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At least 19 recordsLinked to original sources

In vivo analysis of microcirculation following closed soft-tissue injury.

Major loss of tissue is an almost invariable consequence of severe closed soft-tissue injury. Clinically, the extent of soft-tissue trauma determines the outcome of complex injuries and significantly influences bone healing. With use of a new animal model, this study quantitatively analyzed microcirculation, i.e., nutritive perfusion and leukocyte-endothelial cell interaction, in skeletal muscle after standardized closed soft-tissue injury. By means of a computer-assisted controlled-impact technique, a severe standardized closed soft-tissue injury was induced in the left hindlimb of 28 rats. The rats were assigned to four experimental groups (n = 7 per group) that differed by time of analysis (1.5, 24, 72, and 120 hours after injury); rats that were not injured served as controls (n = 7). Intramuscular pressure was measured, and microcirculation in the rat extensor digitorum longus muscle was analyzed by in vivo fluorescence microscopy, which allowed assessment of microvascular diameters, functional capillary density, number of rolling and adherent leukocytes in venules, and microvascular permeability. Edema weight gain was quantified by the ratio of wet to dry weight of the extensor digitorum longus muscle. Microvascular perfusion of the skeletal muscle was characterized by a significant reduction in functional capillary density, which was paralleled by an increase in capillary diameter throughout the 120 hours of observation when compared with the controls. Trauma-induced inflammatory response was reflected by a markedly increased rolling and adherence of leukocytes, primarily restricted to the endothelium of postcapillary venules; this was accompanied by increased microvascular permeability, indicative of a substantial loss of endothelial integrity. The microcirculation surrounding the core of the damaged tissue area resembled that of ischemia-reperfusion injury in skeletal muscle, i.e., heterogeneous capillary perfusion, pronounced microvascular leakage, and adherence of leukocytes. Enhanced vascular leakage and leukocyte adherence (24-72 hours after injury) coincided with the maximum intramuscular pressure (which was not indicative of compartment syndrome) and edema formation. These results demonstrate that initial changes, leading to ultimate tissue death, after closed soft-tissue injury are caused on the microcirculatory level. This standardized model provides further insight into microvascular pathophysiology and cellular interactions following closed soft-tissue injury. Thus, it is an adequate tool for testing novel therapeutic interventions.

Animals↗

[Experimental studies on microcirculation of the hindlimb after ischemia and reperfusion in the rabbits. 1. Establishment of an in vivo method for observing microcirculation using tendon surface microvessels on the dorsum of the foot].

The blood supply system of the extensor digitorum longus tendon in the rabbit hindlimb is observed by the aid of dye injection technique and dissecting microscope. We find that the segment proximal to metatarsophalangeal joint of this tendon is an ideal site for observation of in vivo microcirculation. In this site, there are abundant microvessels on the surface of the tendon, and as red microvessels are on white tendon, it forms a sharp contrast. In addition, the tendon is only covered by skin and little loose connective tissue, so it is easy to expose. On the bases of abovementioned findings, a new in vivo method for observing microcirculation in the rabbit hindlimb is developed. In our experiences, the advantages of this method are as follows: (1) It is simple and convenient; (2) The time required for preparation is short (about 10-15 min), and the observation period can be extended (over 6 h.); (3) Surgical trauma is not serious; (4) The image is clear. This method opens up a new way to using rabbit hindlimb ischemia model to study microcirculation changes in vivo following reperfusion after extremity ischemia.

Animals↗

[Theory of microcirculation. 2. Problems of microcirculation from the viewpoint of the new theoretical concept].

