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PubMedDate not supplied

Microcirculation in hypertrophic scars after burn injury.

Hypertrophic scar formation is a common complication after burn injury. Early active scars show hyperemic appearances that change as the scar matures. This is a report on microcirculation in hypertrophic scars after burn injury among 50 Chinese patients with a laser Doppler flowmeter. The average period of follow-up for the patients was 20 months. The microcirculatory response in scars to vasodilation (heat) stimulus was studied. Significant differences (p less than 0.0001) were demonstrated between scars of different clinical grades of maturity when compared with normal skin. The qualitative and quantitative differences in microcirculatory blood flow were correlated with site variations and different physiologic demands from different grades of scars. The study showed that laser Doppler flowmetry was useful in the clinical grading assessment of or for scar maturity.

Adolescent↗

PubMedDate not supplied

The effects of epinephrine, ibuprofen, and tetrachlorodecaoxide on cutaneous microcirculation in thermally injured hamsters.

Fluctuations in the diameter of selected arterioles in the cutaneous microcirculation of Syrian golden hamster dorsal skin flap chambers, which ranged in size from 10 to 70 microns at different branching order sites, were measured before burn, at the same sites after burn and after injection of the drug. Three different drugs epinephrine (administered intravenously), ibuprofen (administered intravenously), and tetrachlorodecaoxide (administered intravenously and topically) were evaluated. Results show that the response to thermal injury in the control group involved extensive vasodilation in the arterioles, prolonged flow irregularities including flow obstructions and stasis, and a decrease in the level of vasoactivity of the microvessels. In two treatment groups, the ibuprofen and tetrachlorodecaoxide groups, significant improvement as indicated by reduced vasodilation and edema and improved microcirculatory blood flow after injury were observed. Further testing of tetrachlorodecaoxide as a topically applied wound dressing is indicated.

Animals↗

PubMedDate not supplied

Burn-induced alterations in vasoactive function of the peripheral cutaneous microcirculation.

Alterations in the cutaneous vasomotion function caused by scald burns to a large area on the flank were observed and quantified in a dorsal skin flap window with a hamster model. Subsequent to chronic implantation of the window chamber to provide direct microscopic observation of blood flow for an entire thickness of skin, control measurements of vasoactivity in a defined network of arterioles were taken by means of a digital video image splitter over a period of several days. A 100 degrees C, 5-second water scald was then effected over 17% to 55% of the total body surface area, and the vasoactivity was remeasured in the targeted set of sites at serial time intervals for 2 to 4 days. Data were acquired directly into a computer and analyzed for both the magnitude and time pattern of diameter fluctuations during 3-minute observation periods. Average and standard deviations of diameters were computed, and the Prony power spectral analysis method was applied to identify the presence and strength of fluctuation frequencies. In general, vasomotion was suppressed for several hours subsequent to the burn, and the activity was dominated by much slower contractions than control. No direction of vessel diameter changes prevailed uniformly throughout the peripheral microcirculation. Large alternate constrictions and dilations were also observed for some arteriolar and venular components, but others exhibited no significant change at all. The incidence and magnitude of peripheral microvascular response was proportional to the size of the injured area.

Anesthesia, Inhalation↗

PubMed1997

Early white blood cell dynamics after traumatic brain injury: effects on the cerebral microcirculation.

Increasing clinical and experimental evidence suggests that traumatic brain injury (TBI) elicits an acute inflammatory response. In the present study we investigated whether white blood cells (WBC) are activated in the cerebral microcirculation early after TBI and whether WBC accumulation affects the posttraumatic cerebrovascular response. Twenty-four anesthetized rabbits had chronic cranial windows implanted 3 weeks before experimentation. Animals were divided into four experimental groups and were studied for 7 hours (groups I, IIa, and III) or 2 hours (group IIb). Intravital fluorescence videomicroscopy was used to visualize WBC (rhodamine 6G, intravenously), pial vessel diameters, and blood-brain barrier (BBB) integrity (Na+-fluorescein) at 6 hours (groups I, IIa, and III) or 1 hour (group IIb) after TBI. Group I (n = 5) consisted of sham-operated animals. Groups IIa (n = 7) and IIb (n = 5) received fluid-percussion injury at 1 hour. Group III (n = 7) received fluid-percussion injury and 1 mg/kg anti-adhesion monoclonal antibody (MoAb) "IB4" 5 minutes before injury. Venular WBC sticking, intracranial pressure (ICP), and arterial vessel diameters increased significantly for 6 hours after trauma. IB4 reduced WBC margination and prevented vasodilation. Intracranial pressure was not reduced by treatment with IB4. Blood-brain barrier damage occurred at 1 hour but not at 6 hours after TBI and was independent of WBC activation. This first report using intravital videomicroscopy to study the inflammatory response after TBI reveals upregulated interaction between WBC and cerebral endothelium that can be manipulated pharmacologically. White blood cell activation is associated with pial arteriolar vasodilation. White blood cells do not induce BBB breakdown less than 6 hours after TBI and do not contribute to posttraumatic ICP elevation. The role of WBC more than 6 hours after TBI should be investigated further.

