Morphofunctional asymmetry of the microvascular bed of the rabbit concha auriculae

Microvessels of rabbit ears chamber and blood samples drawn from the internal ear vein after 30 min ischemia were studied. In the initial state the length of the left ear microvascular bed was 1.5 times higher, mean microvessel diameter 14.6% less, apparent viscosity of outflowing blood 16.8% less, RBC concentration per volume unity of blood 8% higher, RBC electrophoretic mobility 13.7% higher than those in the right one. It was shown that the left microvessel bed responds to the ischemia with the 13.2% increase of its length and 13.6% increase of the outflowing blood viscosity, the right one--with the 9.7% increase of microvessel diameter and 7.9% decrease of the viscosity.     

Enhanced neovascularization of rat tubed pedicle flaps with low perfusion of the wound margin

To study the role of ischemia due to low perfusion as the inciter of neovascularization, caudally based 3 X 9 cm skin flaps were created on the dorsum of 50 Sprague-Dawley rats. After injection of 0.2 ml 10% fluorescein, the animals were divided into two groups. In group I (n = 25), the distal margin of the flap tip was 1 cm proximal to the border of the fluorescence (good perfusion). In group II (n = 25), the flap was cut 1 cm distally in the nonfluorescent part (poor perfusion). The tips of the tubed flaps were transferred to a wound bed on the right flank. After 10 days, the pedicles were ligated, so that flap survival depended totally on the new vascular supply from the inset area of the flap. The flaps in group I showed a significantly higher rate of necrosis of 52.4 +/- 15.1 percent versus 1.7 +/- 1.4 percent in group II (p less than 0.0001), although the flap length in group I (5.85 +/- 1.16 cm) was less than in group II (7.15 +/- 0.95 cm; p = 0.0001). A nearly three times larger amount of tissue based on the new blood supply survived in group II compared to group I. Xerograms after injection of PbO2-gelatine on day 10 showed an increased ingrowth of blood vessels in group II. After excluding the delay phenomenon as the cause for the difference in necrosis rate, it is concluded that the only possible explanation is an enhancement of neovascularization by a perfusion gradient between the wound margins.     

Early ischemic preconditioning against focal transient and permanent brain ischemia in rats: role of collateral circulation

We hypothesize that early ischemic preconditioning (IPC) can afford protection against focal brief and prolonged cerebral ischemia with subsequent reperfusion as well as permanent brain ischemia in rats by amelioration of regional cerebral blood flow. Adult male Wistar rats (n=97) were subjected to transient (30 and 60 minutes) and permanent middle cerebral artery (MCA) occlusion. IPC protocol consisted of two episodes of 5-min common carotid artery occlusion + 5-min reperfusion prior to test ischemia either followed by 48 hours of reperfusion or not. Triphenyltetrazolium chloride and Evans blue were used for delineation of infarct size and anatomical area at risk (comprises ischemic penumbra and ischemic core), respectively. Blood flow in the MCA vascular bed was measured with use of Doppler ultrasound. The IPC resulted in significant infarct size limitation in both transient and permanent MCA occlusion. Importantly, IPC caused significant reduction of area at risk after 30 min of focal ischemia as compared to controls [med(min-max) 11.4% (3.59-2 0.35%) vs. 2.47% (0.8-9.31%), p = 0.018] but it failed to influence area at risk after 5 min of ischemia [med(min-max) 7.61% (6.32-10.87%) vs. 8.2% (4.87-9.65%), p > 0.05]. No differences in blood flow were found between IPC and control groups using Doppler ultrasound. This is suggestive of the fact that IPC does not really influence blood flow in the large cerebral arteries such as MCA but it might have some effect on smaller arteries. It seems that, along with well established cytoprotective effects of IPC, IPC-mediated reduction of area at risk by means of improvement in local cerebral blood flow may contribute to infarct size limitation after focal transient and permanent brain ischemia in rats.     

