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Biomedical subjects

D L Traber

Publications and source records attributed to D L Traber.

At least 127 records · Page 7Linked to original sources
PubMed1993

Pathophysiology of ovine smoke inhalation injury treated with extracorporeal membrane oxygenation.

An ovine model was used to study the pathophysiology of smoke inhalation injury treated with extracorporeal membrane oxygenation (ECMO). Smoke inhalation is characterized by leukocyte-oxygen free-radical mediated acute lung injury. Treatment with ECMO was by extracorporeal venoarterial or venovenous perfusion using a venous drainage reservoir, roller pump, heat exchanger, and membrane lung oxygenator capable of oxygen delivery to and carbon dioxide removal from a patient. Blood-foreign surface interactions are known to occur during ECMO. We examined the effects of ECMO on circulating leukocytes, oxygen free-radical activity, thromboxane release, and gas exchange after smoke inhalation injury. Animals treated with smoke and ECMO had significantly increased circulating thromboxane B2 levels and oxygen free-radical activity compared with sham-treated animals and animals treated with smoke and mechanical ventilation (MV). Likewise, there was a significant increase in lung wet-to-dry weight ratios in animals treated with smoke and ECMO compared with those treated with smoke and MV. These data may account for the initial deterioration in native lung function after the initiation of ECMO and imply that ECMO may potentiate the pathophysiology of smoke inhalation injury.

Animals↗
PubMed1993

Heparin improves oxygenation and minimizes barotrauma after severe smoke inhalation in an ovine model.

Inhalation injury is one of the main causes of mortality in burn victims. The tracheobronchial epithelium sloughs and combines with a protein rich exudate to form casts of the airways that can lead to obstruction. We studied the effects of a continuous infusion of heparin on the acute pulmonary injury that occurs after smoke inhalation injury in sheep. Twelve ewes with vascular catheters received a standardized smoke inhalation injury and mechanical ventilation according to protocol for 72 hours. The heparin group (n = 6) received a 400 unit per kilogram bolus of heparin followed by a continuous infusion to maintain the activated clotting time between 250 to 300 seconds. The control group (n = 6) received a saline solution vehicle. Hemodynamics, blood gases and plasma samples for conjugated dienes were taken every six hours. At necropsy, pulmonary tissue was collected for histologic findings, polymorphonuclear neutrophil leukosequestration, wet-to-dry weight ratios and conjugated dienes. PaO2 to FIO2 ratios were improved in the heparin group compared with the control group at 12 to 72 hours after injury, and peak airway pressures were higher in the control group compared with the heparin group. Positive end expiratory pressure requirements were higher in the control group compared with the heparin group. There were significantly fewer airway tracheobronchial casts as determined by our tracheobronchial casts scoring system (2.4 +/- 0.4 versus 0.67 +/- 0.21) and confirmed by histologic examination. Pulmonary blood-free wet-to-dry weight ratios were higher in the control group compared with the heparin group (6.4 +/- 0.5 versus 5.2 +/- 0.1; p < 0.05). There were no differences in pulmonary tissue or plasma conjugated dienes; likewise, pulmonary leukosequestration was unaffected by heparin. Heparin decreases tracheobronchial cast formation, improves oxygenation, minimizes barotrauma and reduces pulmonary edema in an ovine model of severe smoke inhalation injury. Heparin does not reduce oxygen free radical activity after smoke inhalation injury.

Analysis of Variance↗
PubMed1992

Mesenteric lymphadenectomy prevents postburn systemic spread of translocated bacteria.

We investigated the role of mesenteric lymph nodes in postburn systemic spread of intestinal bacteria. Group 1 minipigs (n=8) had a 40% third-degree burn. Group 2 minipigs (n=7) had the same burn injury, but their mesenteric lymph nodes were removed immediately after burn. Group 3 minipigs (n=8) had sham burn, and group 4 minipigs (n=6) had mesenteric lymph node removal under anesthesia. All minipigs were killed at 48 hours, and tissues were harvested for bacteriological culture. Group 1 showed a large number of positive cultures from several of the systemic organs. Group 2 demonstrated no positive cultures in any of the tissues except the peritoneal fluid. These data suggest that bacterial translocation occurs mainly via mesenteric lymphatics to mesenteric lymph nodes and, thence, into other systemic tissue. After major burns, mesenteric lymph nodes may become an additional focus of infection.