Animals↗

PubMed1998

Characterization of angiogenesis and microcirculation of high-grade glioma: an intravital multifluorescence microscopic approach in the athymic nude mouse.

The current study follows angiogenesis and microcirculatory changes associated with malignant glioma growth by means of an intravital fluorescence microscopic approach, which allows for the direct and continuous visualization of the glioma microvasculature and its quantitative analysis. Fluorescently labeled C6 rat glioma cells (5 x 10(5)) were implanted into dorsal skinfold chamber preparations of athymic nude mice. Glioma growth, vascularization, microhemodynamics, vascular permeability, and leukocyte-endothelial cell interactions were simultaneously followed over a 22-day observation period using intravital epiillumination microscopy and a multifluorescent labeling technique. Analysis of the process of glioma vascularization revealed three stages with distinct microvascular characteristics: avascular stage (days 0 to 6), lag of glioma growth but initial glioma-induced angiogenesis within the host tissue in peritumoral areas; early vascular stage (days 6 to 14), glioma cell proliferation associated with a spatially homogeneous development of a glioma microvasculature; and late vascular stage (days 14 to 22), exponential tumor growth and expansion (> 400 mm3) with high vascular densities in the peritumoral region and reduced vascularization (microvascular perfusion) in the glioma center. Within the center, the functional vessel length per area correlated inversely with glioma size (P < 0.01). In the peritumoral region, functional vessel length per area was independent of glioma size, indicating persistent, high angiogenic activity throughout the observation period. Thus, the microvasculature of mature gliomas revealed a microvascular zonal division with a progressive reduction of the functional vessel length per area within the tumor center. The perfusion failure of individual microvessels within the glioma center was partly compensated by an increase of diameters (P < 0.05), and thus by an increase of blood flow in these functional microvessels (P < 0.05) over time. Histologic analysis demonstrated both expanding and infiltrating growth patterns, as well as focal necroses on day 22. These are the first data from repeated in vivo analysis of glioma growth, vascularization, and microcirculation.

Animals↗

PubMed1992

Hypertension and the microcirculation: a brief overview of experimental studies.

PURPOSE: To review experimental findings on the importance of the microcirculation in hypertension. RESULTS OF DATA ANALYSIS: A significant part of the increase in vascular resistance found in hypertension involves alterations in the arteriolar network. Changes in vascular reactivity and amplification of normal microvascular autoregulatory loops are among the mechanisms involved in these microvascular alterations. Depending on the organ and the type of hypertension, different types of changes have been observed, including (1) changes in resting arteriolar diameter and increased tone, either throughout the arteriolar network or localized to certain arteriolar segments; (2) temporary closure of a significant fraction of the terminal arteriolar bed; and (3) degenerative processes in terminal arterioles and capillaries inducing anatomical rarefaction of the microvessels. CONCLUSIONS: Microvascular changes are responsible for only a portion of the increased resistance but they are extremely important in the global understanding of the hypertensive process, as they are potentially responsible for tissue damage and may be related to the increased risk of organ failure in hypertension.

Animals↗

PubMed2003

The heart, macrocirculation and microcirculation in hypertension: a unifying hypothesis.