Na(+)/H(+) exchange subtype 1 inhibition reduces endothelial dysfunction in vessels from stunned myocardium

Myocardial ischemia and reperfusion cause myocyte and vascular dysfunction, frequently termed "stunning." We hypothesized that inhibiting the Na(+)/H(+) exchanger subtype 1 isoform (NHE(1)) during ischemia and reperfusion limits myocardial and coronary microvascular stunning. Anesthetized rats completed 2 x 10-min coronary artery occlusions separated by 5-min of reperfusion, followed by 15 or 60 min of reperfusion. Vehicle (saline) or the NHE(1) inhibitor cariporide (HOE-642) was administered 15 min before ischemia and was continued throughout each protocol. After reperfusion, hearts were excised, and the reactivity of resistance arteries (internal diameter, approximately 120 microm) was assessed. The first derivative of left ventricular (LV) pressure, LV developed pressure, and LV systolic wall thickening were depressed (P < 0.05) similarly in vehicle- and cariporide-treated rats during ischemia and after 15 or 60 min of reperfusion compared with sham-operated animals that were not exposed to ischemia (i.e., controls). In vessels obtained after 15 min of reperfusion, the maximal response to acetylcholine-induced relaxation (10(-8)-10(-4) M) was blunted (P < 0.05) in vessels from vehicle- (approximately 35%) and cariporide-treated rats (approximately 55%) compared with controls (approximately 85%). However, the percent relaxation to acetylcholine was greater (P < 0.05) in cariporide-treated rats compared with vehicle-treated rats. Maximal contractile responses to endothelin-1 (10(-11)-10(-7) M) were increased (P < 0.05) similarly in vehicle- and cariporide-treated rats compared with controls. Relaxation to sodium nitroprusside (10(-4) M) was not different among groups. Results were similar in vessels obtained from animals after 60 min of reperfusion. These findings suggest that NHE(1) inhibition before coronary occlusion lessens ischemia-induced microvascular dysfunction for 15-60 min after reperfusion but does not alter myocardial contractile function in the area at risk.     

Calcium channel blockade prevents pressure-dependent inward remodeling in isolated subendocardial resistance vessels

The capacity for myocardial perfusion depends on the structure of the coronary microvascular bed. Coronary microvessels may adapt their structure to various stimuli. We tested whether the local pressure profile affects tone and remodeling of porcine coronary microvessels. Subendocardial vessels (approximately 160 microm, n=53) were cannulated and kept in organoid culture for 3 days under different transvascular pressure profiles: Osc 80: mean 80 mmHg, 60 mmHg peak-peak sine wave pulsation amplitude at 1.5 Hz; St 80: steady 80 mmHg; Osc 40: mean 40 mmHg, 30 mmHg amplitude; St 40: steady 40 mmHg. Under the Osc 80 profile, modest tone developed, reducing the diameter to 81+/-14% (mean+/-SE, n=6) of the maximal, passive diameter. No inward remodeling was found here, as determined from the passive pressure-diameter relation after 3 days of culture. Under all other profiles, much more tone developed (e.g., Osc 40: to 26+/-3%, n=7). In addition, these vessels showed eutrophic (i.e., without a change in wall cross-sectional area) inward remodeling (e.g., Osc 40: passive diameter reduction by 24+/-3%). The calcium blocker amlodipine induced maintained dilation in St 40 vessels and reversed the 22+/-3% (n=6) inward remodeling to 15+/-3% (n=8) outward remodeling toward day 3. Vessels required a functional endothelium to maintain structural integrity in culture. Our data indicate that reduction of either mean pressure or pulse pressure leads to microvascular constriction followed by inward remodeling. These effects could be reversed by amlodipine. Although microvascular pressure profiles distal to stenoses are poorly defined, these data suggest that vasodilator therapy could improve subendocardial microvascular function and structure in coronary artery disease.     

Functional and structural remodeling of the myocardial microvasculature in early experimental hypertension

Advanced hypertension (HT), associated with left ventricular hypertrophy (LVH), impairs myocardial microvascular function and structure and leads to increased myocardial hypoxia and growth factor activation. However, the effect of HT on microvascular architecture and its relation to microvascular function, before the development of LVH (early HT), remains unclear. By way of method, pigs were studied after 12 wk of renovascular HT (n = 7) or control (n = 7) animals. Myocardial microvascular function (blood volume and blood flow at baseline and in response to adenosine) was assessed by using electron beam computed tomography (CT). Microvascular architecture was subsequently studied ex vivo using micro-CT, and microvessels (diameter, <500 microm) were counted in situ in three-dimensional images (40-microm on-a-side cubic voxels). Myocardial expression of vascular endothelial growth factor, basic fibroblast growth factor, and hypoxia-inducible factor-1alpha were also measured. By way of results, left ventricular muscle mass was similar between the groups. The blood volume response to intravenous adenosine was attenuated in HT animals compared with normal animals (+7.4 +/- 17.0 vs. +46.2 +/- 12.3% compared with baseline, P = 0.48 and P = 0.01, respectively). Microvascular spatial density in HT animals was significantly elevated compared with normal animals (246 +/- 26 vs. 125 +/- 20 vessels/cm2, P < 0.05) and correlated inversely with the blood volume response to adenosine. Growth factors expression was increased in HT animals compared with control animals. In conclusion, early HT elicits changes in myocardial microvascular architecture, which are associated with microvascular dysfunction and precede changes in muscle mass. These observations underscore the direct and early effects of HT on the myocardial vasculature.     

