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At least 1,513 records · Page 84Linked to original sources
PubMed1997

Studies on gastric mucosal microcirculation. 1. The nature of regional variations induced by ethanol injury.

BACKGROUND/AIMS: The focal nature of gastric ulcers raises the possibility of underlying regional disturbances in gastric mucosal microcirculation. This study employed fluorescent in vivo microscopy with the aim of directly investigating the response of several areas of the gastric mucosa to 60% ethanol. METHODS: Changes in macromolecular leakage of fluorescein labelled albumin, vessel diameter, and acridine red labelled leucocyte adhesion and rolling were assessed over a period of two hours. A total of 0.5 ml 60% ethanol was topically applied for five minutes to the exteriorised gastric mucosa of anaesthetised rats. RATS: Three distinct patterns of response were found. Areas of lesion formation were small and occurred within five minutes. These areas showed persistent blood flow stasis throughout the course of the experiment, increased leakage (p < 0.02), and no leucocyte adhesion. Peripheral to the lesion, sustained leakage (p < 0.02) was found with adherence of leucocytes (p < 0.01) after lesion formation. Sites more remote to any lesion showed transient leakage and significant numbers of 'rolling' leucocytes (p < 0.01) were observed again after the lesion had formed. CONCLUSIONS: Despite widespread exposure of the entire gastric mucosa to 60% ethanol the resultant mucosal injury was limited. Widespread vascular damage was found reflected by macromolecular leakage, the pattern of which showed regional variation.

Administration, Topical↗
PubMed2002

Hepatic stellate cells: role in microcirculation and pathophysiology of portal hypertension.

Accumulating evidence suggests that stellate cells are involved in the regulation of the liver microcirculation and portal hypertension. Activated hepatic stellate cells have the necessary machinery to contract or relax in response to a number of vasoactive substances. Because stellate cells play a role in both fibrosis and portal hypertension, they are currently regarded as therapeutic targets to prevent and treat the complications of chronic liver disease.

Cell Communication↗
PubMed1995

Diverse interactions of calcitonin gene related peptide and nitric oxide in the gastric and cutaneous microcirculation.

Calcitonin gene related peptide (CGRP) is the major mediator of afferent nerve mediated vasodilatation in the gastric mucosa and skin of the rat. Since receptors for CGRP occur on both the vascular endothelium and smooth muscle, it is conceivable that the vascular actions of CGRP involve multiple mechanisms. The vasodilator effect of rat CGRP-alpha in the rat gastric mucosa is indeed inhibited by blockage of nitric oxide (NO) synthesis, as is the gastric mucosal hyperemia in response to gastric acid challenge, which is mediated by CGRP release from afferent nerve fibres. In contrast, the vasodilator response to rat CGRP-alpha in the rat hind paw and the CGRP-mediated vasodilatation evoked by antidromic stimulation of afferent nerve fibres do not depend on the formation of NO. These data indicate that NO plays regionally different roles in the local vasodilator action of CGRP. NO is a secondary vasorelaxant messenger of CGRP in the gastric, but not in the cutaneous, microcirculation. However, this L-arginine-derived autacoid may have a role in the irritant-induced CGRP release from afferent vasodilator fibres in the skin.

Animals↗
PubMed2006

Time course of changes in nail fold microcirculation induced by acupuncture stimulation at the Waiguan acupoints.

