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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of vasoactive medication on tissue oxygenation and wound healing was investigated in the ear model of the hairless mouse. Ischemia was induced to the ears by ligating 2 of the 3 main vessel bundels and verified by measurements of tcpO2. Reduced tissue oxygenation was followed by a prolongation of the time required for complete healing of standardized wounds. Treatment with the vasoactive drug Buflomedil (3 mg/kg/day iv.) resulted in enhanced recovery of the tissue from reduced oxygenation and likewise reversed the adverse effects of ischemia on wound healing. These results warrant the use of the drug in patients suffering from delayed wound healing due to peripheral arterial disease.
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PMID:Impact of ischemia on tissue oxygenation and wound healing: improvement by vasoactive medication. 128 3

The nutritional blood flow to the tissue is the principle factor determining the outcome of reconstructive procedures in plastic surgery. Beside vasoconstriction, thrombocytes aggregation, leukocytes activation, followed by production of oxygen free radicals and release of proteases, impaired fluidity of erythrocytes and swelling of the microvascular endothelium are responsible for impaired perfusion following ischemia/reperfusion. Therefore, vasoactive drugs known to improve nutritional blood flow are of particular interest in the prevention and therapy of skin flap necrosis. Several methods have been employed to quantify nutritional blood flow in skin flaps but none of them have elucidated the mechanisms underlying potential tissue protection by these drugs. We have developed two skin flap models in the hairless mouse, in which nutritional blood flow can be directly assessed at capillary level by means of intravital microscopy. In the arterial skin flap model, the efficacy of three vasoactive drugs (naftidrofuryl [4.5 mg/kg/day], pentoxifylline [17.0 mg/kg/day] and buflomedil [3.0 mg/kg/day]) to prevent and/or reduce tissue necrosis was investigated. Buflomedil provided the most efficient tissue protection, a phenomenon also verified in a random skin flap model. It was demonstrated that preoperative application of buflomedil preserves functional vascular density in the distal part of skin flaps more efficiently compared to postoperative application. However, there were no significant differences in amount of skin necrosis between the two groups. The tissue protection effect was also observed in random pattern flaps rendered ischemic for six hours after flap elevation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Use of vasoactive substances in prevention of skin necroses]. 158 10

The effect of buflomedil to protect skin tissue from ischemia and necrosis was studied in random cutaneous flaps. Measurements were performed by intravital microscopy on the microcirculatory level of capillary perfusion in a flap model in the hairless mouse. In 30 hairless mice, single-pedicle flaps measuring 6 x 16 mm were raised perpendicular to the spine of the animal. This flap develops a reliable amount of necrosis at its distal edge over a period of 7 days. A group of 10 mice received intravenous injections of buflomedil in doses of 3 mg/kg per day diluted in 0.1 ml normal saline beginning 4 hours before flap elevation and for 6 consecutive days postoperatively. In addition, 10 further animals received the same treatment except that it was started 5 minutes after flap elevation. In 10 mice serving as controls, normal saline in equal volumes as in the experimental groups was applied. By means of intravital microscopy, functional vessel density (FVD) was determined in 2.5-mm increments from the flap's base to its distal edge at 1, 6, and 24 hours after elevation. Skin-flap survival was quantified by measuring the necrotic area on day 7 by means of digital planimetry. Functional vessel density was preserved in the distal flap of animals pretreated with buflomedil, revealing a higher functional vessel density at 10.0 mm (p less than 0.01), 12.5 mm (p less than 0.05), and 15.0 mm (p less than 0.001) from the flap's base as compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Increase in skin-flap survival by the vasoactive drug buflomedil. 198 57