Selective recruitment of endothelial progenitor cells to ischemic tissues with increased neovascularization

Tissue ischemia remains a common problem in plastic surgery and one for which proangiogenic approaches have been investigated. Given the recent discovery of circulating endothelial stem or progenitor cells that are able to form new blood vessels, the authors sought to determine whether these cells might selectively traffic to regions of tissue ischemia and induce neovascularization. Endothelial progenitor cells were isolated from the peripheral blood of healthy human volunteers and expanded ex vivo for 7 days. Elevation of a cranially based random-pattern skin flap was performed in nude mice, after which they were injected with fluorescent-labeled endothelial progenitor cells (5 x 10(5); n = 15), fluorescent-labeled human microvascular endothelial cells (5 x 10(5); n = 15), or media alone (n = 15). Histologic examination demonstrated that endothelial progenitor cells were recruited to ischemic tissue and first appeared by postoperative day 3. Subsequently, endothelial progenitor cell numbers increased exponentially over time for the remainder of the study [0 cells/mm2 at day 0 (n = 3), 9.6 +/- 0.9 cells/mm2 at day 3 (n = 3), 24.6 +/- 1.5 cells/mm2 at day 7 (n = 3), and 196.3 +/- 9.6 cells/mm2 at day 14 (n = 9)]. At all time points, endothelial progenitor cells localized preferentially to ischemic tissue and healing wound edges, and were not observed in normal, uninjured tissues. Endothelial progenitor cell transplantation led to a statistically significant increase in vascular density in ischemic tissues by postoperative day 14 [28.7 +/- 1.2 in the endothelial progenitor cell group (n = 9) versus 18 +/- 1.1 in the control media group (n = 9) and 17.7 +/- 1.0 in the human microvascular endothelial cell group (n = 9; p < 0.01)]. Endothelial progenitor cell transplantation also showed trends toward increased flap survival [171.2 +/- 18 mm2 in the endothelial progenitor cell group (n = 12) versus 134.2 +/- 10 mm2 in the media group (n = 12) and 145.0 +/- 13 mm2 in the human microvascular endothelial cell group (n = 12)], but this did not reach statistical significance. These findings indicate that local tissue ischemia is a potent stimulus for the recruitment of circulating endothelial progenitor cells. Systemic delivery of endothelial progenitor cells increased neovascularization and suggests that autologous endothelial progenitor cell transplantation may have a role in the salvage of ischemic tissue.     

Skin microvascular adaptations during maturation and aging of hairless mice

Using intravital fluorescence microscopy in the ears of hairless mice, we determined skin microvascular adaptations during the process of aging from juvenile to adult and senescent life (6-78 wk). Despite an increase of ear area within the first 36 wk, the number and branching pattern of both arteriolar and venular microvessels remained constant during the whole life period. Both arterioles and venules exhibited an increase in length, diameter, and intervascular distance up to the age of 36 wk. With the increase of the size of the ears, the observation that cutaneous capillary density remained unchanged implied new capillary formation. During aging to 78 wk, capillary density in the ears was reduced to approximately 40%. Functional analysis revealed an appropriate hyperemic response to a 2-min period of ischemia during late juvenile and adult life, which, however, was markedly reduced during senescence. Thus, except for capillaries, there is no indication for age-related new vessel formation. The process of aging from adult to senescent life does not cause any significant remodeling but is associated with a decrease of nutritive perfusion and a functional impairment to respond to stimuli such as ischemia.     