Epidemiological studies in the past decade have stressed the importance of both pulse pressure and mean arterial pressure (MAP) as important risk factors in hypertension-related cardiovascular disease. Pulse pressure and MAP are determined by different segments of the cardiovascular system. Pulse pressure is the pulsatile component of the blood pressure curve. It is determined by left ventricular ejection, the cushioning capacity (compliance) of the large arteries, and the timing and intensity of wave reflections from the microcirculation. MAP is the steady component; it is determined by cardiac output and peripheral (micro)vascular resistance. To a large degree, the structural design of the heart and vascular tree determine the pulse pressure and MAP, in addition to the propagation of the pressure wave through the vasculature. Pressure and flow, in contrast, influence the composition and geometry of the heart and vasculature. Hypertensive disease is associated with important structural alterations of the heart, such as hypertrophy and fibrosis, and of the vasculature, such as large artery stiffening, small artery remodelling and microvascular rarefaction. Recent basic research has revealed some of the molecular pathways involved in the remodelling of the cardiovascular system under the influence of physical forces. For correct understanding of the pathophysiology of hypertensive disease, its risks for target-organ damage and its effective treatment, both the pulsatile and steady components of the blood pressure curve must be considered.

Antihypertensive Agents↗

PubMed1990

Human immunodeficiency virus (HIV) leukoencephalopathy and the microcirculation.

We studied the brains of three patients with acquired immune deficiency syndrome (AIDS), all of whom developed subacutely progressive dementia unassociated with opportunistic infection or neoplasm in the central nervous system. Computed tomographic (CT) scans of the head revealed cortical atrophy, ventricular dilation, and diffuse hypodensity of the centrum semiovale. On microscopic examination, the cerebral and cerebellar white matter in all cases showed diffuse and focal, angiocentric regions of myelin pallor, focal vacuolization, and extensive gliosis. Variable axonal loss and axonal spheroids were evident. The microvasculature showed striking changes, including mural thickening, increased cellularity, and enlargement and pleomorphism of endothelial cells with variable numbers of macrophages and multinucleated giant cells (MNGC), which often contained hemosiderin pigment. Human immunodeficiency virus type 1 (HIV-1) antigens were identified immunocytochemically within perivascular macrophages and MNGC and in some microglial cells. We suggest that the morphologic abnormalities of the microcirculation may be associated with an alteration of the blood-brain barrier. The increased vascular permeability could contribute to damage and loss of the white matter including both myelin and axons, and result in subcortical cerebral atrophy. The HIV-1 infected cells present in relation to the microvasculature may play a role in mediating the vascular injury.

Acquired Immunodeficiency Syndrome↗

PubMed1991

A study of the microcirculation in whole villi of neonatal mice using a peroxidase histochemical staining method.

The anatomy of the microcirculation of intestinal villi from the upper, middle, and lower small intestine of neonatal mice from 8 to 14 days old was studied using a histochemical peroxidase technique that specifically stained erythrocytes. Over 8-14 days, there was little chronological variation between the same regions of gut; the exception was the lower intestine, which, in younger mice, was noticeably less well perfused with erythrocytes. Vascular beds in the middle and lower intestine comprised a hairpin loop with cross-connections. In the upper intestine, the capillary beds were generally more complex, particularly in apical regions of the villi. Most villi were well perfused with erythrocytes, but a minority (less than 10%) contained considerably fewer red cells, some to the point of being totally ischemic. Other villi (less than 5%) were hyperemic, and the vascular beds packed and engorged with red cells. Usually, the packing density (hematocrit) of red cells within blood vessels increased progressively from villus base to apex. Red-cell deformation was more prevalent at villus apices, with marked crenation in some villi, yet in the basal regions of these same villi, the red cells were of normal discoid shape. The peroxidase staining technique produces a reliable histological picture of red cells circulating through villi. It also reveals differential perfusion of erythrocytes between and within villi, and that blood vessels pass through hypertonic zones in the apical regions of villi.

Animals↗

PubMed1991

Effects of endothelin-1 on coronary microcirculation in isolated beating hearts of rats.

