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W D Suval

Publications and source records attributed to W D Suval.

8 recordsLinked to original sources
PubMed1989

Dexamethasone attenuates microvascular ischemia-reperfusion injury in the rat cremaster muscle.

We examined the effect of dexamethasone (DXM) pretreatment on microvascular transport of macromolecules in ischemia-reperfusion injury. The rat cremaster muscle was splayed, placed in a Lucite intravital chamber, and suffused with bicarbonate buffer. The clearance of fluorescein isothiocyanate-dextran 150 (FITC-Dx 150) was measured as an index of microvascular transport. After determination of baseline data, the muscle was made ischemic for 2 hr by clamping its vascular pedicle, and subsequently reperfused for 2 hr. Ischemia-reperfusion produced a marked increase in clearance of FITC-Dx 150. After an initial peak of 13 times baseline value clearance fell to approximately 4 times baseline level 30 min into the reperfusion period. Clearance increased slowly throughout the remainder of the experiment, reaching 6 times baseline after 2 hr of reperfusion. The treated animals received DXM 3 hr prior to and immediately preceding the pedicle clamping. DXM reduced macromolecular clearance significantly after the first 30 min of reperfusion, and prevented the increase in clearance over time. After an initial peak, clearance values fell to near twice baseline in DXM-treated animals, and remained at this level for the 2 hr of reperfusion. Our data demonstrate that DXM attenuates the alternations in microvascular macromolecular transport produced by ischemia-reperfusion injury.

Analysis of Variance↗
PubMed1989

Hypercoagulability in arterial disease.

Isolated human monocytes generate tissue factor when stimulated with endotoxin. Tissue factor generation provides a marker for activation of the monocyte and of the clotting system. Determination of the recalcification time of blood after incubation with endotoxin detects minute changes in coagulability. This clotting assay was utilized to assess the presence of a hypercoagulable state in patients with peripheral arterial occlusive disease when compared with healthy volunteers. Citrated blood was incubated with endotoxin for two hours, CaCl2 was added, and the recalcification time determined. Hypercoagulability was indicated by shortened recalcification time. The recalcification time +/- standard deviation for saline (control) and endotoxin-activated samples from 19 healthy volunteers was 6.55 +/- 0.8 and 5.69 +/- 0.7 minutes, respectively, whereas it was 4.93 +/- 1.2 and 4.55 +/- 0.9 minutes for 31 patients with peripheral arterial occlusive disease (p less than .001 for each). This hypercoagulable state can accentuate the arterial occlusive process in patients with peripheral vascular disease and may prove to be of diagnostic, therapeutic, and prognostic significance.

Arterial Occlusive Diseases↗
PubMed1988

Detection of sepsis in the postoperative patient.

It becomes evident, therefore, that there is no one indicator, either clinical or laboratory, sufficient to diagnose infection in the postoperative patient. Only a skillful clinician using the multiple modalities available and combining them with a careful history and physical examination and a high index of suspicion will be able to diagnose and treat infection in a timely manner and so avoid the physical, emotional, and fiscal costs of a late or missed diagnosis.

Abdomen↗
PubMed1987

Microvascular transport and endothelial cell alterations preceding skeletal muscle damage in ischemia and reperfusion injury.

We determined the leakage of macromolecules using FITC-dextran-150 as a tracer and measured the extent of no-reflow phenomenon by video field analysis. The cremaster muscle of anesthetized rats was fashioned as a single layer, splayed on a lucite chamber and suffused with bicarbonate solution at 35 degrees C. After a 1 hour period of baseline data collection, ischemia was produced by cross-clamping the cremasteric vascular pedicle for periods of 30 minutes and 2 hours in separate experiments. Macromolecular leakage was visualized after reinstitution of perfusion. Leakage occurred at postcapillary venules 15 to 50 micron in diameter and quickly spread to the interstitium. The magnitude of leakage decreased as a function of time with continuous buffer suffusion, but remained higher than in the control period. No reflow occurred in approximately 30 percent of the muscle microvasculature upon reperfusion. The no-reflow values at 30 minute and 2 hour periods of ischemia were significantly different from the control values but were not from each other. Electron micrographs demonstrated endothelial cell swelling and migration of leukocytes and normal myocytes after 1 hour of reperfusion following 2 hours of ischemia. Our results demonstrate that permeability changes, occurrence of no reflow, and leukocyte migration precede the onset of damage to skeletal muscle in ischemia and reperfusion injury.