Estimation of age-related changes in the regulation of peripheral blood flow in humans

The age-dependent features in the state of skin microvascular bed has been studied with laser Doppler flowmetry in healthy volunteers of different age groups. To reveal the reaction of skin blood flow in response to short-term ischemia, the occlusive test has been carried out. To estimate the contribution of rhythmic components to blood flow signal, continuous wavelet-transform spectral analysis was used. Age-dependent increase of pulse-wave amplitude and decrease of respiratory wave amplitude reflecting age-dependent changes in functioning of arteriolar and venular links of microvascular bed have been observed at rest. In response to short-term ischemia the age-dependent reduction of reserve resources has been revealed in functioning of arteriolar link of microvascular bed. The reduction of activity of myogenic, neurogenic and endothelial regulation systems have been shown at rest in ageing.     

Static Magnetic Field Versus Systemic Calcium Channel Blockade Effect on Microcirculation: Possible Mechanisms and Clinical Implementation

The goal was to compare static magnetic field (SMF, generated by Nd₂–Fe₁₄–B magnets) vasodilator capacity with verapamil (VER, a potent, clinically verified Ca²⁺ channel-blocking agent), aimed to assess SMF implementation in conditions with vascular ischemia. Skin microcirculatory blood flow measured by microphotoelectric plethysmogram was recorded in conscious rabbits after 40 min of 0.25 T SMF regional exposure to ear microvascular net (SMF-Vas, n = 20), or 0.35 T to carotid baroreceptors (SMF-Car, n = 14), and compared with that after 30 min VER intravenous infusion (20 µg/kg/min, n = 20). The principal finding is that SMF-Vas, SMF-Car, and VER significantly increased microcirculatory blood flow by 17.9 ± 9.58%, 22.6 ± 11.11%, and 30.5 ± 14.06% (mean ± SEM) respectively, and there was no significant difference between all three treatments (P = 0.986). Microvascular dilation was accompanied by significant decrease of blood pressure in VER and SMF-Car cases. The decrease of arterial baroreflex sensitivity in VER contrasted with its increase in SMF-Car, coupled with improved vessel sensitivity to nitric oxide (NO) dilatory effect. This suggests that SMF can have a strong vasodilator property tailored to address diabetic, mainly NO-deficient, neural, and myogenic microvascular dysfunction, especially employing both SMFs’ vasodilation synergy. Bioelectromagnetics. 2020;41:447–457. © 2020 Bioelectromagnetics Society.     

Vascular adaptation to deconditioning and the effect of an exercise countermeasure: results of the Berlin Bed Rest study.

Deconditioning is a risk factor for cardiovascular disease. The physiology of vascular adaptation to deconditioning has not been elucidated. The purpose of the present study was to assess the effects of bed rest deconditioning on vascular dimension and function of leg conduit arteries. In addition, the effectiveness of resistive vibration exercise as a countermeasure for vascular deconditioning during bed rest was evaluated. Sixteen healthy men were randomly assigned to bed rest (BR-Ctrl) or to bed rest with resistive vibration exercise (BR-RVE). Before and after 25 and 52 days of strict horizontal bed rest, arterial diameter, blood flow, flow-mediated dilatation (FMD), and nitroglycerin-mediated dilatation were measured by echo Doppler ultrasound. In the BR-Ctrl group, the diameter of the common femoral artery decreased by 13 +/- 3% after 25 and 17 +/- 1% after 52 days of bed rest (P < 0.001). In the BR-RVE group this decrease in diameter was significantly attenuated (5 +/- 2% after 25 days and 6 +/- 2% after 52 days, P < 0.01 vs. BR-Ctrl). Baseline blood flow did not change after bed rest in either group. After 52 days of bed rest, FMD and nitroglycerin-mediated dilatation of the superficial femoral artery were increased in both groups, possibly by increased nitric oxide sensitivity. In conclusion, bed rest deconditioning is accompanied by a reduction in the diameter of the conduit arteries and by an increased reactivity to nitric oxide. Resistive vibration exercise effectively attenuates the diameter decrease of leg conduit arteries after bed rest.     

MDA, oxypurines, and nucleosides relate to reperfusion in short-term incomplete cerebral ischemia in the rat.