By means of network analysis and the use of a model which stimulates continuous blood supply to the tissue the basis of Starling's hypothesis of microcirculation is challenged. Contrary to the Starling's conception, we found that the microcirculation in the tissue is a stable process, whereby the interstitial hydraulic pressure (IHP) depends on the intracapillary blood pressure, on the permeability of the capillary wall, on the colloid-osmotic pressure and on the static pressure in the vessels and form a characteristic gradient along the capillary wall. The main effect of the colloid-osmotic pressure cannot be regarded as counteracting to the blood pressure, but instead consists in reduction of the IHP. Based on a theoretical conception about elastic interactions in the tissue a new method for measurement of the capillary filtration coefficients (CFC) is developed. Applying the method on the rabbit skeletal muscle the CFC is found to be 0.130 ml/min.mm Hg.100 g. This value is substantially higher than the values obtained from similar experiments reported in the literature (0.008 ml/min.mm Hg.100 g). The lymphatic fluid is not a result of a disbalance between filtration and resorption across the capillary wall, but it is a consequence of the protein recirculation in the following manner: blood vessels--interstitial space--lymphatic vessels--blood vessels. This recirculation is essential for the vital function of the tissue cells.

Animals↗

[Effect of topical timolol on microcirculation in the rabbit optic nerve head evaluated with a laser speckle microcirculation analyser].

The effect of topical 0.5% timolol on the microcirculation in albino rabbit optic nerve head (ONH) tissue was examined using a laser speckle microcirculation analyser. In the first experiment, normalized blue (NB) in ONH, a quantitative index of peripheral blood flow in ONH, intraocular pressure (IOP), blood pressure (BP) and pulse rate (PR) were measured under general anesthesia before, and 30, 60, 90 and 120 minutes after a 20 microliters instillation of timolol in one eye and a placebo in the other eye in a masked randomized manner. In the second experiment, one eye of another group of rabbits received timolol twice daily for 20 days and a placebo in the fellow eye in a randomized masked manner. The NB in ONH and IOP were measured before treatment and 2 hours after the last instillation on the 20th day. After a single instillation of timolol, PR showed a maximum reduction of 11% and the IOP in the timolol-treated eyes showed a maximum decrease of 18%, but the NB in ONH and BP did not show any significant change during the experiment. After the 20-day treatment, IOP showed a maximum decrease of 28% in the timolol-treated eyes and 17% in the placebo-treated eyes. The NB in the timlol-treated eyes increased significantly (p < 0.01), but in the placebo-treated eyes it showed no significant change. Thus, the long-term use of topical timolol may increase peripheral blood flow in ONH tissue in the living rabbit eye.

Administration, Topical↗

[Effect of calcium antagonist on retinal microcirculation evaluated with the laser speckle retinal microcirculation analyzer].

The effect of intravenous administration of a calcium antagonist on the retinal microcirculation in rabbit eyes was examined with a laser speckle retinal microcirculation analyzer. Under general anesthesia, 40 micrograms/kg of nicardipine, a calcium antagonist, was injected intravenously in the nicardipine group, and 0.4 ml/kg of saline in the control group. A quantitative index of blood flow velocity, the normalized blur (NB) value, in a retinal area (0. 62 x 0.62 mm) free of visible vessels, was recorded at 1-minute intervals for the first 5 minutes and at 5 minute-intervals for the next 85 minutes. The retinal NB value in the nicardipine group was significantly greater than in the control group, averaging 119%, 115%, 111%, 112%, and 116% of the initial value at 65, 75, 80, 85, and 90 minutes after injection, respectively. The blood pressure in the nicardipine group decreased significantly from 1 to 20 minutes after injection. The pulse rate, arterial pH, partial CO2 pressure, partial oxygen pressure, body temperature and intraocular pressure did not show significant change during the experiment. These results suggest, for the first time, that nicardipine increases the blood flow velocity in the retinal microvasculature in the living eye.

Animals↗

Studies on the gastric mucosal microcirculation. 2. Helicobacter pylori water soluble extracts induce platelet aggregation in the gastric mucosal microcirculation in vivo.

