In the control group (n = 7), an equivalent volume of normal saline was infused. MEASUREMENTS AND MAIN RESULTS: Videomicroscopy was performed on 6-10 villi of ileum mucosa at M1 and was repeated at M2 and M3. Blood was drawn to determine plasma levels of AVP and interleukin-6. At M1, both study groups were hypotensive compared with preseptic data (mean arterial pressure, -25%). The increase in mean arterial pressure was linked to supraphysiologic AVP plasma levels and was accompanied by a decrease in mean mucosal blood flow by 76% at M2 and 81% at M3 (p <.001 vs. control). Red blood cell velocity fell by 45% and 47%, respectively (p <.05 vs. control). Whereas periods of arrested villus blood flow increased from 8.1 +/- 2.6 secs/min to 43.8 +/- 5.2 and 47 +/- 6.2 secs/min at M2 and M3 (p <.001), the diameter of terminal arterioles remained unchanged. In addition, AVP infusion further augmented the sepsis-associated increase in interleukin-6 levels (AVP, 905 +/- 160 vs. control, 638 +/- 55 pg/mL; p =.022). CONCLUSIONS: This study provides evidence for severe abnormalities in gut mucosal blood flow after AVP infusion in septic rats, accompanied by an augmented inflammatory response to the septic injury. The effects of AVP on microvascular blood flow in this model may be related to AVP activities on larger arterioles (>40 microm), a concomitant reduction in cardiac output, or even both.

Animals↗

PubMed2003

Dehydroepiandrosterone protects the microcirculation of muscle flaps from ischemia-reperfusion injury by reducing the expression of adhesion molecules.

Adhesion molecules contribute to ischemia-reperfusion injury by increasing the endothelial adhesion and extravasation of leukocytes. Scientific evidence suggests that presurgical treatment with dehydroepiandrosterone may protect the microvasculature against this damage, but the exact mechanism is not known. The purpose of this study was to investigate the effects of presurgical dehydroepiandrosterone treatment on microcirculatory hemodynamic parameters and the expression of adhesion molecules in a rat cremaster muscle flap model. Twenty male rats were randomly assigned to three experimental groups. In group I (n = 5), the muscle flaps did not receive presurgical treatment. In group II (n = 6), propylene glycol (30 mg/kg), the vehicle for dehydroepiandrosterone, was injected intravenously before ischemia was induced. In group III (n = 9), dehydroepiandrosterone (30 mg/kg) was injected intravenously before ischemia was induced. All flaps were subjected to 6 hours of ischemia and 90 minutes of reperfusion. Microcirculatory variables (functional capillary density, red blood cell velocity in the main flap arteriole, and numbers of rolling, sticking, and transmigrating leukocytes), blood levels of three adhesion molecules (L-selectin, Mac-1 integrin, and CD44), and the numbers of leukocytes expressing those molecules were analyzed. Analysis of the microcirculatory parameters revealed that dehydroepiandrosterone treatment before ischemia had significant preservative effects on the red blood cell velocity and functional capillary density 30 and 90 minutes after reperfusion, compared with the control and vehicle-treated groups. Leukocyte-endothelial cell interactions were also affected by dehydroepiandrosterone treatment, as reflected by significant decreases in the numbers of sticking and transmigrating leukocytes 30 and 90 minutes after reperfusion. In dehydroepiandrosterone-treated animals, leukocytes exhibited lower levels of expression of adhesion molecules after the onset of ischemia, compared with the control groups. In this study, intravenous dehydroepiandrosterone administration reduced the activation of leukocytes and improved red blood cell velocity and capillary perfusion in the muscle flap microcirculation during ischemia-reperfusion injury. This protective effect was most likely the result of delayed expression of Mac-1 integrin, L-selectin, and CD44 molecules on leukocytes.

Animals↗

PubMed2005

Live demonstration of microcirculation in the deep fascia and its implication.

The rich vascular network in the deep fascia has been emphasized by various scientists, but the actual demonstration of live circulation in the deep fascia has not previously been witnessed. Encouraged by the sight of live circulation in the web membrane of toad hind limb, a successful attempt was made to demonstrate the live circulation in the vascular network of the deep fascia. Fascial extensions of inferiorly based fasciocutaneous flaps were dissected in five patients with distal leg and heel defects. The fascial extension in continuity with a proximal retrograde fasciocutaneous flap was mounted on a glass slide and examined under a microscope. The authors witnessed the live microcirculation and the movement of individual red blood corpuscles in vascular channels of the deep fascia. The authors also noticed that the deep fascia has two layers with circulations that are independent of one other. A video recording was made to document these important features.

Adolescent↗

PubMed2003

Urinary trypsin inhibitor improves peripheral microcirculation and bronchospasm associated with systemic anaphylaxis in rabbits in vivo.