Acupuncture has been used widely to treat disease; however, the time course for acupuncture to have an effect remains unclear. Therefore, the aim of the present study was to investigate the time course of changes in nail fold microcirculation (NFM) induced by acupuncture stimulation (AS) at the right and left Waiguan acupoints (WAs). A total of 38 healthy female volunteers, age range from 21 to 33, were studied. We recorded NFM of the right middle finger before, and 5 min, 10 min, 15 min and 20 min after initiating AS; NFM was also recorded 5 min and 10 min after secessions of AS. Nitric oxide (NO) and endothelin-1 levels were measured from the left cubital vein, before AS and 10 min after stopping AS. The results indicated that capillary density of NFM increased 5 min after AS at the right Waiguan acupoint (WA); however, similar changes were not noted at the left WA. The capillary density decreased beginning 15 min after AS at the right and left WA. Capillary red blood cell velocity increased 5 min and 10 min after AS at the right and left WAs, but decreased 5 min and 10 min after stopping AS at the left WA. NO and endothein-1 levels were similar before AS and 10 min after stopping AS. Therefore, we suggest that a segmental effect of the spinal nerve contributes to the increasing capillary density of NFM induced by AS. The effect of acupuncture on NFM lasts about 10-15 min. The changes of balance between the sympathetic nerve activities and parasympathetic nerve activities may be induced by AS.

Acupuncture↗
PubMed2000

Monitoring of tumor microcirculation during fractionated radiation therapy in patients with rectal carcinoma: preliminary results and implications for therapy.

PURPOSE: To measure microcirculatory changes during chemoirradiation and to correlate perfusion index (PI) values with therapy outcome. MATERIALS AND METHODS: Perfusion data in 11 patients with cT3 (clinical staging, tumor invaded the perirectal tissue) rectal carcinoma who underwent preoperative chemoirradiation were analyzed. Perfusion data were acquired by using a T1 mapping sequence with a whole-body magnetic resonance (MR) imager. After contrast medium was intravenously infused at a constant rate, concentration-and-time curves were evaluated for arterial blood and tumor. All patients underwent MR imaging before and at constant intervals during chemoirradiation. Clinical stages before therapy were compared with surgical stages after therapy. RESULTS: Spatial and temporal resolution on dynamic T1 maps were sufficient to reveal changes in contrast medium accumulation in the tumor. Comparison of PI values and radiation dose showed a significant increase in the 1st (P: =.003) and 2nd weeks (P: =.01) of treatment; values subsequently returned to pretreatment levels or showed a renewed increase. High initial PI values correlated with greater lymph node downstaging (P: =.042). CONCLUSION: Dynamic T1 mapping provides a suitable tool for monitoring tumor microcirculation during chemoirradiation and offers the potential for individual optimization of therapeutic procedures. Furthermore, these results indicate that the PI map may serve as a prognostic factor.

Adenocarcinoma↗
PubMed2006

Roles of anandamide in the hepatic microcirculation in cirrhotic rats.

Cannabinoids have been reported to participate in the pathogenesis of peripheral vasodilatation in cirrhosis. However, their roles in increased intrahepatic resistance (IHR) in cirrhotic livers are unknown. We aimed to investigate the effects of cannabinoids in the hepatic microcirculation of cirrhotic rats produced by bile duct ligation. In isolated liver perfusion, portal perfusion pressure (PPP) and the production of eicosanoids in the perfusate were measured. In addition, various hepatic protein levels [cyclooxygenase (COX) isoform and 5-lipoxygenase (5-LOX)] were also determined. Finally, concentration-response curves for PPP and the corresponding production of eicosanoids in response to anandamide (1.44 x 10(-10)-1.44 x 10(-3) M) after indomethacin (COX inhibitor), piriprost (5-LOX inhibitor), or furegrelate (thromboxane A(2) synthase inhibitor) preincubation were obtained. The study showed that cirrhotic livers had significantly higher levels of PPP, COX-2 and 5-LOX protein expression, and production of thromboxane B(2) (TXB(2)) and cysteinyl leukotrienes (Cys-LTs) than normal livers. Anandamide induced a dose-dependent increase in PPP in both normal and cirrhotic livers. The anandamide-induced increase in PPP was found concomitantly with a significant increase in TXB(2) and Cys-LT production in the perfusate. In response to anandamide administration, cirrhotic livers exhibited a significantly greater increase in IHR and production of TXB(2) and Cys-LTs than normal livers. Indomethacin and furegrelate, but not piriprost, significantly ameliorated the anandamide-induced increase in IHR in cirrhotic livers. In conclusion, anandamide plays, in part, an important role in increased IHR of cirrhotic livers. The anandamide-induced increase in IHR in cirrhotic livers may be mediated by increased COX-derived eicosanoid (mainly thromboxane A(2)) production.