Animals↗
PubMed1992

Endorphin mediation of mesenteric blood flow after endotoxemia in sheep.

BACKGROUND AND METHODS: The administration of endotoxin in small dosages to sheep results in an acute decrease followed by an increase in cardiac output. It has previously been determined that the initial decrease in output was the result of a reduction in blood flow to the mesenteric areas. These changes were associated with increased blood concentrations of beta endorphin. The present study was accomplished to determine if the systemic cardiovascular response to endotoxin could be affected by the administration of an opiate receptor-blocking agent. Female range sheep (n = 12) were prepared for chronic study by implantation of cardiopulmonary catheters and a flow probe on the cephalic mesenteric artery. Endotoxin (Escherichia coli, 1 microgram/kg) was administered to these animals. Half of the sheep were treated with naloxone (2 mg/kg + 2 mg/kg.hr), and the remainder with an equivalent volume of sodium chloride (0.9%). RESULTS: In untreated sheep, cardiac indices decreased by 15% to 20% (5.1 +/- 0.1 to 4.2 +/- 0.4 L/min.m2) between 0 and 1 hr and 2 and 5 hrs after endotoxin (4.5 +/- 0.2 L/min.m2), and then increased to a value 40% (7.2 +/- 0.6 L/min.m2) above baseline by 12 hrs. Flow in the cephalic mesenteric artery decreased in a pattern similar to the reduction in cardiac index (962 +/- 152 [time, T = 0] to 379 +/- 111 [T = 0.8] and 384 +/- 88 mL/min [T = 4.0], p less than .05) but did not increase to the same extent (1008 +/- 153 mL/min [T = 4.0], p greater than .05). There was a concomitant increase in the plasma beta-endorphin concentrations as the blood flow decreased (5 +/- 4 [T = 0] to 40 +/- 15 pg/mL [T = 0.8; untreated group], p less than .05; and 10 +/- 4 to 50 +/- 7 pg/mL [T = 0.8; naloxone-treated group], p less than .05). In the naloxone-treated group, the same pattern of cardiac output change was noted with endotoxin; however, reduction of mesenteric artery flow was only 30% (1118 +/- 129 to 908 +/- 122 mL/min, p less than .05) of the value seen in the untreated animals (962 +/- 152 to 379 +/- 111 mL/min, p less than .05). These changes in mesenteric blood flow were statistically significant from one another. As the cardiac output increased in the sheep treated with the opiate antagonist, mesenteric blood flows increased 20% above the baseline value (1391 +/- 199 mL/min, p less than .05). CONCLUSIONS: The decrease in cardiac output noted with endotoxin can be accounted for by the decrease in the blood flow in the cephalic mesenteric artery. This phenomenon can be attributed, at least in part, to the release of endorphins. There is both a vasodilation and constriction during endotoxemia in the ovine model.

Animals↗
PubMed1992

Effects of hypertonic saline dextran resuscitation on oxygen delivery, oxygen consumption, and lipid peroxidation after burn injury.

We compared the effects of lactated Ringer's (LR) and hypertonic saline dextran (HSD) on postburn cardiovascular function, O2 consumption, lipid peroxidation, and bacterial translocation. Miniature pigs with 40% total body surface area (TBSA), third-degree burns received, 30 minutes postburn, either Parkland resuscitation (LR group, n = 8) or HSD, 10 mL/kg/30 minutes, followed by LR, 4 mL/kg/%burn over the next 23 hours (HSD group, n = 8). The HSD prevented the early decrease in cardiac index (CI); the early increase in the resistance of the systemic, mesenteric, celiac, and renal vascular beds; and the decrease in mesenteric O2 consumption seen after burns when LR alone is used for resuscitation. The HSD also moderated the systemic and mesenteric lipid peroxidation. Bacterial translocation was less in the HSD group (3 of 8 animals) compared with the LR group (5 of 8 animals), but was not statistically different. Hypertonic saline dextran may be beneficial in improving the postburn microcirculation and attenuating postburn oxidant-induced lipid peroxidation in the systemic tissues and the gut.