Short-term incomplete cerebral ischemia (5 min) was induced in the rat by the bilateral clamping of the common carotid arteries. Reperfusion was obtained by removing carotid clamping and was carried out for the following 10 min. Animals were sacrificed either at the end of ischemia or reperfusion. Controls were represented by a group of sham-operated rats. Peripheral venous blood samples were withdrawn from the femoral vein from rats subjected to cerebral reperfusion 5 min before ischemia, at the end of ischemia, and 10 min after reperfusion. Neutralized perchloric acid extracts of brain tissue were analyzed by a highly sensitive high-performance liquid chromatography (HPLC) method for the direct determination of malondialdehyde, oxypurines, nucleosides, nicotinic coenzymes, and high-energy phosphates. In addition, plasma concentrations of malondialdehyde, hypoxanthine, xanthine, inosine, uric acid, and adenosine were determined by the same HPLC technique. Incomplete cerebral ischemia induced the appearance of a significant amount (8.05 nmol/g w.w.; SD = 2.82) of cerebral malondialdehyde (which was undetectable in control animals) and a decrease of ascorbic acid. A further 6.6-fold increase of malondialdehyde (53.30 nmol/g w.w.; SD = 17.77) and a 18.5% decrease of ascorbic acid occurred after 10 min of reperfusion. Plasma malondialdehyde, which was present in minimal amount before ischemia (0.050 mumol/L; SD = 0.015), significantly increased after 5 min of ischemia (0.277 mumol/L; SD = 0.056) and was strikingly augmented after 10 min of reperfusion (0.682 mumol/L; SD = 0.094). A similar trend was observed for xanthine, uric acid, inosine, and adenosine, while hypoxanthine reached its maximal concentration after 5 min of incomplete ischemia, being significantly decreased after reperfusion. From the data obtained, it can be concluded that tissue concentrations of malondialdehyde and ascorbic acid, and plasma levels of malondialdehyde, oxypurines, and nucleosides, reflect both the oxygen radical-mediated tissue injury and the depression of energy metabolism, thus representing early biochemical markers of short-term incomplete brain ischemia and reperfusion in the rat. In particular, these results suggest the possibility of using the variation of malondialdehyde, oxypurines, and nucleosides in peripheral blood as a potential biochemical indicator of reperfusion damage occurring to postischemic tissues.     

Neutrophil retention in model capillaries: deformability, geometry, and hydrodynamic forces

The initial retention of neutrophils within the pulmonary microvascular bed occurs in both physiological and pathological states, yet the factors responsible for this retention are poorly understood. Because the diameter of the neutrophil is approximately 7.03 micron and the mean pulmonary capillary diameter is 5.5 micron, we postulated that geometric constraints imposed by the microvascular bed, the deformability of the neutrophil, and the hydrodynamic characteristics of blood were important determinants of neutrophil retention. We used a filtration system wherein 111In-labeled human neutrophils (111In-N) suspended in a serum-containing buffer were passed through Nuclepore filters of known pore size. Compared with 99mTc-labeled erythrocytes (99mTc-RBC), the passage of 111In-N was delayed and a higher percentage was retained within the filter. Because the neutrophil and RBC are approximately equal in diameter, the deformability of the neutrophil must be less than that of RBC. As the flow rate increased, retention in the filters decreased logarithmically from 72 +/- 5% (flow rate 0.5 ml/min) to 15 +/- 4% (10.0 ml/min). As the number of RBC in the buffer increased, neutrophil retention in 5-micron filters decreased in a linear fashion from 65 +/- 6% at hematocrit of 0 to 33 +/- 2% at hematocrit of 10. The perfusion pressure and shear stress were of critical importance, and there was a logarithmic relationship between retention and perfusion pressure or shear stress (tau), whether the increase in pressure or tau was generated by increasing flow or by increasing the hematocrit of the perfusate. As the pore size of the filter increased, the retention of neutrophils decreased in a logarithmic fashion: from 75 +/- 5% in the 3-micron filter to 4 +/- 1.3% in the 12-micron filter.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of thermal factors on the state of microcirculation of the small intestine in acute ischemia

The influence of normo- (38 degrees C), hyper- (42 degrees C) and hypothermia (20 degrees C) on microcirculatory disturbances caused by acute local ischemia of the small intestine was investigated with the help of biomicroscopy as well as morphological methods. Ischemia was modeled by ligation of the intestine look eventrated through the abdominal wall incision of a rat onto the microscope stage for 1 h. It was shown that hyperthermia intensified microcirculatory disorders and stimulated destructive processes in tissues and hypothermia promoting microcirculation and decreasing metabolism and restrained the development of these processes. Important peculiarity of the microvascular response to ischemia, hyper- and hypothermia was revealed: heterogeneity of the reaction of different parts of microvascular bed. Appropriate evaluation of the microcirculation state in such conditions can be obtained taking into account not only the qualitative character of microvascular reaction but also an extent of this reaction manifestation in different parts of microvascular bed.     