6-Ketoprostaglandin F1 alpha↗
PubMed2003

Embolization by sinusoidal lining cells obstructs the microcirculation in rat sinusoidal obstruction syndrome.

Mechanisms leading to the obstruction of the microcirculation in sinusoidal obstruction syndrome (SOS) have been unclear. Because this occurs at the onset of disease, this is a potential key target for therapeutic intervention. Rats were treated with monocrotaline with or without continuous intraportal infusion of glutathione and were studied at 0.5, 1, 2, 4, 6, and 10 days after monocrotaline treatment with the use of in vivo microscopy and transmission electron microscopy. Sinusoidal perfusion decreased from days 1 through 10 with a nadir on day 4. At 12 h, numerous swollen sinusoidal endothelial cells (SECs) were observed. Subsequently, red blood cells penetrated into the space of Disse through gaps between and through swollen SEC and dissected the sinusoidal lining away from the parenchymal cells. Sinusoidal blood flow was obstructed by an embolism of aggregates of sinusoidal lining cells, red blood cells, and adherent monocytes. All changes were prevented by glutathione infusion, notably the initial swelling of SEC. SOS is initiated by changes in SEC. Microcirculatory obstruction is due to dissection of the sinusoidal lining, followed by embolization of the sinusoid by sinusoidal lining cells, compounded by aggregates of monocytes adherent in the sinusoids. Glutathione prevents SOS by preserving an intact sinusoidal barrier.

Animals↗
PubMed1985

Rat gastric mucosal microcirculation in vivo.

The superficial gastric mucosal microcirculation was observed microscopically by transillumination in the anesthetized rat. The vessels surrounding the gastric crypts were monitored on a television screen through a microscope and the pictures stored on a videotape for off-line analysis of red cell velocity (VRBC) and vessel diameter. From these measurements microvascular volume flows were calculated. VRBC reached steady values after 1-4 h (mean 2 h) and showed a regular pulsatile flow (4-7 cycles/min) in most experiments. Acid output was measured at regular intervals; 50% of the rats showed no spontaneous acid output, but the others secreted up to 100 mu eq/h. The microvessels in the superficial mucosa were classified into three orders according to their branching hierarchy and relative dimensions, and their distribution per unit mass was estimated. VRBC and volume flow were shown to decrease in the successive orders of the microvessels. Calculation of organ blood flow from microvascular flow data and vessel distribution gave values (21 ml.min-1.100 g tissue-1) that agree with earlier reported values. A higher flow velocity was detected in rats with spontaneous acid output than in those without, but there was a poor correlation between the magnitude of the acid output and VRBC. Pentagastrin (96 micrograms.kg-1.h-1) induced a significant increase in both blood flow and acid secretion. Results from this study indicate that this experimental model is potentially useful for studies of the correlation between acid secretion and mucosal blood flow.

Animals↗
PubMed1994

ET-1 induced alterations of hepatic microcirculation: sinusoidal and extrasinusoidal sites of action.

Using epifluorescence microscopy, we investigated the dynamic changes in hepatic sinusoidal hemodynamics in vivo during continuous infusion of endothelin-1 (ET-1) in pentobarbital-anesthetized rats. ET-1 was infused for 20 min at rates of 2 or 10 pmol/min either systemically or into the portal vein, followed by a 90-min recovery period. In contrast to systemic application of ET-1 that did not cause a consistent hepatic microvascular effect, we observed two different patterns of microcirculatory alterations during portal application. Infusion of 2 pmol/min elicited a rapid, reversible decrease in sinusoidal diameter that was paralleled by a slight increase in red cell velocity, resulting in conservation of volumetric flow and sinusoid density. Infusion of 10 pmol/min resulted in a biphasic narrowing followed by transient increase in sinusoidal diameter and a profound and lasting decrease in red cell velocity, leading to an almost complete cessation of hepatic microvascular blood flow. These results indicate that ET-1 is a potent constrictor in the liver microcirculation in vivo and acts at both extrasinusoidal and sinusoidal sites, although the sinusoidal sites appear to be more sensitive to lower concentrations.