BACKGROUND: The exact mechanisms by which Helicobacter pylori infection results in gastric mucosal injury are unclear. AIMS: To assess in vivo whether H pylori extracts could initiate an inflammatory response in the rat gastric mucosal microcirculation. METHODS: Extracts of H pylori, Escherichia coli, or distilled water were administered topically to the gastric mucosa of anaesthetised animals. Fluorescence in vivo microscopy assessed macromolecular leakage of labelled albumin from mucosal vessels, leucocyte adherence/rolling, and platelet activity for 90 minutes. RESULTS: H pylori induced increases (p < 0.001) in adherent platelet thrombi and circulating platelet emboli after five and 15 minutes respectively. Adherent platelet thrombi (mean of four per field of view) remained significantly increased throughout the experiment, but circulating emboli (maximum of five at 30 minutes) decreased with time. Leucocyte adherence did not occur although early transient rolling was observed. An 11% increase (p < 0.02) in albumin leakage occurred after five minutes only. The induction of platelet aggregation was only observed following H pylori administration. CONCLUSION: This in vivo study demonstrated the ability of H pylori extracts to promote platelet aggregation within gastric mucosal microvessels. Recruitment of leucocytes was not observed. The results suggest that the early events associated with H pylori infection are platelet aggregation with perhaps subsequent leucocyte recruitment by activated platelets.

Animals↗

Microcirculation of the epimyocardial layer of the heart. I. A method for in vivo observation of the microcirculation of superficial ventricular myocardium of the heart and capillary flow pattern under normal and hypoxic conditions.

To study microcirculation of the heart in vivo, we developed a new technique of epi-illumination of the beating rat ventricular myocardium. Five tiny needles connected to the operation table were horizontally inserted into the ventricular myocardium just beneath the epicardium in order to restrict cardiac movement during contraction and to enhance the amount of light reflected from the structures under study. The in vivo light and fluorescent microscopy were performed with the Ultropak and the Fluopak systems (Leitz) combined with a highly sensitive television camera and recording system. In 142 individual in vivo measurements (6 animals) the mean capillary diameter amounted to 6.0 +/- 1.0 mu. In the same experiments, the mean intercapillary distance was 18.7 +/- 1.7 mu. In agreement with the literature, the capillaries of the epimyocardial layer of the rat heart demonstrate a mixed countercurrent flow pattern. In contrast to other authors, we observed no recruitment of resting capillaries after hypoxia.

Animals↗

A pharmacological and histological examination of the microcirculation of the rat subcutaneous air-pouch: microcirculation of the rat air-pouch.

The effects of histamine, 5-hydroxytryptamine (5-HT) and prostaglandin E2 (PGE2) on plasma protein extravasation in the rat subcutaneous air-pouch have been studied. Both histamine and 5-HT produced increases in plasma protein extravasation which were inhibited by specific receptor antagonists. Plasma protein extravasation induced by PGE2 was partially inhibited by either a 5-HT receptor antagonist (methysergide) or by a combination of H1 and H2 receptor antagonists (mepyramine and cimetidine). A combination of all three antagonists further reduced plasma protein extravasation. These results suggest that PGE2 increases vascular permeability indirectly via the degranulation of mast cells. This supposition was confirmed by histological evidence of extensive mast cell degranulation following the injection of PGE2 but not following histamine, 5-HT or saline injection. Using a technique of vascular labelling, following the intravenous injection of Monastral blue dye, plasma extravasation induced by histamine, 5-HT or PGE2 was observed to be restricted to post-capillary venules and was not observed in arterioles or capillaries. Electron microscopic examination of the tissue revealed the presence of monastral blue particles trapped between endothelial cells. These findings suggest that the microcirculation of the rat subcutaneous air-pouch behaves in an analogous manner to that of other tissues.

Air↗

Recombinant human erythropoietin and its effects on macro- and microcirculation during normovolemia. A physiological study of hemodynamics, fluid status and skin microcirculation.