Capillary reperfusion following four hours of regional ischemia was determined in the ear skin microvasculature of 10 homozygous hairless mice. Selective arteriolar ligation was used to produce flow stasis in capillaries within an ischemic risk zone (RSK) without direct compression of the microvasculature under study. Reperfusion capillary RBC velocities (CBV), diameters, and flow times in both RSK and nonischemic capillaries (NRSK) were measured and compared to baseline values after flow stasis was verified in the RSK capillaries. Baseline values of CBV, diameter and flow time did not differ between RSK and NRSK. In the RSK capillaries, the post-ischemic mean CBV was significantly less than baseline (120 +/- 22 vs. 212 +/- 31 microns/s, p less than 0.01), whereas in NRSK capillaries no differences were detected (195 +/- 41 vs. 174 +/- 22 microns/s). The decrease in mean CBV in RSK capillaries was mainly due to an increase in the number of capillaries with low or zero reflow. The percentage of capillaries having CBV less than 100 microns/s increased from 10% at baseline to 45% after ischemia. These results indicate that when capillary flow stasis is produced, durations of skin ischemia of four hours may subject the microvasculature to significant reperfusion deficits.
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PMID:Skin capillary reperfusion after regional ischemia. 206 Sep 94

The homozygous hairless mouse ear provides a reproducible model for the study of the microcirculatory changes of the burn wound during and following a scald burn injury. This model has allowed us to correlate the dynamic changes of the microcirculation to progressive zones of injury, which show an approximate tenfold increase in the area of complete capillary occlusion during the first 48 hours after injury. Platelet thromboembolism appears to be the major factor causing this progression of postburn dermal ischemia. Edema (increased skin water content) was greatest in the burned ear at 6 hours after the burn (20 percent greater than control values); edema of the unburned, contralateral ear was significant at 2 hours after the burn (9 percent greater than control values).
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PMID:In vivo microcirculation of a scald burn and the progression of postburn dermal ischemia. 740 9

We present an experimental model that makes it possible to investigate the effects of global ischemia and reperfusion on microvascular perfusion and viability of ill-proportioned (poorly designed) arterial pattern skin flaps in hairless mice. Skin flaps were created on the ears of hairless mice by dissecting two of three nutritional vessel bundles at the ear base. Under these nonischemic conditions, 19 percent of the total flap area went on to necrose (as a result of poor flap design). Global ischemia was induced to the flap tissue for 6 hours with a tourniquet clamp directly after flap incision. The extension of perfused tissue area and flap viability were assessed at the microcirculatory level by intravital video microscopy at 1, 3, 6, and 18 hours and 7 days after reperfusion in animals treated with either normal saline (control) or the vasoactive drug buflomedil hydrochloride (3 mg/kg of body weight per day, i.v., starting 4 hours prior to flap creation and continued at daily intervals until the end of the experiments). In untreated animals (n = 18), 1 hour after clamp release we observed reperfusion of 39.55 percent (38.5/44.9) of total flap area. Reperfusion remained unchanged within the following 5 hours. Within the next 12 hours, reperfused flap area was dramatically reduced to 21.9 percent (15.1/58.4). Seven days thereafter, only 18.8 percent (10.9/42.2) of total flap area remained viable. In contrast, we found in buflomedil-treated animals (n = 18) that 57.3 percent (53.5/62.9) of the total flap tissue was reperfused within the first hour after clamp release (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Visualization of nutritive perfusion following tourniquet ischemia in arterial pattern skin flaps: effect of vasoactive medication. 793 88

The use of intravital fluorescence microscopy in the models of the hamster dorsal skin fold chamber and the ear of the hairless mouse allows for the quantitative analysis of post-ischemic microvascular reperfusion injury in striated muscle and skin. Prolonged periods of ischemia (4 hours in striated muscle and 6 hours in skin) are associated with 1) perfusion failure of nutritive capillaries at the onset of reperfusion (no-reflow) and 2) activation, accumulation and microvascular adherence of white blood cells, formation of reactive oxygen metabolites and release of potent mediators (leukotrienes, platelet-activating factor) with the consequence of increased microvascular permeability due to the loss of endothelial integrity, interstitial edema and cell damage (reflow-paradox). Prophylactic and/or therapeutic regimens may, therefore, include improvement of capillary perfusion by hemodilution, and inhibition of leukocyte adherence, radical formation and mediator release by appropriate counteracting compounds, including anti-oxidants, antibodies directed against adhesion molecules, leukotriene synthesis inhibitors and platelet-activating factor receptor antagonists.
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PMID:In vivo analysis of microvascular reperfusion injury in striated muscle and skin. 796 63

