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PubMed2002

The role of quantitative myocardial contrast echocardiography in the study of coronary microcirculation in athlete's heart.

Quantitative myocardial contrast echocardiography was performed with harmonic power Doppler analysis using the background subtraction and Levovist (Schering AG, Berlin, Germany) as contrast agent in a triggered modality. Quantitative analysis of echocontrast was performed offline with PC software, obtaining the transit curves of microbubbles through the coronary capillary system. Coronary microcirculation in athletes showed a behavior substantially comparable with control participants, although at a higher level. Training determines a physiologic left ventricular hypertrophy that counterbalances the dilatation in the left ventricular chambers because of the higher blood volume in athletes compared with control participants. Angiogenesis and several functional adaptations (relaxation of small coronary arteries, increased production of nitric oxide by the coronary endothelium, or both), represent the potential mechanisms that allow an optimal distribution of oxygen and of substrates to the hypertrophied myocardium of the athletes.

Adult↗

PubMed2002

Cutaneous microcirculation in the neuropathic diabetic foot improves significantly but not completely after successful lower extremity revascularization.

OBJECTIVE: The purpose of this study was the examination of the effect of successful large vessel revascularization on the microcirculation of the neuroischemic diabetic foot. RESEARCH DESIGN AND METHODS: We measured the cutaneous microvascular reactivity in the foot in 13 patients with diabetes with peripheral arterial disease and neuropathy (group DI) before and 4 to 6 weeks after successful lower extremity arterial revascularization. We also compared them with age-matched and sex-matched groups of 15 patients with diabetes and neuropathy, seven patients without neuropathy, and 12 healthy patients for control. We used single-point and laser Doppler scan imaging for the measurement of the foot skin vasodilatation in response to heating to 44 degrees C and to iontophoresis of 1% acetylcholine (endothelial-dependent response) and 1% sodium nitroprusside (endothelial-independent response). RESULTS: The group DI response to heat increased from 289% +/- 90% before surgery (percent increase over baseline measured in volts) to 427% +/- 61% (P <.05) after surgery but was still comparable with the response of the patients with diabetes and neuropathy (318% +/- 51%) and lower than the responses of the patients without neuropathy (766% +/- 220%) and the healthy patients for control (891% +/- 121%; P <.0001). The group DI acetylcholine response also improved from 6% +/- 4% before surgery to 26% +/- 8% after surgery (P <.05) and was similar to the responses of patients with diabetes and neuropathy (18% +/- 3%) and patients without neuropathy (38% +/- 8%) but still lower when compared with the response of the patients for control (48% +/- 9%; P <.001). The sodium nitroprusside response for group DI improved from 10% +/- 4% to 29% +/- 9% (P <.05) and was similar to the responses of the neuropathic (25% +/- 9%), nonneuropathic (32% plus minus 6%), and control (40% +/- 5%) groups. The group DI neurovascular response, which depends on the healthy function of the C-fiber nociceptors, was similar at baseline (5% +/- 9%) and after surgery (14% +/- %10) and in the neuropathic group (33% +/- 21%), but it was dramatically reduced when compared with the nonneuropathic (110% +/- 40%) and control (198% +/- 54%) groups (P <.001). CONCLUSION: Impaired vasodilation in the diabetic neuropathic lower extremity leads to functional ischemia, which improves considerably but is not completely corrected with successful bypass grafting surgery. Therefore, patients with diabetes and neuropathy may still be at high risk for the development of foot ulceration or the failure to have an existing ulcer heal despite adequate correction of large vessel blood flow.

Acetylcholine↗

PubMed2005

Cardiomyopathy associated with microcirculation dysfunction in laminin alpha4 chain-deficient mice.