Using intravital microscopy of the rabbit ear for quantitative studies of microvascular dynamics, we examined the impact of urinary trypsin inhibitor (UTI), a proteolytic enzyme inhibitor, on microvascular changes during immune complex-mediated anaphylaxis. A total of 50 rabbits, previously sensitized with horse serum, were anesthetized and mechanically ventilated with pentobarbital and isoflurane for the intravital microscopy. Rabbits were then challenged with intravenous injection of horse serum to induce systemic anaphylaxis. One minute after the challenge, each rabbit was randomly assigned to receive saline (group C), 50,000 units x kg(-1) of UTI (group U1), or 150,000 units x kg(-1) (group U2). There were no statistical differences between hemodynamic variables, including heart rate (HR), mean arterial pressure (MAP), and central venous pressure (CVP), among the survivors in each treatment group. Peak inspiratory pressure rose in all three groups but at a much higher rate in group C (P < 0.05). In contrast with the moderate effects of UTI on the above parameters, microscopic evaluation revealed a substantial difference among treatment groups: upon the initiation of anaphylaxis, the arteriole started to reduce in diameter, but UTI prevented vasoconstriction in the arteriole in a dose-dependent manner. Similar results were observed with blood flow velocity. Because flow rate was calculated as the product of blood flow velocity and vascular cross-sectional area proportional to the square of the vessel diameter, these results indicate that UTI preserves microvascular flow rate during anaphylaxis. Rabbit ear microcirculation is highly preserved in the UTI-treated groups during systemic anaphylactic shock.

Anaphylaxis↗

PubMed2006

Comparison of the protective effects of type III phosphodiesterase (PDE3) inhibitor (cilostazol) and acetylsalicylic acid on intestinal microcirculation after ischemia reperfusion injury in mice.

Antiplatelet therapy has been proposed as the treatment of choice for ischemia/reperfusion injury. The aim of this study is to elucidate the difference in effect between cilostazol (CZ) and acetylsalicylic acid (ASA) on microcirculatory disturbance in ischemia/reperfusion injury. Either 10 mg/kg of CZ (n = 14) or 100 mg/kg of ASA (n = 14) was administered orally to mice. Thereafter, 20 min of intestinal ischemia, followed by 60-min reperfusion, was applied; then, the status of submucosal microcirculation was observed under intravital microscopy. The blood cell counts and organ damage markers were examined in the portal blood. Next, 5 mm of the ileum was excised and was then histologically examined. Platelet-leukocyte aggregates were often observed in the postcapillary venules, and this formation was significantly reduced by both CZ and ASA. The number of adherent leukocytes was significantly lesser in the CZ-treated mice than in the ASA-treated mice (P < 0.01). The leukocyte number, lactate dehydrogenase, and lactate levels were best maintained in the CZ-treated mice (P < 0.05). The villus height was best preserved in the CZ-treated mice. Cilostazol inhibited not only the platelet aggregation but also the leukocyte adhesion to the endothelium, thereby inducing organ protection.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1975

The autoregulation of the microcirculation.

The paper reviews August Krogh's contribution to capillary physiology stressing his formulation of useful new concepts such as "tissue cylinder model", capillary intermittency and the intimate matching of capillary perfusion and cellular metabolism. Looked upon from a control theory viewpoint. Krogh was very early in considering the microcirculation as an autoregulated system with tissue oxygen tension as the controlled parameter. Recent work on Krogh's theories is briefly summarized.

Animals↗

PubMed1992

Intravital video-capillaroscopy for the study of the microcirculation in psoriasis.

Intravital capillaroscopy using a video-microscopy system permits real-time imaging of the skin microvasculature with retrospective analysis of capillary dynamics. The addition of fluorescein angiography improves contrast and detects aspects of blood vessel behaviour, such as perfusion homogeneity and transcapillary solute diffusion, not detectable under native conditions. This study was performed to evaluate whether the method can be applied to the investigation of a skin disease and in particular the understanding of the role of the blood vessel in the pathogenesis of psoriasis. Results demonstrated clear differences between normal and psoriatic skin. More capillaries were red-cell perfused in both plaque and uninvolved skin compared to normal skin (P less than 0.001) and 0.01 less than P less than 0.02, respectively). The capillaries in psoriatic plaque skin were much larger than those in normal skin (P less than 0.001). The density of capillaries was not increased in plaque or uninvolved psoriatic skin, indicating expansion of existing vessels and not new vessel formation. The area of fluorescence seen around each capillary at 60 s was greater in plaque (P less than 0.001) and in uninvolved psoriatic skin (P less than 0.001) than in normal skin, indicating greater vessel transcapillary diffusion. This study confirms the value of video-microscopy as a non-invasive technique for the examination of the cutaneous microcirculation in vivo.

Adolescent↗

PubMed1990

Skin microcirculation and regional peripheral resistance in patients with chronic renal anaemia treated with recombinant human erythropoietin.

Skin microcirculation and regional peripheral resistance were studied in 14 patients with renal anaemia during therapy with recombinant human erythropoietin. Haematocrit was raised from 20.0 to 31.3% after 10-12 weeks of treatment and remained stable over another period of 12 weeks. Antihypertensive treatment had to be intensified in five patients. Regional calf blood flow decreased significantly; accordingly, calculated peripheral vascular resistance was increased by more than 100%. However, transcutaneous oxygen pressure (37 degrees C and 44 degrees C) increased significantly. The pathological vasoconstrictor response of skin capillaries was not influenced. There were no significant differences of any parameter between the patients requiring reinforced antihypertensive therapy and those with stable blood pressure. In conclusion skin oxygenation may be improved by erythropoietin treatment to a large extent despite an increase in calculated total limb vascular resistance.