The problem of adaptation and oscillatory processes in the microvascular bed

Healthy people (n = 16), patients with autonomic dystonia syndrome (n = 38), and patients with traumatic rupture of the median nerve before and after nerve suture (n = 28) were examined by laser Doppler flowmetry (LDF) with a computer wavelet analysis of blood flow oscillations. Functional states (FSs) of the microcirculatory bed wеre assessed using energetic and information indices of microvascular blood flow oscillations. The variation coefficient and the information regime (multistable or resonance) were used as key characteristics. Oscillatory processes are an integral part of adaptation and the FS formation in the microvascular bed. FSs were classified as adaptive, hyperadaptive, hypoadaptive, and failure of adaptation. Because supporting the optimal function of nutritive microvessels is a leading component of the adaptation process, FSs of nutritive and nonnutritive microvessels may differ. A selective contribution of the autonomic sympathetic regulatory channel was related to maintaining considerable hyperadaptation in the microvascular bed with overstrain or marked overstrain of regulatory systems, as in emotional stress. Hypoadaptive FSs formed when skin blood flow increased, an excess decrease in flow resistance was unnecessary, and especially when regulatory factors were in deficiency, e.g., in neurodystrophic syndrome.     

L-propionylcarnitine and myocardial performance in stunned porcine myocardium

Recently, we showed that L-propionylcarnitine did not affect recovery of regional contractile function of porcine myocardium subjected to 1 h of low-flow ischemia followed by 2 hr of reperfusion. In that study, ischemia may have been too severe and/or the duration of reperfusion too short to detect a beneficial effect of the compound. Therefore, in the present study we investigated the effects of saline (control group; n = 14) or pretreatment with L-propionylcarnitine (3 days of 50 mg/kg p.o. b.i.d. + 50 mg/kg i.v. prior to the experiment; n = 13) on recovery of regional contractile function of the myocardium in open-chest anesthetized pigs, subjected to two cycles of 10 min of left anterior descending coronary artery (LADCA) occlusion, each followed by 30 min of reperfusion. In the control animals, at the end of the second reperfusion period, systemic vascular resistance had increased by 18%, which, however, was not observed in the L-propionylcarnitine-treated pigs. In the control group, during the first occlusion, systolic segment length shortening (SSLS) of the LADCA-perfused area decreased from 18.5 ± 5.5% to - 3.7 = 3.2%. After 30 min of reperfusion, SSLS of the LADCA-perfused area had only partially recovered to 6.2 ±5.9%. During the second occlusion-reperfusion cycle similar values for SSLS were observed. In the treated animals., SSLS of the LADCA-perfused area was slightly improved after the second occlusion-reperfusion cycle (p = 0.056). This effect did not result in an overall improvement in cardiac pump function. We conclude that in a model of myocardial stunning, L-propionylcarnitine prevents systemic vasoconstriction in response to ischemia and reperfusion and, possibly as a result of this effect, slightly ameliorates post-ischemic hypofunction. (Mol Cell Biochem116: 147–153, 1992)     

Microvascular polytetrafluoroethylene prostheses: the cellular events of healing and prostacyclin production

This study was undertaken to obtain more insight into the morphologic and functional performance of microvascular polytetrafluoroethylene (PTFE) prostheses. Therefore, both the cellular events of healing (n = 30) and the prostacyclin production (n = 18) of microvascular polytetrafluoroethylene prostheses (length 10 mm, internal diameter 1.5 mm) were evaluated from 1 hour up to 3 months after implantation into the abdominal aorta of rats. After implantation, the graft surface became scarcely covered with platelets. From 1 week onward, endothelial cells originating from the anastomotic sides grew in over the graft surface, covered only about half the prostheses after 3 months of implantation, but did produce normal amounts of prostacyclin as compared to normal endothelium. Only near the anastomotic sides one to two layers of smooth-muscle-like cells developed underneath the neoendothelial lining. Perigraft tissue ingrowth into the wall of the polytetrafluoroethylene prostheses was scarce. The overall patency rate was 98 percent. It was concluded that optimalization of the healing characteristics of microvascular polytetrafluoroethylene prostheses may provide a prosthesis that is more suitable for clinical microsurgery.     