The influence of hyperbaric oxygen on reepithelialization and on microvascular perfusion of wounds in normal and ischemic skin tissue was investigated by using a standardized model, in ears of hairless mice. Animals were treated within 2 hours of wound creation and then twice daily with 100% oxygen at 2 atmospheres of absolute pressure. Ischemia was induced by ligating two of the three major vessels of the ear 2.5 days before wound creation. Wound surface area was measured every third day after wound creation. In addition, microvascular blood flow before and during the wound healing process was measured by scanning the ear with a new laser Doppler perfusion imager. In normal tissue (n = 13), hyperbaric oxygen therapy significantly accelerated wound healing by 2 days (p < 0.01) as compared with controls (n = 16). In ischemic tissue (n = 16), treatment with hyperbaric oxygen reduced time for reepithelialization in control animals (n = 16) from 14.3 to 9.9 days (p < 0.001). Laser Doppler data showed no difference in tissue blood flow between treated and untreated animals. In comparison with normal tissue, wound healing in ischemic tissue was characterized by a reduced and less intense hyperemic response. These data suggest that hyperbaric oxygen therapy improves reepithelialization in normal and ischemic skin tissue. The beneficial effect is not associated with changes in microvascular perfusion and therefore is probably due to high arteriolar oxygen content and oxygen diffusion.
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PMID:Hyperbaric oxygen improves wound healing in normal and ischemic skin tissue. 813 43

To determine the effect of ischemia on tissue oxygenation and the healing of experimental wounds, chronic ischemia was induced in the ears of hairless mice by ligating 2 of the 3 main nutritional arteries. Tissue ischemia was verified by measurement of transcutaneous pO2 (tcpO2) prior to and on days 3, 6, 9, 12 and 15 after vessel ligation. TcpO2 values decreased from 24 to 6 mm Hg at day 2 after ligation, and slowly recovered to 12 mm Hg at day 12 after vessel ligation. In animals treated with the vasoactive drug buflomedil (3 mg/kg BW i.v., startling 2 days after vessel ligation) tcpO2 values were significantly higher on days 6 and 9 when compared to saline-treated control animals. In order to find out whether the enhanced tissue oxygenation resulted in enhancement of healing of wounds, we created circular wounds (diameter = 2.5 mm, depth 0.1 mm) on ischemic ears 2 days after vessel ligation. The wound surface area was measured by means of intravital fluorescence microscopy and digital planimetry at 3-day intervals until the time of wound closure. These experiments were performed on buflomedil-treated and control animals receiving equivalent amounts of saline. The reduction of wound surface area was accelerated and wound closure time was reduced from 15 days in control animals to 12 days in buflomedil-treated animals (p < 0.01). Functional capillary density as well as the microhemodynamic parameters microvessel diameter and red blood cell velocity were not different between buflomedil-treated and control animals.
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PMID:Impact of ischemia on tissue oxygenation and wound healing: intravital microscopic studies on the hairless mouse ear model. 848 3

The primary critical ischemia time of the hairless mouse ear was determined using a probit analysis. An atraumatic clamp was used across the pedicle base of the ear to induce total ischemia at 0, 2, 4, 6, 7, 7.5, 8.0, 8.5, 9.0, 9.5, and 12 hours of normothermic ischemia. Seventy-seven ears were examined 7 days after the ischemic interval for evidence of necrosis. The median critical ischemia time was determined to be 8.2 hours with 95 percent fiducial limits of 7.74 hours and 8.69 hours.
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PMID:Primary critical ischemia time in the hairless mouse ear. 939 75


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