In 9 chronic hemodialysis patients, treated with recombinant human erythropoietin (rHuEpo), longitudinal studies were performed to investigate possible changes in macro- and microcirculatory parameters during normovolemia, as assessed echographically by determining the inferior vena cava diameter and adjusting dialysis dry weight. Hematocrit increased from 19 +/- 4 to 33 +/- 5% (p less than 0.001). Systemic vascular resistance increased from 1,020 +/- 259 to 1,283 +/- 245 dyn/s/cm-5 (p less than 0.02), while mean arterial pressure remained unchanged. Cardiac index decreased (4.9 +/- 1.4 to 3.8 +/- 0.9 liters/min/m2; p less than 0.02), caused by a decrease in heart rate (87 +/- 21 to 75 +/- 16 beats/min; p less than 0.02) and stroke index (59.9 +/- 15.2 to 51.0 +/- 10.7 ml/m2; p less than 0.02). Red blood cell volume increased (468 +/- 105 to 858 +/- 203 ml/m2; p less than 0.001) and plasma volume decreased inversely ([125I]-albumin; 2,008 +/- 338 to 1,664 +/- 225 ml/m2; p less than 0.001), whereas total blood volume remained unaltered (2,476 +/- 397 to 2,518 +/- 352 ml/m2; n.s.). Total body weight increased (57.8 +/- 12 to 62.1 +/- 12 kg; p less than 0.02), indicative of an anabolic effect of rHuEpo therapy. Skin capillary circulation as measured by transcutaneous oxymetry at 37 degrees C skin temperature impaired, reflected by the increase of the time to peak after arterial occlusion (82 +/- 21 to 121 +/- 25 s; p less than 0.02). The reactive hyperemic response following the release of occlusion showed a significant increase at high hematocrit (10.7 +/- 4.2 to 16.6 +/- 5.3 mm Hg; p less than 0.02), whereas resting transcutaneous Po2 values showed a slight but not significant increase (2.3 +/- 1.3 to 4.7 +/- 3.3 mm Hg; n.s.). The high number of pathological capillaries in hemodialyzed patients might be an additional factor for the increase in systemic vascular resistance.

Adult↗

Cerebral microcirculation: heterogeneity of pial arterial network controlling microcirculation of cerebral cortex.

Analysis of the functional behaviour of pial arterial ramifications feeding small areas of the cerebral cortex of rabbits uncovered well-defined heterogeneity of vascular responses during development of functional hyperemia. In the network of the smaller pial arteries, under 100 microns in diameter, the most active segments, the sphincters of offshoots of smaller arterial branches from larger trunks and the precortical arteries just before their penetration as the radial arteries into the cerebral cortex, have been discovered. The frequency of their dilatation was found to be higher, the latent periods of the vascular responses significantly shorter, and the degree of vasodilatation greater than of the adjacent arterial segments. An abundant amount of cholinergic nerve plexuses (containing the cholinesterase) was found in the walls of these active vascular segments, and microapplication of atropine resulted in a considerable decrease of their dilatation. These experimental results indicate the involvement of the cholinergic neurogenic mechanism in the functional vasodilatation, as distinct from the largely accepted effect of the humoral mechanism accomplished by diffusion of active vasodilatory substances from tissue elements to the walls of the feeding arterial branches.

Animals↗

[The theory of microcirculation. 3: Role of blood pressure amplitude on tissue microcirculation].

The blood pressure amplitude of the pulsatile blood supply evokes elastic interactions in the tissue, in which the noncompressible tissue fluid functions as mediator of strength. The particular morphological structure round the tissue capillary gives rise to the suggestion that in the result of these interactions a tissue pump is working which supports the blood flow as well as the exchange of substances at the capillary wall. The effectiveness of this pump depends upon the blood pressure amplitude, the heart rate and upon the elastic tissue properties and can be regulated with changes of these parameters. With the help of a hydraulic model an engineer-technical solution is built up and tested which in analogy to the tissue structure functions as pump and shows the properties of elastic interactions mentioned.

Blood Pressure↗