Laminin alpha4 chain is a component of extracellular matrix (ECM) laminin-8 and -9 and serves dual roles as a structure protein and as a signaling molecule. The abundance of laminin alpha4 chain transcripts in the heart suggests an important role of this protein in cardiovascular development and function. In this study, we demonstrate that laminin alpha4 deficient mice gradually develop cardiac hypertrophy with impaired function. We show that depletion of laminin alpha4 chain did not alter the levels of dystrophin-glycoprotein complex (DGC) components or affect cell membrane integrity. No alteration in integrin beta 1D protein was observed in terms of expression level or distribution pattern, indicating that the postnatal development of cardiac hypertrophy and cardiomyopathy in these mice is unlikely associated with the stability of sarcolemmal DGC and integrin complexes. Moreover, cardiomyocytes isolated from Lama4-/- mutant hearts maintained their contractility in vitro. In contrast, elevated levels of hypoxia-inducible factor 1alpha (Hif1alpha) and vascular endothelial growth factor A (Vegfa) transcripts, along with multiple foci of cardiomyocyte degeneration and fibrosis suggested sustained cardiac ischemia. Electron microscopy confirmed malformed blood vessels and wide pericapillary ECM spaces, suggesting the presence of microcirculation abnormalities in Lama4-/- mutant hearts. We thus conclude that mutation in the laminin alpha4 chain leads to abnormal cardiovascular ECM structure that cause insufficient oxygen supply to the heart and the subsequent ischemic cardiac phenotype observed. Our study links the genetic deficiency of an ECM protein to cardiomyopathy and implies a novel pathway of idiopathic cardiomyopathy in human.

Animals↗

PubMed1999

Quantitative analysis of leukocyte dynamics in retinal microcirculation of rats with short-term ischemia-reperfusion injury.

PURPOSE: To characterize the time course of complete recovery of leukocyte velocities in the retinal microcirculation of rats from short-term (5-minute) retinal ischemia. METHODS: After 5 minutes of retinal ischemia produced by clamping the optic nerve, resulting in the occlusion of both central retinal artery and the central retinal vein, we used acridine orange (AO) and a scanning laser ophthalmoscope (SLO) to observe the velocities of leukocytes in precapillary arteriole ( v(a)), capillary (v(c)) and postcapillary venule (v(v)). Measurements were taken at reperfusion time points of 5, 10, 15, 20, 30, 40, 50, 60 and 80 minutes for the ischemic eyes and at 12, 22, 42 and 62 minutes for the control eyes, respectively. RESULTS: Each control velocity was arteriole 25.1 +/- 4.3 mm/ s; venule 16.9 +/- 3.2 mm/s; and capillary 1.54 +/- 0.31 mm/s, respectively. The leukocyte velocities after 5 minutes of ischemia in arteriole and venule recovered completely within 80 minutes of reperfusion; however, the recovery patterns were different. The recovery pattern showed a biphasic increase in arterioles and a monophasic increase in venules. The velocity in capillaries half recovered rapidly, within 5 minutes of reperfusion, but the subsequent recovery was slower and was not complete even at 80 minutes of reperfusion. CONCLUSIONS: In this study, leukocyte velocities in arterioles, venules and capillaries exhibited different recovery patterns following retinal ischemia and subsequent reperfusion. Capillaries, at least within 80 minutes of reperfusion, may have difficulty recovering completely from even short-term (5-minute) ischemia.

Acridine Orange↗

PubMed1999

Nitric oxide synthase inhibitor augments post-ischemic leukocyte adhesion in the cerebral microcirculation in vivo.

The objective was to examine the effect of the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME) on leukocyte adhesion in the cerebral microcirculation during reperfusion following partial forebrain ischemia in the rat. Intravital fluorescence video-microscopy through a closed cranial window was used to visualize leukocyte-endothelium interaction in small pial veins of 15-100 microns diameter. Forebrain ischemia was produced by the ligation of both common carotid arteries plus elevation of the intracranial pressure to 20 mmHg for 60 min. The number of leukocytes adhering to the endothelium for longer than 3 sec was determined during ischemia (5 min and 60 min) and during reperfusion (5 min and 60 min). Two experimental groups were treated with either L-NAME or its inactive enantiomer D-NAME (20 mg kg-1 i.v.) 30 min prior to reperfusion. In a third group, also treated with D-NAME, post-ischemic hyperemia was prevented by lowering the ICP without removing the occlusion of common carotid arteries (partial reperfusion). The velocity of flow adjacent to the endothelial surface of pial veins was measured by tracking the movement of fluorescently labeled red blood cells as flow markers before and after ischemia. During ischemia, the number of adhering leukocytes increased approximately two-fold at 5 min, and three-fold at 60 min. In the D-NAME-treated group with complete reperfusion, leukocyte adhesion returned to the baseline level by 60 min of reperfusion. However, in the L-NAME-treated group, leukocyte adhesion remained elevated at 60 min of reperfusion. Post-ischemic flow velocity was significantly decreased (-66%) from control after L-NAME treatment whereas it was increased (+53%) in the D-NAME-treated group. In the partial reperfusion group, leukocyte adhesion continued to increase after the first hour of ischemia and reached a level 2.7-fold over baseline at 60 min reperfusion. Flow velocity remained below control (-26%) at 60 min reperfusion. Leukocyte adhesion was absent in pial arteries and no plugging by leukocytes was observed in cortical capillaries. The results suggest that leukocyte adhesion in small pial veins increases during 1 h forebrain ischemia and continues to increase during reperfusion if the velocity of flow or shear rate is low. The increase in leukocyte adhesion is reversible if flow velocity is elevated during reperfusion. L-NAME prevents post-ischemic hyperemia and augments leukocyte adhesion principally via a decrease in velocity or shear rate.