An intravital fluorescence videomicroscope system was used to investigate the pharmacological effects of endothelin-1 (ET-1) on the coronary microcirculation in isolated beating hearts of rats. The heart was perfused by retrograde aortic steady flow with an oxygenated Krebs-Ringer solution containing FITC-dextran. Cumulative injections of ET-1 (1-30 pmol) elicited a dose-dependent increase in perfusion pressure from 52 +/- 15 mm Hg (mean +/- SEM; n = 6) before the ET-1 injection to 104 +/- 23 mm Hg at the ET-1 dose of 30 pmol. A dose-dependent narrowing of microvessels was also observed on a monitor screen. This diffuse vasoconstriction was especially prominent in small arterioles; the maximum vasoconstriction of the smaller arterioles was significantly higher than that of the larger arterioles. These findings suggest that ET-1 may have an important role in governing the coronary resistance and regulating the capillary flow in myocardium.

Animals↗

PubMed1992

Effects of manidipine hydrochloride on the renal microcirculation in spontaneously hypertensive rats.

We wished to clarify the effects of a newly developed calcium antagonist, manidipine hydrochloride (HCl), on renal microcirculation in hypertensive rats by using the micropuncture technique. Oral administration of manidipine HCl for 2 months reduced systemic blood pressure (BP), did not change the single-nephron glomerular filtration rate (SNGFR), but increased the SNG plasma flow (SNGPF). Moreover, the glomerular transcapillary hydraulic pressure difference (delta P), which is assumed to be the parameter most related to development of glomerulosclerosis, was significantly reduced. Both afferent and efferent arteriolar resistance (RA and RE) were reduced. Intravenous (i.v.) infusion of manidipine HCl (20 micrograms/kg) decreased systemic BP but did not change SNGFR, SNGPF, or delta P. Both RA and RE were also significantly decreased. These results indicate that chronic administration of manidipine HCl increases renal blood flow (RBF) by dilating the afferent arterioles and improves glomerular hypertension by dilating the efferent arterioles. Thus, manidipine HCl might be a beneficial antihypertensive agent for patients with renal diseases. Because acute i.v. infusion of manidipine HCl did not change delta P, apparently time must elapse before glomerular hypertension is corrected.

Animals↗

PubMed2000

Adenosine and angiotensin system interact in the regulation of renal microcirculation in humans.

We sought to evaluate the possible interaction between the adenosine and angiotensin systems in the regulation of renal microcirculation in humans. Twenty normotensive patients entered the study. Ten patients (group 1) were pretreated with 50 mg of captopril, an inhibitor of angiotensin-converting enzyme, whereas 10 patients (group 2) were pretreated with placebo. Incremental doses of adenosine (from 10(-5) to 1 mg) were injected into a renal artery to all patients at 5-min intervals. Adenosine injection reduced mean renal blood flow velocity in both groups (from 17.3+/-2.8 and 16.7+/-2 cm/s to 5.1+/-1.1 and 3.8+/-0.8 cm/s, in groups 1 and 2, respectively). The decrease in flow velocity was immediate after adenosine, and its duration was proportional to dosage (y = 3.05 x -2.7; R2 = 0.46; p < 0.01). However, group 1 had a slope of regression lower than group 2 (2.37 vs. 3.82 s; p < 0.03). The index of renal resistance (mean arterial pressure/mean blood flow velocity) increased linearly in both groups with adenosine, but group I showed a lower slope of increment (2.77 vs. 5.57 mm Hg/cm/s; p < 0.01). Adenosine administration induced a marked and transient increase in human renal resistance. This vasoconstrictive effect of adenosine was blunted by captopril pretreatment.

Adenosine↗

PubMed2000

Endothelin receptor blockade as a therapeutic strategy in ameliorating postischemic damage to the liver microcirculation.