Animals↗
PubMed1997

Interleukin-2-induced hepatic injury involves temporal patterns of cell adhesion in the microcirculation.

The treatment of metastatic cancer with interleukin-2 (IL-2) is limited by systemic toxicities, including hepatic dysfunction. The objective of this study was to determine the cellular mechanisms of IL-2-induced hepatic injury. Intravital microscopy was used for the direct observation of the murine hepatic microcirculation after 2 h, 2 days, and 4 days of IL-2 treatment. At each interval, leukocyte- and platelet-endothelial adherence were observed and quantitated. Simultaneously, sinusoidal perfusion, serum levels of glutamate pyruvate transaminase, and edema were measured as indexes of hepatic toxicity. IL-2 increased neutrophil adhesion acutely in association with decreased sinusoidal perfusion. Leukocyte adhesion subsided at 2 days, but platelet-endothelial interactions were enhanced and 40% of mice receiving IL-2 had microvascular thrombi. These effects occurred in conjunction with decreased sinusoidal perfusion and the development of hepatic edema. After 4 days of IL-2, maximal hepatic edema, hypoperfusion, and increased serum levels of glutamate pyruvate transaminase were associated with increased lymphocyte adhesion and microvascular thrombosis. These data suggest coordinated, temporal roles of leukocytes and platelets in the generation of IL-2-induced hepatic injury.

Animals↗
PubMed1999

Assessment of the mechanism of juxtacrine activation and adhesion of leukocytes in liver microcirculation.

Leukotriene C4 (LTC4), histamine, and other mediators can induce expression of P-selectin and platelet-activating factor (PAF) on venular endothelium to recruit leukocytes in vivo and in vitro via a juxtacrine mechanism of adhesion. The objective of this study was to assess the effect of histamine and LTC4 on the leukocyte recruitment in the liver and to study the components and molecular mechanisms involved in this process. We visualized the hepatic microvasculature using intravital microscopy and we determined that LTC4 (20 nM) but not histamine (0.1, 0.3, or 1 mM) induced leukocyte recruitment in the liver microcirculation. Histamine could induce leukocyte recruitment but only in the presence of an antihistaminase. The LTC4-induced leukocyte recruitment occurred primarily in sinusoids (not venules) and was not inhibitable by three different anti-P-selectin antibodies (5H1, RMP-1, and RB40). Leukocyte recruitment in P-selectin-deficient mice, intercellular adhesion molecule 1 (ICAM-1)-deficient mice, and mice treated with a PAF antagonist was of the same magnitude as in wild-type animals in response to LTC4. Although PAF alone could induce adhesion in both sinusoids and postsinusoidal venules, this chemotactic agent was not involved in LTC4-induced adhesion in the liver. Finally, an overlapping role for P-selectin and ICAM-1 was ruled out as LTC4 induced leukocyte recruitment in P-selectin and ICAM-1 double-deficient mice. These data demonstrate that LTC4 does not activate the known early mechanisms of leukocyte recruitment, including P-selectin, PAF, or ICAM-1 in the hepatic microvasculature.

Animals↗
PubMed2004

Oxygen delivery and consumption in the microcirculation after extreme hemodilution with perfluorocarbons.