Animals↗

PubMed2006

Effects of Diaspirin Crosslinked Hemoglobin (DCLHb) on microcirculation and local tissue pO2 of striated skin muscle following resuscitation from hemorrhagic shock.

The hemoglobin based oxygen carrier (HBOC) Diaspirin Crosslinked Hemoglobin (DCLHb) has been developed to substitute not only the blood volume, but also to restore the oxygen-carrying properties of blood during hemorrhagic shock. However, it has been suggested that HBOCs may enhance the formation of free oxygen radicals through the release of free iron ions via the Haber-Weiss reaction. The aim of this study was to investigate the effects of DCLHb on the microcirculation, leukocyte-endothelial cell interaction and local tissue oxygenation in striated skin muscle of Syrian golden hamsters during and after resuscitation from hemorrhagic shock. In particular we focused on the local tissue oxygenation after resuscitation with DCLHb (hemoglobin content 10 g%) compared to resuscitation using autologous blood diluted to a hemoglobin content of 10 g%. Hemorrhagic shock was induced for 45 minutes by bleeding the animals at a rate of 33 ml/kg BW maintaining a mean arterial pressure of 30 +/- 5 mmHg. Animals were resuscitated either with 33 ml/kg BW 6% Dextran-60.000 or with 10 g% DCLHb. The control group received shed blood diluted with Ringers to a hemoglobin content of 10 g%. Intravital microscopy was used for investigation of the microcirculatory parameters and a multiwire platinum surface electrode for measurement of local tissue pO2 in striated skin muscle in the dorsal skinfold chamber of Syrian golden hamsters. Resuscitation from hemorrhagic shock with 10 g% AUB revealed significant increase of leukocytes rolling in postcapillary venules at 30 to 120 minutes after resuscitation compared to baseline values. DCLHb turned out to reduce the number of firmly adherent leukocytes after resuscitation compared to 10 g% AUB. Microvascular permeability as an indicator for functional endothelial integrity revealed no significant differences between the groups. DCLHb and 10 g% AUB led to a significant increase in local tissue oxygenation after resuscitation from hemorrhagic shock. However, 10 g% AUB turned out to be most effective to restore the local tissue pO2 compared to Dx-60. Our findings indicate that DCLHb restores microvascular perfusion after critical hemorrhagic shock as efficient as Dx-60 and 10 g% AUB. The absence of enhanced leukocyte-endothelium interaction after resuscitation with DCLHb implies that this HBOC does not exacerbate formation of oxygen free radicals during reperfusion. DCLHb effectively increases local tissue pO2 after resuscitation from hemorrhagic shock; however, not as effectively as 10 g% AUB.

Animals↗

PubMedDate not supplied

Lymphatic biology and the microcirculation: past, present and future.