Ischemia leads to profound endothelin- (ET) related constriction of hepatic microvessels, causing disturbances in blood and oxygen supply. The aim of the study was to modulate hepatic microvascular diameters by blocking ET receptors to find the optimal therapeutic vessel width for reduction of ischemia-reperfusion injury. In an in vivo model (84 female Wistar rats, 250-300 g) with portal decompression by means of a splenocaval shunt, normothermic hepatic ischemia was induced for 30 min by crossclamping of the hepatoduodenal ligament. The ET receptor antagonist (ERA) bosentan was administered before induction of ischemia in different dosages [0.1, 1.0 and 10.0 mg/kg body weight (BW) i.v. and 10 mg/kg BW intraportally (i.p.)]. The effect on microcirculation was assessed by in vivo microscopy and influence on hepatocellular function by measurement of aspartate aminotransferase (AST) levels. Sinusoidal diameters were reduced as a result of ischemia to 76.3 +/- 7.4% compared with values received from sham-operated animals. After application of 0.1 mg/kg of bosentan, sinusoids remained constricted (89.7 +/- 9.9%, AST 255.0 +/- 12.8 U/l). Blocking ET receptors with 1 mg/kg bosentan avoided sinusoidal constriction (99.0 +/- 8.8%, p < 0.05) and led to the most effective reduction of AST level peak after 6 h of reperfusion (244.0 +/- 34.2 U/l vs 422.9 +/- 163.3 U/l in untreated ischemia). Bosentan (10 mg/kg i.v.) caused an increase in sinusoidal diameter to 109.1 +/- 6.4% (AST 311.7 +/- 33.6 U/l) and 10 mg/kg i.p. to 136.8 +/- 19.3% and even increase AST levels (618.90 +/- 209.32 U/l). After intravenous application of 1 and 10 mg/kg BW bosentan the perfusion rate was significantly increased and sticking of leukocytes in sinusoids and venules reduced (p < 0.05). In our model, diameters of sinusoids and postsinusoidal venules could be regulated gradually. We conclude that the avoidance of constriction, but not an excessive vasodilation leads to increased perfusion rate and hence improved hepatocellular function.

Animals↗

PubMed2001

Changes in the local blood and lymph microcirculation in response to direct mechanical trauma applied to leg: in vivo study in an animal model.

BACKGROUND: The aim of this study was to investigate changes in the blood microcirculation of skin, subcutaneous tissue, and striated muscle, and the venous and lymphatic outflow from hind limb, after a standardized mechanical trauma. METHODS: Trauma, defined as 50% of the minimal energy needed for tibia fracture (3.7 J/g), was applied to the leg of hairless mice. Intravenously injected fluorescein isothiocyanate-dextran 150 kDa and Rhodamine-6G were used for intra-vital fluorescence microscopy of blood vessels. Lymphatics were stained with fluorescein isothiocyanate-dextran injected into the footpad. A computer-assisted analysis system allowed measurement of the functional capillary density (FCD), vessel diameters, velocity of blood flow, and edema value expressed as extravasation index (EV). The percentage of slowly rolling and sticking leukocytes in postcapillary venules was estimated. RESULTS: At the site of injury, trauma resulted in significant reduction of FCD in skin, subcutaneous tissue, and striated muscle. There were no significant differences in the vessel diameter (skin subcutaneous and muscle arterioles and venules, and superficial saphenous artery and vein) or velocity of blood flow (subcutaneous tissue and muscle venules). The EV increased significantly in muscle venules and was higher in muscles, subcutaneous tissue, and superficial saphenous veins than in controls (nonsignificantly). An increased percentage of slowly rolling and sticking leukocytes was noted in the superficial saphenous vein at the site of injury and proximal to it. The lymphatics remained patent, with faster visualization and increased summarized cross-sectional areas in traumatized extremities. CONCLUSION: Early changes occurring in soft tissues in response to mechanical injury were characterized by reduction in FCD of skin and muscles, and less in subcutis; increased EV, reflecting leakage of macromolecules; increased percentage of slowly rolling and sticking leukocytes; maintenance of lymphatic vessel continuity; and increased lymph formation and flow rate.

Animals↗

PubMed1991

Effects of sympathectomy on skin and muscle microcirculation during dorsal column stimulation: animal studies.