The oxygen transport capacity of fluorocarbons was investigated in the hamster chamber window model microcirculation to determine the rate at which oxygen is delivered to the tissue in conditions of extreme hemodilution [hematocrit (Hct) 11%]. Hydroxyethlyl starch (HES 200; 200 kDa molecular mass) was used as a plasma expander for two isovolemic hemodilutions performed with 10% HES 200 until a Hct of 65%. A third step reduced the Hct to 75% of baseline and was performed with either HES 200 or a 60% perfluorocarbon (PFC) emulsion. Comparisons of HES 200-only-hemodiluted animals versus 4.2 g/kg PFC emulsion-hemodiluted animals were made at 21% and 100% normobaric oxygen ventilation. It was found that systemic and microvascular oxygen delivery was 25% and 400% higher in the PFC animals compared with HES 200 animals, respectively, showing that PFCs deliver oxygen to the tissue when combined with hyperoxic ventilation in the present experiments, with no evidence of vasoconstriction or impaired microvascular function. Oxygen ventilation (100%) led to a positive base excess for the PFC group (5.5 +/- 2.5 mmol/l) versus a negative balance (-0.8 +/- 1.4 mmol/l) for the HES 200 group, suggesting that microvascular findings corresponded to systemic events.

Animals↗
PubMed1982

Anesthetic depression of microcirculation, central hemodynamics, and respiration in decerebrate rats.

The objectives of this study were the development of a skeletal muscle microcirculatory preparation, in which the complications of drug anesthesia were minimized, and the quantitation of the effects of urethan and chloralose anesthesia on the microcirculation. Rats were initially anesthetized with urethan and chloralose and decerebrated by a midcollicular transection. The cremaster skeletal muscle, with intact circulation and innervation, was prepared for intravital microscopy by placement in a tissue bath. Arterioles (9-70 micrometers diam) at several anatomic levels were observed during the initial period of urethan-chloralose anesthesia (period 1), after recovery from the anesthesia (period 2), and again following reanesthetization (period 3). During period 2, respiratory rate, heart rate, and mean arterial pressure were significantly greater than during periods 1 and 3. Smaller arterioles (8-50 micrometers diam) exhibited vasomotion (mean amplitude 35% of mean diameter; mean frequency 31 cycles/min) during period 2. Urethan-chloralose anesthesia during periods 1 and 3 inhibited vasomotion and increased arteriolar diameters by 16-36%. This study quantitates the depressant effects of urethan-chloralose anesthesia on the cardiovascular system and demonstrates the feasibility of using decerebration to circumvent the necessity of continuous drug anesthesia for in vivo microvascular studies.

Animals↗
PubMed1986

Effect of hypoxia and hypercapnia on ACE activity in the cerebral microcirculation of anesthetized dogs.

Angiotensin-converting enzyme (ACE) activity of the cerebral microcirculation of anesthetized dogs was measured from cerebral venous outflow curves after bolus injection of a synthetic ACE substrate, [3H]benzoyl-phenylalanyl-alanylproline ([3H]BPAP), into a common carotid artery. Cerebral BPAP metabolism was quantified by measuring the concentration of [3H]benzoyl-phenylalanine (the product of BPAP hydrolysis by ACE) in blood samples from the sagittal sinus after occlusion of the lateral sinuses with bone wax. Instantaneous BPAP metabolism in each sample increased as a function of time after injection, suggestive of perfusion heterogeneity, and averaged 59 +/- 4% (n = 8) over a single pass during normoxia and normocapnia. The ratio of Vmax (the maximal rate of cerebral BPAP metabolism) to Km (the concentration at Vmax/2), was calculated from instantaneous outflow curves using a model based on first-order kinetics. Increases in cerebral blood flow during either hypoxia or hypercapnia significantly reduced BPAP metabolism to 33 +/- 3 (n = 7) and 24 +/- 3% (n = 5), respectively; however, Vmax/Km of ACE activity (0.19 +/- 0.03 ml/s) was not affected by either condition. The lack of change in apparent kinetics of ACE activity (i.e., in Vmax/Km) during hypoxia or hypercapnia suggests that recruitment of cerebral capillaries was not a quantitatively significant factor in controlling BPAP metabolism with this degree of either hypoxia or hypercapnia.

