Biomedical subjects

K Duke

Publications and source records attributed to K Duke.

6 recordsLinked to original sources

PubMed1991

Timing and interpretation of the hemodynamic effects of the pneumatic antishock garment.

STUDY OBJECTIVES: To clarify apparently conflicting reports on the hemodynamic effects of the pneumatic antishock garment (PASG). DESIGN: Ten anesthetized dogs with hemorrhagic hypotension had hemodynamics measured without PASG inflation (group 1) and were compared with ten dogs with PASG inflation (group 2). MEASUREMENTS AND MAIN RESULTS: Baseline and immediate posthemorrhage data were similar in both groups. Group 1 maintained a carotid artery pressure of 85 +/- 9 mm Hg while group 2, by design, maintained baseline CP at 119 +/- 12 mm Hg. After PASG inflation, carotid artery flow increased by 50%, and femoral artery flow decreased tenfold. There was an immediate but transient increase (2.4 +/- 0.1 to 2.7 +/- 0.1 L/min, P less than .05) and a later decrease in cardiac output to 1.9 +/- 0.9 L/min and an increased pulmonary artery wedge pressure and central venous pressure over one hour. Saline (342 +/- 12 mL) reversed the decreased cardiac output without changing pulmonary artery wedge pressure or central venous pressure. CONCLUSION: PASG inflation, therefore, not only increases venous return and cardiac output initially by compressive venous emptying but also decreases venous return and cardiac output later by further venous compression without cardiac decompensation. Thus, apparently conflicting data are explained by the timing and interpretation of the raw hemodynamic measurements.

Animals↗

PubMed1991

Pneumatic antishock garment decreases hemorrhage and mortality from splenic injury.

The effect of the pneumatic antishock garment (PASG) in controlling hemorrhage and death from splenic injury was studied in a canine model. Twelve (two groups of 6) anesthetized dogs had their spleens crushed. Carotid blood pressure, carotid blood flow, splenic artery flow and abdominal aortic flow, as well as the death rate and blood loss, were measured. Group 1 dogs did not have PASG inflation, but group 2 dogs had PASG inflation to an intraperitoneal pressure of 60 mm Hg. All group 1 dogs died within 27 to 58 minutes, but all group 2 dogs survived. Blood loss was 9.4 +/- 1.4 mL/min in group 1 and 1.6 +/- 0.9 mL/min in group 2. In group 1 carotid artery blood pressure, carotid artery flow, splenic artery flow and abdominal aortic flow fell from 120 +/- 10 mm Hg, 284 +/- 12 mL/min, 194 +/- 18 mL/min and 285 +/- 10 mL/min respectively to 0 with death of the animals. By 2 hours in group 2 dogs the carotid artery blood pressure had dropped from 116 +/- 12 to 99 +/- 12 mm Hg, and over the same period carotid artery flow, splenic artery flow and abdominal aortic flow fell from 296 +/- 8 mL/min, 190 +/- 26 mL/min and 279 +/- 16 mL/min respectively to 259 +/- 14 mL/min, 39.0 +/- 6 mL/min and 45 +/- 11 mL/min respectively. Thus, inflation of the PASG maintained carotid artery blood pressure wh ile decreasing splenic, abdominal and aortic flow as well as splenic hemorrhage, with a decrease in the death rate, over a 2-hour period.

Abdomen↗

PubMed1987

Effect of bumetanide in capillary permeability pulmonary oedema.

UNLABELLED: To determine if bumetanide, like furosemide, improves shunt through pulmonary vasoactivity, 20 dogs with unilobar oleic acid pulmonary oedema were studied. Fractional perfusion and intrapulmonary shunt of the oedematous lobe were measured at: baseline, 1 1/2 hours after oleic acid infusion, 15 minutes later after either 0.1 mg X kg-1 of bumetanide in ten dogs (Bumetanide Group) or without bumetanide in ten dogs (Control Group), and 2 1/2 hours after the oleic acid, the bumetanide being administered immediately after the 1 1/2 hours post-oleic acid measurements. Lobar shunts for the Bumetanide Group were: 9.3 +/- 4.0, 54.3 +/- 13.6, 54.7 +/- 13.6, 38.6 +/- 12.0 per cent and for CONTROLS: 8.7 +/- 1.6, 45.1 +/- 8.8, 48.3 +/- 7.8, 70.4 +/- 6.2 per cent. Fractional perfusions of the oedematous lobe were: 29.9 +/- 1, 14.7 +/- 1.1, 14.6 +/- 0.7, 19.3 +/- 1.9 per cent in the Bumetanide Group and 28.6 +/- 2.1, 14.2 +/- 1.1, 14.2 +/- 1.5, and 9.9 +/- 1.1 per cent in CONTROLS. Oedema (wet to body weight ratio) was less (p less than 0.05) in the contralateral lobe (2.5 +/- 0.2 vs. 2.9 +/- 0.3) and the oedematous lobe (4.7 +/- 0.4 vs 6.0 +/- 0.5) after bumetanide-induced diuresis. We conclude that bumetanide decreases shunt by decreasing oedema and not through pulmonary vasoactivity.