Animals↗
PubMed1987

Assessment of ischemia reperfusion injury in skeletal muscle by macromolecular clearance.

Qualitative changes in skeletal muscle injury after ischemia are well known; however, quantitative assessments have not been well documented. We have determined microvascular permeability changes by measuring the clearance of fluorescein-labeled dextran of MW 150,000 (FITC-Dextran-150). The cremaster muscle of anesthetized rats was fashioned as a single layer, splayed on a lucite chamber and suffused with bicarbonate buffer solution at 35 degrees C. Clearance is the product of suffusion rate times the ratio of suffusate to plasma concentrations of FITC-Dx 150. After a 1-hr period of baseline data collection, ischemia was produced by cross-clamping the cremasteric vascular pedicle for periods of 30 min and 2 hr in separate experiments. Clearance of FITC-Dx 150 increased from a control value (mean +/- SE) of 8.3 +/- 2.7 to 29.9 +/- 8.1 microliters/min/g after reperfusion following a 30-min period of ischemia, and from a control value of 36.2 +/- 13.6 to 274 +/- 94.5 after 2 hr of ischemia. The differences were statistically significant (P less than 0.05). Our results show a significant increase in microvascular permeability occurring after only 30 min of ischemia. They also demonstrate a direct relationship between the extent of the permeability change and the duration of the ischemic period.

Animals↗
PubMed1986

Paradoxical effect of burns in diabetic mice.

Since the microcirculation is impaired in diabetes and since burn injury is associated with microvascular thrombosis, the purpose of this study was to determine whether diabetes increases the severity of burns. Swiss white mice were made diabetic with alloxan, and control animals received saline. One week later, animals with over 2000 mg/dl urine sugar and the control animals were anesthetized and burned uniformly on the back with a steel disc at 100 C for 10 sec. At 24 hr, burn severity was evaluated on a scale of 0 to 4 using gross and microscopic criteria. The mean burn severity of the diabetic mice was 0.80 +/- .15 and that of the control mice was 3.22 +/- .09 at 24 hr (P less than 0.001.). At 5 days, the differences of the burn severity between the two groups were still significant, but 5/10 (50%) of the diabetic mice and none of the control mice died. In diabetic mice, through burn severity appears mild in the wound, the mortality is high. Therefore, the criteria for initial evaluation of the diabetic with burns need to be reassessed.

Alloxan↗
PubMed1984

The effect of age on severity of murine burns.

There is a higher mortality in elderly subjects with burns. Whether the same amount of heat will cause a greater degree of thermal injury in elderly subjects and thus account, in part at least, for this increased mortality has not been determined and was, therefore, the purpose of this study. Swiss white mice, 1-year-old (elderly) and 3-months-old (young) were anesthetized with pentobarbital sodium and burned uniformly on a depilated area of the back with a steel disc at 100 F for 10 seconds (10% body burn). Burn severity was evaluated in a blinded manner by gross and microscopic criteria at 1, 2, and 4 days postburn. The mean burn severity 1 day postburn was significantly less in the elderly mice compared with the young mice (1.72 versus 3.22, (P less than 0.001). On the 2nd and 4th days postburn, no differences were noted in the degree of burn severity between the two groups. The early apparent diminished burn severity in the elderly mice was unexpected. Possible mechanisms to account for this difference in the old animals may relate to decreased cutaneous microcirculation, alteration in chemical composition of the skin, and the effects of thromboxane A2 and prostaglandin I2. The clinical relevance of these findings concerns the need for more careful clinical management with intentional overassessment of the initial degree of the thermal damage.

Aging↗