Anesthesia↗
PubMed1988

Vasomotion in cerebral microcirculation of awake rabbits.

Cerebral arterioles of unanesthetized rabbits equipped with chronically implanted cranial windows exhibited spontaneous rhythmic variation in vessel caliber characteristic of vasomotion. This variation was noted in all examined vessels. The vasomotion was independent of arterial blood pressure or respiration. The average frequency was 0.74 cycles/min and was independent of vessel size. The mean amplitude of the oscillations had a statistically significant inverse relationship to vessel diameter (r = 0.69). Vasodilation induced by arterial hypercapnia, topical adenosine, or topical acetylcholine had no significant effect on the frequency or amplitude of vasomotion. Anesthesia significantly reduced the frequency in arterioles of all sizes and markedly reduced amplitude in large arterioles. Topical verapamil resulted in a statistically significant reduction in frequency and in peak amplitude. Variations in vessel diameter occurred simultaneously in arterioles and their companion venules. We conclude that the cerebral microcirculation displays active vasomotion, which is significantly depressed by anesthesia or topical verapamil. The results also suggest that vasomotion is probably controlled by local factors.

Acetylcholine↗
PubMed1989

Laser-Doppler assessment of brain microcirculation: effect of systemic alterations.

There is a need for new technical approaches whereby the cerebral microcirculation can be easily and continuously assessed. The objective of this study was to determine whether laser-Doppler (LD) flowmetry can be utilized to assess changes in cerebral cortical blood flow and to determine whether changes in blood perfusion measured by LD flowmetry correlate with simultaneously measured changes in flow measured by H2 clearance in cats or with changes in pial arteriolar diameter measured with a microscope in rabbits equipped with a closed cranial window. In the rabbit experiments a 0.84-mm-diam LD probe was inserted through a cranial window port, and in the cat experiments the probe was fixed adjacent to the H2 probe. The probe was fixed at a distance of 1-2 mm from the cortical surface, where it and its associated electronics detect changes in blood cell velocity and blood volume within a tissue volume of approximately 1 mm3. Volume and velocity are multiplied to provide a flow signal. When cerebral blood flow in cats was decreased by hyperventilation-induced hypocapnia and increased by norepinephrine-induced hypertension, the percent changes in LD flow and H2 clearance flow changed linearly (r = 0.94, slope = 0.97). When arterial PCO2 was increased from 28 to 48 mmHg in the rabbit experiments, the pial arterioles dilated 19 +/- 4% (mean +/- SE) and LD flow increased by 74 +/- 9%, LD flow changes which would be predicted by a third power relationship of diameter to flow.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Influence of endothelin on piglet cerebral microcirculation.

The purpose of this study was to determine responses of the newborn pig cerebral microcirculation to endothelin. Pial arterioles were observed directly using a closed cranial window in chloralose-anesthetized piglets. Topical application of endothelin derived from porcine endothelial cells produced increases in pial arteriolar diameter at the lowest concentration (0.1 ng/ml) (159 +/- 6 to 180 +/- 8 microns) and concentration-dependent decreases in pial arteriolar diameter at higher concentrations (141 +/- 6, 127 +/- 5, and 110 +/- 4 microns at 1, 10, and 100 ng/ml, respectively). Indomethacin (5 mg/kg iv) and aspirin (50 mg/kg iv) blocked dilator responses to endothelin and attenuated constrictor responses. Endothelin produced concentration-dependent increases in cortical periarachnoid cerebrospinal fluid levels of 6-ketoprostaglandin (6-keto-PG) F1 alpha, PGE2, PGF2 alpha, and thromboxane B2. Thus endothelin can produce either dilation or constriction of cerebral arterioles in newborn pigs, depending on concentration. Furthermore, prostanoids appear to mediate vasodilation induced by the lowest concentration of endothelin and contribute to constriction induced by higher concentrations of endothelin.

Animals↗