Adult↗

PubMed1991

Cysteinyl leukotriene actions on the microcirculation of the normal and split hydronephrotic rat kidney.

The effects of leukotriene D4 (LTD4) and leukotriene E4 (LTE4) on renal microcirculation were determined on normal and hydronephrotic female Wistar rats. In normal kidneys, the effects of LTD4 on total renal blood flow and glomerular filtration rate were measured by a flow meter and by inulin clearance. In the split hydronephrotic kidney, the LTD4- and LTE4-mediated vascular effects were localized by intravital microscopy. Intravenous infusion of low-dose LTD4 (1 x 10(-9) mol min-1 kg-1) over 15 min induced a strong decrease in renal blood flow (-43% and -70%) in the normal and the hydronephrotic kidney. After the infusion the glomerular filtration rate of the normal kidney was significantly reduced by 65% and the filtration fraction by 32%. The fall in filtration fraction is in accordance with the significant decrease in luminal diameters of the arcuate artery (-28%) and the proximal interlobular artery (-12%) in the hydronephrotic kidney under LTD4. The decrease in renal blood flow, glomerular filtration rate, filtration fraction and luminal diameters persisted in the normal as well as in the hydronephrotic kidney for more than 60 min beyond cessation of infusion. Local application of LTD4 (1 x 10(-10) mol l-1 up to 1 x 10(-7) mol l-1) and LTE4 (1 x 10(-10) mol l-1 up to 1 x 10(-8) mol l-1) induced a dose-dependent constriction of the arcuate artery and the proximal interlobular artery. The distal interlobular artery, the afferent and the efferent arteriole were not significantly affected by LTD4 or LTE4. The glomerular blood flow was dose-dependently reduced up to 48% under local LTD4 and 43% under LTE4. The LTD4/LTE4 antagonist FPL 55712 (1 x 10(-8) mol min-1 kg-1, iv) significantly attenuated the effects of LTD4 infusion and local LTE4 application in the hydronephrotic kidney. This is indicative of the presence of receptors for LTD4 and LTE4 in the larger preglomerular vessels of the rat kidney. The LTD4 effects on the normal kidney were attenuated by simultaneous infusion of dopamine (5 microgram min-1 kg-1) or plasma expansion, two principal methods in the treatment of acute renal failure. The results in the normal and hydronephrotic kidney demonstrate a preferential preglomerular vasoconstriction under LTD4 and LTE4 causing a marked decrease in renal and glomerular blood flow, glomerular filtration rate and filtration fraction.

Animals↗

PubMed1990

Age-related differences in testicular microcirculation.

Different aspects of testicular microcirculation were studied in rats aged 20, 24 or 90 days, in order to determine if maturational changes in the testis could influence its vasculature. Using laser Doppler flowmetry, it was found that vasomotion was not present in 20-day-old rats, but it could be induced by hCG-treatment given 32 h prior to flow measurements. In rats aged 24 days vasomotion was present in the testis but it was not influenced by hCG treatment, in contrast to adult rats in which testicular vasomotion disappeared after hCG treatment. In all age-groups, hCG treatment induced an increase in testicular interstitial fluid (IF) volume, which was most pronounced in young rats. In young rats, as in adults, there was an increase in the volume density of polymorphonuclear (PMN) leucocytes in testicular blood vessels after hCG treatment. However, rats aged 20 or 24 days did not exhibit any significant extravascular migration of leucocytes as occurred in adult rat testis after hCG injection. The deposition of colloidal carbon particles observed in adult rats after hCG-treatment was also not seen in young rats. It is concluded that the vasculature of the immature rat testis responds to hCG stimulation with an increase in IF volume. However, when compared to adult rats, different mechanisms may be operating because no evidence for opening of inter-endothelial cell gaps was observed in the testis of young rats.

Aging↗

PubMed1992

In-vivo confocal scanning laser microscopy of the cerebral microcirculation.

Confocal scanning laser microscopy (CSLM) was used to study the microcirculation of the brain neocortex in anaesthetized rats. After removal of the dura mater, implantation of a closed cranial window, and intravenous injection of fluorescein, three-dimensional reconstructions of cortical capillaries were performed down to a depth of 250 microns below the pial surface. Using a one-dimensional approach (single line scanning), erythrocyte (negative contrast in fluorescently labelled plasma) and leucocyte (labelled with rhodamine 6 G) velocity and supply rate in cortical capillaries were measured. The effect of CO2-inhalation on capillary blood flow dynamics was studied. Capillaries were imaged continuously for up to 1 h without changes in flow or fluorescence pattern. However, by increasing the laser power 10-100-fold, aggregate formation was induced and capillaries were occluded, possibly due to damage to vascular endothelium. We conclude that CSLM can be used to study morphological and dynamic aspects of fluorescently labelled subsurface structures in organs of experimental animals.

Angiography↗