Animals↗

PubMed1987

Does indomethacin affect shunt and its response to PEEP in oleic acid pulmonary edema?

We assessed hemodynamics, lobar perfusion, and shunts at base line 1.5 h after unilobar oleic acid edema, 15 min after indomethacin (10 mg/kg iv), and 15 min after positive end-expiratory pressure (PEEP) (10 cm) in 10 dogs. In 10 additional dogs (control) the same measurements were made but no indomethacin was administered. Shunts of the edematous lobe were: 10.6 +/- 6.3, 54.1 +/- 22.8, 30.8 +/- 16.6, and 12.4 +/- 6.3% for dogs administered indomethacin and 10.9 +/- 4.2, 53.8 +/- 13.1, 72.3 +/- 14.6, and 11.5 +/- 4.1% for the controls. Perfusions (% cardiac output) to the edematous lobe were 27.6 +/- 3.6, 14.6 +/- 2.0, 9.9 +/- 1.5, and 27.9 +/- 2.9% in the dogs administered indomethacin and 27.3 +/- 3.1, 14.0 +/- 1.7, 13.2 +/- 1.3, and 26.9 +/- 2.8% in controls. The decrease in lobar perfusion was similar before indomethacin with a further decrease in lobar perfusion and an increase in lobar vascular resistance 15 min after indomethacin. The increase in vascular resistance of the edematous lobe was three times that of nonedematous lobes after indomethacin (149.6 +/- 76% vs. 58.0 +/- 43%). Indomethacin, therefore, decreases shunt possibly by enhancing alveolar hypoxic vasoconstriction and does not block the improvement in shunt with PEEP.

Animals↗

PubMed1987

Decreasing hydrostatic pressure does not uniformly decrease high-pressure pulmonary edema.

Pulmonary artery wedge pressure (PAWP) of 30 mm Hg with left atrial balloon inflation for 1 1/2 hours produced pulmonary edema in eight dogs. PAWP was then decreased to 10 mm Hg for two hours, and shunt, lung water (extravascular thermal volume, or ETV, by thermal dye), and perfusion distribution (radiomicrosphere technique) were measured and compared with four other dogs (group 1) whose PAWP was maintained at 10 mm Hg. The eight dogs with PAWP of 30 mm Hg for 1 1/2 hours were retrospectively subdivided into two groups of four based on ETV (group 2, double baseline ETV; group 3, triple baseline ETV). Baseline ETV and shunt were similar for all groups and remained unchanged for group 1. At 1 1/2 hours, 2 hours (1/2 hour after decreasing PAWP), 2 1/2 hours, and 3 1/2 hours, respectively, ETV were: 13.9 +/- 1.9, 12.8 +/- 2.0, 9.3 +/- 1.5, and 8.5 +/- 1.0 ml/kg in group 2; and 21.9 +/- 2.1, 22.7 +/- 2.2, 22.5 +/- 2.0, and 22.2 +/- 2.0 ml/kg in group 3. A more variable rate of edema formation was detected in eight additional dogs, but failure to resolve higher levels of edema after decreasing PAWP was also demonstrated in this group. Edema was greatest in lower lobes and decreased lobar perfusion. Shunt was higher in group 3 than in group 2 at 1 1/2 hours and decreased in group 2 but not in group 3 at 3 1/2 hours. Changes in colloid osmotic pressure may account for the differences in edema formation and resolution, but our data suggest that, independent of the rate of edema formation, a decrease in vascular exchange surface area at higher levels of edema may inhibit edema resolution when PAWP is decreased.

Animals↗

PubMed1987

Colloid osmotic pressure in pulmonary edema clearance with furosemide.

After tripling of baseline lung water (EVLW), decreasing wedge pressure (PWP) alone for two hours did not decrease EVLW. In 11 of 16 dogs, triple baseline EVLW and a decrease in plasma colloid osmotic pressure (COP) from 21.1 +/- 0.8 to 17.8 +/- 0.8 mm Hg resulted from left atrial balloon inflation at PWP of 28 to 30 mm Hg. With subsequent lowering of PWP to 10 mm Hg, intravenously administered furosemide (1 mg/kg) was given to these 11 dogs. One half hour after furosemide, shunt decreased slightly without decreasing EVLW in all 11 dogs, but by two hours, seven dogs (group 1) decreased EVLW (from 23.2 +/- 1.8 to 11.1 +/- 1.4 ml/kg) and shunt (37.4 +/- 2.0 to 12.9 +/- 2.9 percent), while four dogs (group 2) did not (EVLW: 22.3 +/- 1.4 to 22.5 +/- 0.6 ml/kg: shunt, 36.8 +/- 1.7 to 36.5 +/- 1.9 percent). Group 1 had diuresis, maintained normal blood urea nitrogen and creatinine levels, and increased COP from 17.7 +/- 0.7 to 23.6 +/- 0.5 mm Hg while group 2 was oliguric with elevated BUN and creatinine values and showed no change in COP (17.9 +/- 0.9 to 18.3 +/- 0.6 mm Hg) after furosemide. After decreasing PWP in massive pulmonary edema (triple baseline EVLW), furosemide appeared to enhance edema clearance by changes in COP with diuresis.

Animals↗