Because of the role that lymphatics have in fluid and macromolecular exchange, lymphatic function has been tightly tied to the study of the microcirculation for decades. Despite this, our understanding of many basic tenets of lymphatic function is far behind that of the blood vascular system. This is in part due to the difficulty inherent in working in small, thin-walled, clear lymphatic vessels and the relative lack of lymphatic specific molecular/cellular markers. The application of cellular and molecular tools to the field of lymphatic biology has recently produced some significant developments in lymphatic endothelial cell biology. These have propelled our understanding of lymphangiogenesis and related fields forward. Whereas the use of some of these techniques in lymphatic muscle biology has somewhat lagged behind those in the endothelium, recent developments in lymphatic muscle contractile and electrical physiology have also led to advances in our understanding of lymphatic transport function, particularly in the regulation of the intrinsic lymph pump. However, much work remains to be done. This paper reviews significant developments in lymphatic biology and discusses areas where further development of lymphatic biology via classical, cellular, and molecular approaches is needed to significantly advance our understanding of lymphatic physiology.

Animals↗

PubMedDate not supplied

A computer-based method for determination of the cell-free layer width in microcirculation.

OBJECTIVES: The cell-free layer between the erythrocyte column and the vessel wall is an important determinant of hydrodynamic resistance in microcirculatory vessels. The authors report a method for continuous measurement of the width of this layer. METHODS: The light intensity of a linear array of pixels perpendicular to the vessel axis is continuously determined from a video image of a microcirculatory vessel. A threshold level based on Otsu's method is used to establish the interface between the cell-free layer and the erythrocyte column. To test the method, video images at 750-4500 frames/s were obtained from venules and arterioles in rat spinotrapezius muscle at normal and reduced arterial pressures before and after induction of erythrocyte aggregation with Dextran 500. The current measurements were compared to manual measurements of the same images. RESULTS: Values obtained by the manual and the new methods were in agreement within the 95% confidence limit by the Bland-Altman analysis and within 90-95% range by the correlation coefficient (R2). The more frequent measurements reveal substantial, rapid variations in cell-free layer width and changes in mean values with alteration of arterial pressure and red cell aggregability. CONCLUSIONS: A new, computer-based technique has been developed that provides measurements of rapid, time-dependent variations in the width of the cell-free layer in the microcirculation.

Animals↗

PubMed2006

Effect of inflammation on the aging microcirculation: impact on skeletal muscle blood flow control.

To meet the metabolic demands of skeletal muscle, the vasculature supplying these vascular beds has to be connected to respond in a coordinated uniform manner, thus providing the necessary oxygen and nutrients during increased activity. The skeletal muscle microcirculation is the major resistance network controlling vascular blood supply and it is the integrity of the endothelium lining the blood vessels that is paramount in facilitating this action. Aging is a major risk factor for cardiovascular disease and is associated with significant increases in inflammatory agents that negatively impact the vasculature. Several inflammatory agents such as cytokines (tumor necrosis factor-a), advanced glycation products (AGEs), and matrix metalloproteinases (MMPs) along with storage cells for inflammatory mediators (mast cells) are associated with a chronic "low-grade inflammation" state that has been observed over the course of the aging process. Current research suggests that these age-related increases in inflammatory agents can disrupt the microvascular endothelium and thus impair blood flow. This impairment could exacerbate the common age-related disease states such as hypertension, diabetes, congestive heart failure, and sarcopenia, leading to increased mortality and morbidity.

Aging↗

PubMed2004

Free radical activity depends on underlying vasoconstrictors in renal microcirculation.

We examined the role of free radicals in renal microvascular tone induced by various vasoactive stimuli. Isolated perfused rat hydronephrotic kidneys were used for direct visualization of renal microcirculation. The effect of tempol on angiotensin II-, norepinephrine-, KCl-, and pressure-induced afferent arteriolar constriction was evaluated. Under angiotensin II-induced constriction, tempol (3 mmol/L) caused 57 +/- 8% dilation of afferent arterioles. In contrast, tempol elicited only 38 +/- 8% and 26 +/- 9% dilation of norepinephrine- and KCl-induced constriction. Similarly, myogenic response induced by elevating renal arterial pressure from 80 to 180 mmHg was resistant to the vasodilator action of tempol (22 +/- 7% inhibition). Furthermore, tempol failed to reverse nitro-L-arginine methylester-induced afferent constriction, nor had vasodilator effect on the angiotensin II-induced constriction in the presence of nitro-L-arginine methylester. In contrast, nitroprusside elicited marked vasodilation of angiotensin II- (97 +/- 5% reversal) and norepinephrine-induced afferent constriction (89 +/- 6% reversal), but had less effect on KCl- (46 +/- 8% reversal) and pressure-induced constriction (26 +/- 9% reversal). These different actions were also observed when polyethylene-glycolated superoxide dismutase was used as an antioxidant. In conclusion, the role of free radicals in afferent arteriolar tone varies, depending on the underlying vasoconstrictor stimuli, with greater contribution of free radicals to angiotensin II-induced constriction. The heterogeneity in the responsiveness to free radical scavengers is attributed to both magnitude of free radicals produced and sensitivity of the underlying vasoconstrictors to nitric oxide.