Improved healing of microvascular PTFE prostheses by induction of a clot layer: an experimental study in rats

This study was undertaken to test the hypothesis that the induction of a clot layer on the graft surface of microvascular polytetrafluoroethylene (PTFE) prostheses might improve their healing. PTFE microvascular prostheses (n = 18), mechanically roughened PTFE microvascular prostheses (n = 18), and Chitosan-impregnated PTFE microvascular prostheses (n = 18) (all prostheses: length 1 cm, inside diameter 1.5 mm, fibril length 30 microns) were implanted into the abdominal aortas of rats and were evaluated at 3 days (n = 3), 10 days (n = 3), 3 weeks (n = 6), and 6 weeks (n = 6) with regard to the presence or absence of a clot layer and with regard to the amount of graft healing. All untreated PTFE prostheses were never found to be covered with a clot layer, only scarcely with some platelets, and showed poor neoendothelial healing; even at 6 weeks after implantation, there was only endothelial cell coverage near the anastomotic sides (coverage = 19 +/- 4 percent). The endothelial cells were present directly on the graft surface. In contrast, both the roughened and the Chitosan-impregnated PTFE prostheses were completely covered with a thin clot layer upon implantation and demonstrated significantly better neoendothelial healing (endothelial cell coverage at 6 weeks = 76 +/- 22 percent and 75 +/- 18 percent, respectively; p less than 0.001); moreover, in these prostheses, the endothelial cells were present on a matrix of smooth-muscle cells, which covered the graft surface completely. These results confirm our hypothesis that the induction of a clot layer on the graft surface of microvascular PTFE prostheses improves their healing.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of helium-neon laser radiation on restoration of the structure of the microcirculatory bed and neurocytes of the small intestine following experimental ischemia

Influence of helium-neon laser lg-75 rays on the microcirculatory bed and neurocytes of the small intestine after its experimental ischemia has been studied. When a normal small intestine is radiated, dilatation of the luminal diameter is observed in all links of the microcirculatory bed (MCB) and also hypertrophy of neurocytes, when phenomena of distrophic processes are absent. In 30 days after 3-hours' ischemia of the intestinal loop and its successive radiation, spasm of arterial and dilatation of the venous link of MCB is registered; they normalize by the 45th day. In the control, after ischemia (without radiation) in 45 days venous plethora of the vessels in the intermuscular plexus of the intestinal wall is kept. In the nervous elements of the muscular-intestinal plexus at early stages of the experiment against the background of ischemia reactive and distrophic changes appear. By the 30th day after radiation, the volume of neurocytic bodies increases, processes grow out, nuclear-cytoplasmic index increases. Nonspecific character of the laser rays is supposed; their effect is realised via regional microvascular and nervous formations.     

The influence of heart disease on characteristics, quality of life, use of health resources, and costs of COPD in primary care settings

Background

Ectonucleotidase dependent adenosine generation has been implicated in preconditioning related cardioprotection against ischemia-reperfusion injury, and treatment with a soluble ectonucleotidase has been shown to reduce myocardial infarct size (IS) when applied prior to induction of ischemia. However, ectonucleotidase treatment according to a clinically applicable protocol, with administration only after induction of ischemia, has not previously been evaluated. We therefore investigated if treatment with the ectonucleotidase apyrase, according to a clinically applicable protocol, would reduce IS and microvascular obstruction (MO) in a large animal model.

Methods

A percutaneous coronary intervention balloon was inflated in the left anterior descending artery for 40 min, in 16 anesthetized pigs (40-50 kg). The pigs were randomized to 40 min of 1 ml/min intracoronary infusion of apyrase (10 U/ml, n = 8) or saline (0.9 mg/ml, n = 8), twenty minutes after balloon inflation. Area at risk (AAR) was evaluated by ex vivo SPECT. IS and MO were evaluated by ex vivo MRI.

Results

No differences were observed between the apyrase group and saline group with respect to IS/AAR (75.7 ± 4.2% vs 69.4 ± 5.0%, p = NS) or MO (10.7 ± 4.8% vs 11.4 ± 4.8%, p = NS), but apyrase prolonged the post-ischemic reactive hyperemia.

Conclusion

Apyrase treatment according to a clinically applicable protocol, with administration of apyrase after induction of ischemia, does not reduce myocardial infarct size or microvascular obstruction.