Animals↗
PubMed1992

Immediate positive pressure ventilation with positive end-expiratory pressure (PEEP) improves survival in ovine smoke inhalation injury.

BACKGROUND: The purpose of this study was to compare the effects of immediate initiation of positive pressure ventilation (PPV) with positive end-expiratory pressure (PEEP) versus the initiation of PPV with PEEP only after hypoxemia ensued following severe smoke inhalation injury. METHODS: We prospectively evaluated chronically instrumented adult sheep treated with immediate versus delayed PPV with PEEP and compared oxygen requirements, hemodynamics, pleural fluid formation, postinjury survival, and tracheobronchial pathologic processes among groups. The immediate group (group I; smoke, n = 6; sham, n = 2) underwent tracheostomy and bilateral chest tube placement before they received inhalation injury. They were then immediately placed on PPV with PEEP (12 cm H2O). The animals in the delayed group (group D) (n = 6) were placed on PPV with PEEP when arterial hypoxemia (PaO2 < 80 mm Hg [11.2 kPa] on 0.4 FIO2) or respiratory distress developed. RESULTS: Groups were matched for smoke exposure and peak carboxyhemoglobin. Both groups developed a characteristic decrease in PaO2/FIO2 ratio. Initiation of PPV + PEEP improved PaO2 in the delayed group (69 +/- 7 to 126 +/- 21 mm Hg [9.2 +/- 0.9 to 16.7 +/- 2.8 kPa]). Pleural fluid output was greater in the immediate group compared with the delayed group (1559 +/- 415 vs. 426 +/- 236 mL). At 96 hours after injury five of six animals in the delayed group had died. In contrast, six of six animals in the immediate smoke group survived 96 hours (p < 0.05 versus delayed group). The immediate group had fewer and less extensive tracheobronchial casts at necropsy. CONCLUSIONS: Immediate PPV + PEEP did not prevent the development of hypoxia and was associated with increased pleural fluid formation. Death within 96 hours in the delayed group was the result of respiratory failure aggravated by bronchial cast formation despite vigorous pulmonary toilet. Early positive pressure ventilation with PEEP, preferably initiated immediately after the inhalation insult, significantly increases short-term survival and is associated with decreased tracheobronchial cast formation in this ovine model of severe smoke inhalation injury.

Animals↗
PubMed1992

Pulmonary hemodynamics and tissue damage after one lung infusion of Pseudomonas aeruginosa in sheep.

The relative roles of hematogenous mediators and direct bacterial toxicity due to phagocytosis by pulmonary intravascular macrophages were determined by selective bacterial infusion into the left pulmonary artery and comparison of right and left lungs at 24 h. Chronically instrumented sheep received 15-min pulmonary arterial infusions of live Pseudomonas aeruginosa (0.35-2.9 x 10(9), n = 6) or saline (n = 5). The saline group demonstrated stable cardiopulmonary function over time. Left lung blood flow, measured by Doppler flow probe, decreased 15 min into the bacterial infusion, with a concomitant sevenfold increase in left lung pulmonary vascular resistance index. The right lung pulmonary vascular resistance index doubled at 1 h, in association with increased plasma thromboxane B2 levels. An increase in cardiac index and decrease in systemic vascular resistance occurred at 12 h. The wet-to-dry weight ratio of the Pseudomonas-infused left lung was increased compared with that of the sham-infused lung. The tissue count of neutrophils in the lungs was doubled in both sides, but neutrophils on the left were more degranulated. The left lung tissue damage was caused by direct bacterial toxicity, including activation of phagocytic cells. Hematogenous mediators induced pulmonary and systemic hemodynamic changes and right lung neutrophil sequestration, but they did not damage the noninfused lung.

Animals↗
PubMed1992

Mechanical alteration of blood flow in smoked and unsmoked lung areas after inhalation injury.