Electric stimulation of the dorsal spinal cord (DCS) in the treatment of pain in peripheral vascular disease is known to enhance peripheral circulation, but the mechanisms are still obscure. An earlier study has provided indirect evidence that the vasodilator effect is dependent upon alteration of sympathetic vasomotor activity. In the present study, surgical interruption of sympathetic pathways was performed to define the role of the sympathetic system for the stimulation-induced vasodilation. Three groups of normal rats were used: one group subjected to lumbar sympathectomy, one group sham-operated about 1 week before performing spinal cord stimulation, and a third group, without pretreatment, serving as a second control. Stimulation was applied to one dorsal column at the thoracolumbar junction, and peripheral microcirculation was recorded in hind limb skin and muscle by laser Doppler technique. The stimulation parameters were chosen to correspond with those used clinically in man. A cold test with monitoring of cold-induced changes in peripheral blood flow was used to assess the completeness of the sympathectomy. The preoperative cold test induced a reciprocal response, vasoconstriction in the skin and vasodilation in muscle. DCS with clinical parameters did not produce this reciprocity in the control and sham-operated rats, but induced a vasodilation in both skin and muscle. After complete sympathectomy, defined as postoperative disappearance of the vasomotor responses to cold, the vasodilation in skin and muscle in response to DCS was abolished; however, the vasodilatory response to high-intensity stimulation (approximately 10 times the motor threshold) was not affected. Incomplete sympathetic denervation in some animals resulted in partial preservation of a vasodilatory response to DCS.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1980

In vivo microcirculation of a scald burn and the progression of postburn dermal ischemia.

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).

Animals↗

PubMed1989

The hairless mouse ear for in vivo studies of skin microcirculation.

The homozygous (hr/hr) hairless mouse ear was introduced in 1980 by Eriksson and coworkers as a model for in vivo studies of the skin microcirculation. Herein we expand on this work, presenting results of in vivo microvascular parameter measurements and morphologic studies in the intact ear. The in vivo measurements include microvascular diameter, RBC velocity, capillary density, and the frequency and amplitude of arteriolar vasomotion. In connection with the in vivo studies, a detailed anatomic description of the overall and vascular anatomy is given. Additionally, the preparation techniques for carrying out these in vivo and morphologic studies in the mouse ear are presented in detail.

Animals↗

PubMed1993

Morphologic analysis of the microcirculation during reperfusion of ischemic skeletal muscle and the effect of hyperbaric oxygen.

The morphologic events in the microcirculation that lead to reperfusion injury of ischemic skeletal muscle remain incompletely understood. The purpose of this experiment was to evaluate leukocyte endothelial adherence characteristics and dynamic changes in microvessel caliber during reperfusion of an in vivo skeletal muscle ischemia preparation. In addition, the effect of hyperbaric oxygen treatment on these microcirculatory changes also was studied. An intravital microscopy preparation of a transilluminated gracilis muscle in 27 rats was used to observe a total of 101 arterioles and 63 venules (13 to 73 microns diameter). Baseline hemodynamics were videotaped for 30 minutes following muscle isolation. The animals were divided into six groups: (1) sham, no ischemia, (2) 4 hours of global ischemia only, (3) no ischemia plus hyperbaric oxygen (one 2.5 ATA/1 hour of treatment with 100% oxygen), (4) 4 hours of ischemia plus hyperbaric oxygen during ischemia, (5) 4 hours of ischemia plus hyperbaric oxygen immediately on reperfusion, and (6) 4 hours of ischemia plus hyperbaric oxygen 1 hour after reperfusion. Changes in arteriolar and venular diameters at specific times during 3 hours of reperfusion were recorded, and the number of adherent and slow-rolling leukocytes in 100-microns venular segments were counted and compared with baseline measurements. The proximity of arterioles to venules was classified as adjacent (< 15 microns) or distant (> 15 microns). No significant changes in leukocyte endothelial adherence or arteriolar diameter were noted in group 1 sham or group 3 nonischemic hyperbaric oxygen-treated rats when compared with baseline measurements. A significant increase in adherent leukocytes was observed in group 2 ischemic venules (+14.9 +/- 2.5) within 5 minutes of reperfusion, which was maintained for 3 hours. Reperfusion measurements of arteriolar diameter in group 2 ischemic muscle preparations demonstrated an initial vasodilation that was followed at 1 hour by a progressive and severe vasoconstriction (-46.9 +/- 11.3 percent at 3 hours) in arterioles adjacent to venules that was not seen in distant arterioles. The increase in adherent leukocytes seen in group 2 ischemic venules was significantly reduced by hyperbaric oxygen treatment given during ischemia (group 4) or up to 1 hour during reperfusion (groups 5 and 6). In addition, the progressive ischemic arteriolar vasoconstriction was inhibited in all groups (4, 5, and 6) treated with hyperbaric oxygen.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