Angiotensin II↗

PubMed1964

PRODUCTION OF INFLAMMATORY CHANGES IN THE MICROCIRCULATION BY CATIONIC PROTEINS EXTRACTED FROM LYSOSOMES.

Lysosomal granules of rabbit exudate polymorphonuclear (PMN) leucocytes were isolated and then lysed by freezing-thawing. Topical application of this material to rat and rabbit mesentery produced sticking and emigration of leucocytes, stasis of blood flow, and petechial hemorrhage. The granule-free, supernatant fraction of the homogenized leucocytes failed to produce any of these reactions. Cationic proteins extracted from these granules by weak acid and precipitated by ethanol at concentrations of 20 and 45 per cent, were also tested on heterologous, homologous, and autologous mesenteric vessels. The 20 per cent ethanol-precipitated fraction produced all of the aforementioned injury reactions, whereas the 45 per cent fraction was inactive. The intensity of inflammatory changes produced by the active cationic protein fraction was greater than that produced by lysed whole granules. Both the 20 per cent and 45 per cent ethanol fractions of cationic protein induced clumping of rabbit platelets, in vitro. The 20 per cent ethanol fraction also caused a slight acceleration in rate of swelling of isolated rabbit liver mitochondria. The active material proved to be non-pyrogenic in rabbits. This material exhibited no kinin-like effects when tested on isolated smooth muscle preparations (rabbit aorta and guinea pig ileum). In the rat, the protein produced a transient vasodepression which was inhibited by pretreatment of the animal with an antihistamine. Ultraviolet absorption data and ribose assays showed that the 20 per cent ethanol fraction contained only 4 per cent or less of ribonucleic acid. Upon electrophoresis in starch gel, using acid buffer, this fraction separated into at least three major components which migrated towards the cathode. Precipitation of one of the slowly migrating components by titration of the fraction to pH 10.5 greatly increased the inflammatory activity of the material. The inflammatory basic protein fraction was essentially devoid of acid phosphatase, beta glucuronidase, acid ribonuclease, lysozyme, and catalase activity. The non-inflammatory basic protein fraction contained appreciable quantities of acid ribonuclease and lysozyme. The foregoing data demonstrate that certain of the cationic proteins present in lysosomes of rabbit exudate PMN leucocytes can reproduce one of the cardinal features of the inflammatory response; namely, adhesion and emigration of leucocytes in the microcirculation. These findings offer fresh support for the role of lysosomes in the pathogenesis of tissue injury, and may help to account for the propagation of leucocyte emigration to peak numbers during inflammatory reactions.

Acid Phosphatase↗

PubMed2004

Oxygen distribution and respiration by the microcirculation.

Longitudinal and radial oxygen gradients in the microcirculation due to oxygen release from arterioles show that in some tissues oxygen is primarily supplied by arterioles and secondarily by capillaries. In several tissues, the arteriolar rate of oxygen exit is too large to be explained by diffusion alone, indicating that in these tissues oxygen consumption of the arteriolar wall in vivo is much greater than that shown in in vitro studies of endothelium and vascular smooth muscle, a phenomenon that may be related to the synthesis autocoids by the endothelium in vivo. The functional significance of the high metabolic rate of the arteriolar vessels may be related to the need of providing a metabolic barrier for protecting the parenchymal tissue from high oxygen levels in arterial blood, thus reducing formation of oxygen free radicals in the perivascular tissue, a supposition supported by the finding that the radial oxygen gradient at the microvascular wall and therefore its rate of oxygen consumption are proportional to local blood oxygen partial pressure (pO(2)). Oxygen consumption by the endothelium and/or smooth muscle is also a factor in causing terminal lymphatic pO(2) to have the lowest oxygen level in the tissue, rendering this compartment most vulnerable in hypoxic conditions.

Animals↗

PubMed2004

Blood substitutes and redox responses in the microcirculation.

Transfusion of hemoglobin-based blood substitutes, designed for their plasma expansion and oxygen transport capabilities, has resulted in some major problems, such as organ dysfunction, during clinical trials. Experimental evidence demonstrates that these hemoglobins damage tissue by producing highly reactive oxygen species. Although cell-free hemoglobin may present a low risk to people with normal redox status, patients who are sick and have a poor antioxidant status may be at risk. Oxidative damage is particularly dangerous in the microcirculation because excess leakage of plasma components into the interstitium will disturb the fluid balance between blood and tissue and alter the kinetics of delivery of intravascularly injected drugs, and endogenous enzymes and hormones, to various tissues. In this review, the redox chemistry of hemoglobin-based blood substitutes is briefly described, and their effects on cultured endothelial cells, and on the exchange properties of the microvasculature, are discussed. Taking into account the possible mechanisms by which oxidative damage can occur, various methods to reduce the deleterious effects of blood substitutes in vivo are evaluated. Finally, several possible cell signaling pathways that are triggered in endothelial cells, in response to modified hemoglobins, are considered in terms of protecting microvascular function.

Animals↗

PubMedDate not supplied

A computational model for free radicals transport in the microcirculation.

Nitric oxide (NO), superoxide (O(2)(-)), and peroxynitrite (ONOO(-)) interactions in pathophysiologic conditions such as cardiovascular disease, hypertension, and diabetes have been studied extensively in vivo and in vitro. A reduction in bioavailability of NO is a common event that is known as the endothelial dysfunction in these conditions. Despite intense investigation of NO biotransport and O(2)(-) and ONOO(-) biochemical interactions in vasculature, we have very little quantitative knowledge of distributions and concentrations of NO, O(2)(-), and ONOO(-) under normal physiologic and pathophysiologic conditions. Based on fundamental principles of mass balance, vessel geometry, and reaction kinetics, we developed a mathematical model of these free radicals transport in and around an arteriole during oxidative stress. We investigated the role of O(2)(-) and ONOO(-) in inactivating vasoactive NO. The model predictions include (a) NO interactions with oxygen, O(2)(-), and ONOO(-) have relatively little effect on the NO level in the vascular smooth muscle under physiologic conditions; (b) superoxide diffuses only a few microns from its source, whereas peroxynitrite diffuses over a larger distance; and (c) reduced superoxide dismutase levels significantly increase O(2)(-) and peroxynitrite concentrations and decrease NO concentration. Model results indicate that the reduced NO bioavailability and enhanced peroxynitrite formation may vary depending on the location of oxidative stress in the microcirculation, which occurs at diverse vascular cell locations in diabetes, aging, and cardiovascular diseases. The results will have significant implications for our understanding of these free radical interactions in physiologic and pathophysiologic conditions resulting from endothelial dysfunction.

Arterioles↗

PubMed1991

Effects of Nd:YAG laser irradiation on microcirculation.

Changes in microcirculation after irradiation by Nd:YAG laser were evaluated using the "rabbit ear chamber" method. Morphological changes of the vascular network related to time elapsed after irradiation was observed by a microscope-video system. Findings such as vascular shrinkage, degeneration, coagulation, and stasis associated with irradiation were recognized shortly after the Nd:YAG laser was applied. Damage increased with irradiation energy increase. Expansion of the stasis region and appearance of hemorrhagic spots decreased, and vascularization began. On the seventh to tenth days, the damaged region was restored by a newly formed capillary network. When no change was noticed microscopically in the case of low-energy irradiation, transient increase of blood flow, determined by laser Doppler flowmeter, was observed. The results suggest that the effects of Nd:YAG laser irradiation are primarily thermal. It has good hemostatic and coagulation ability and some of the changes are nerve-mediated by low-energy irradiation.

Animals↗

PubMed1994

The effects of pressure and shear on skin microcirculation in elderly stroke patients lying in supine or semi-recumbent positions.

The effects of external pressure and shear on the skin microcirculation over the sacral area, which is known as a high risk area for pressure sore formation, were studied in 30 elderly patients. The skin blood cell flux (SBF) was measured using the laser Doppler technique, with the patient first at rest in lateral position, then lying for 30 minutes in supine or semi-recumbent 45 degrees position, and finally in lateral position. Elderly high-risk patients (G2), most of them more than two years post-stroke, had a lower body mass index and a reduced sacral skin-fold compared with non-risk patients (G1). The SBF in G2 decreased 28% in supine and 14% in 45 degrees position, whereas the SBF in G1 increased 35% in supine and 13% in 45 degrees position. Spontaneous movements up to seven times per 30 minutes were registered, even during sleep, and were evident by direct observation of the recorded charts as a temporary SBF increase. The risk for skin ischaemic damage over the sacral area of elderly risk patients was evident in both positions, especially with the patients lying in supine position. When increasing the upper body slope in G2 from horizontal to 45 degrees, an inability to recover a satisfactory blood supply after the ischaemic insult was found. Discomfort from compressive and shear forces initiates changes in posture, even in elderly patients prone to tissue breakdown. Occasional relief of pressure was in most patients followed by temporary increase in skin blood flow with concomitant temperature increase. This most probably protected them from developing skin lesions.

Aged↗

PubMed1993

Effect of chronic alcohol intake on rat liver microcirculation assessed by the multiple indicator dilution technique.

To study the hepatic microcirculatory disturbance in alcoholic liver injury, rats were chronically (8-12 weeks) fed with alcohol via a gastric fistula according to the method of Tsukamoto and French (1986). The hepatic microcirculation was studied by measuring the sinusoidal volume (SV) and the apparent space of Disse (DS) volume using a multiple-indicator dilution technique. Both the SV and the DS volume were significantly decreased in the alcohol-fed rats at 8-12 weeks despite the absence of microscopically detectable hepatic fibrosis. Similar changes were noted in the alcohol-fed and control rats regarding expansion of the SV and the DS volume with alterations in portal pressure. However, since the volumes in the alcohol-fed group increased with the increase of portal pressure, they maintained a steady difference from the control values. These results suggested that the decrease of the SV and the DS volume may have been secondary to compression caused by steatosis and/or hepatocyte enlargement, although a possible role for microscopically undetectable hepatic fibrosis could not be ruled out.

Alcoholism↗

PubMed1991

Influence of hypertonic volume replacement on the microcirculation in cardiac surgery.

We have studied the effects of two types of volume replacement on the microcirculation in an open, controlled study in 45 patients undergoing aorto-coronary bypass grafting whose pulmonary capillary wedge pressure (PCWP) was less than 5 mm Hg. Hypertonic saline prepared in hydroxyethylstarch solution (HS-HES, n = 15) and 6% HES 200/0.5 solution (6% HES; n = 15) were infused randomly before operation in order to double the PCWP. Patients not given an infusion served as controls (n = 15). Skin microcirculatory blood flow was investigated by laser Doppler flow (LDF) measured simultaneously at the forearm and forehead before and after cardiopulmonary bypass (CPB). Less HS-HES (3.8 (SD 0.3) ml kg-1) than 6% HES-solution (9.7 (1.5) ml kg-1) was necessary to double baseline PCWP. There were no differences in heart rate and mean arterial pressure (MAP) between the groups. Cardiac index (CI) increased significantly in both volume groups (HS-HES max. +54%; 6% HES max. +30%). Systemic vascular resistance (SVR) decreased after infusion of HS-HES (-30%) and after 6% HES(-19%) and remained almost unchanged in the control group. Plasma viscosity decreased after infusion of HS-HES and increased slightly in control patients (+4%). In comparison with the 6% HES and particularly with the control group, LDF was significantly greater after infusion of HS-HES (forearm +80%; forehead +28%). LDF during CPB and thereafter was always greater than baseline values in the HS-HES group, whereas after bypass LDF was reduced in the 6% HES (-5%) and particularly in the control patients (-30%).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