The degree of pulmonary perfusion may have an important role in the pathogenesis of inhalation injury. We studied this in sheep that had only one lung exposed to smoke. The right lung and upper airway of 12 chronically instrumented sheep were insufflated with cotton smoke. In six animals, the left pulmonary artery was occluded between 4 and 10 h after smoke insufflation. All animals were studied for 24 h and then killed, and lung tissue was harvested. The smoked as well as the air-insufflated lung of all animals showed an increase in wet-to-dry weight ratio and tissue conjugated dienes (products of lipid peroxidation). Neither the intermittent blood flow increase to the smoked lung nor the simultaneous blood flow reduction with a concomitant polymorphonuclear neutrophil entrapment in the air-insufflated lung significantly affected the histopathological outcome of the respective lung. We conclude that tissue damage after inhalation injury cannot be diminished by increasing the flow to smoked areas. Ischemia-reperfusion injury does not have a major role in the lung damage seen with inhalation injury.

Animals↗
PubMed1992

Reversal of hyperdynamic response to continuous endotoxin administration by inhibition of NO synthesis.

Septic shock is characterized by an increase in cardiac output and a fall in systemic vascular resistance index and mean arterial pressure. Endotoxin alters the smooth muscle function of blood vessels, probably by means of an increased production of the potent vasodilator nitric oxide (NO). The present study was accomplished to determine how the inhibition of NO synthesis influences cardiovascular performance in an ovine model of hyperdynamic endotoxemia. Endotoxemia was induced in five range ewes (41 +/- 2 kg) by continuous infusion of Escherichia coli endotoxin (LPS, 10 ng.kg-1.min-1) over the entire study period. After 24 h of LPS infusion, cardiac output increased from 5.2 +/- 0.3 to 7.9 +/- 0.6 (SE) 1/min (P less than 0.05) and mean arterial pressure and systemic vascular resistance index fell from 92 +/- 5 to 79 +/- 6 mmHg (P = 0.08) and from 1,473 +/- 173 to 824 +/- 108 dyn.s.cm-5.m2 (P less than 0.05), respectively. The pulmonary shunt fraction increased from 0.23 +/- 0.03 to 0.32 +/- 0.03 (P less than 0.05). The intravenous administration of the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (25 mg/kg) 24 h after the start of the LPS infusion changed these values to approximately baseline levels over the subsequent 4 h. Although N omega-nitro-L-arginine methyl ester increased pulmonary arterial pressure and pulmonary vascular resistance (P less than 0.05), right and left ventricular stroke volume index showed no significant changes. It is concluded that NO has a major function in cardiovascular performance in endotoxemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Systemic blood flow to sheep lung: comparison of flow probes and microspheres.

Discrepancies exist between experimental measurements of the systemic blood flow to sheep lung by use of microsphere techniques and flow probes on the bronchial artery. In these studies, we simultaneously measured the blood flow through the bronchial artery, using a transit time flow probe, and the systemic blood flow to left lung, using radioactive microspheres. All measurements were made on conscious sheep previously prepared with chronic catheterizations of the left atrium, aorta, and vena cava and a flow probe around the bronchial artery. Inflatable occluder cuffs were placed around the pulmonary and bronchoesophageal arteries. Bronchial artery blood flow in six sheep was 25.3 +/- 5.2 ml/min or 0.4% of the cardiac output. Systemic blood flow to left lung, measured with microspheres, was 54.1 +/- 14.2 ml/min. Calculated systemic blood flow to that portion of sheep lung perfused by the bronchial artery was 127.6 +/- 35.3 ml/min or 1.9% of cardiac output. Occlusion of the bronchoesophageal artery reduced bronchial artery flow to near zero, whereas total systemic blood to the lung was reduced by only 55%. Blood flow to the intraparenchymal cartilaginous airways was reduced 60-90% after occlusion of the bronchoesophageal artery. Sheep, like most mammals, have multiple and complex systemic arterial inputs to the lungs. We conclude that multiple branches of the bronchoesophageal artery provide most but not all of the systemic blood flow to the intraparenchymal cartilaginous airways but that over one-half of the total systemic blood flow to sheep lung comes from sources other than the common bronchial artery.

Animals↗
PubMed1992

Lymph and blood flow responses in central airways.

The lymphatic drainage of the lung has been used as a quantitation of pulmonary microvascular fluid flux in normal animals and after various forms of injury. This review supports the importance of the bronchial microvasculature in the formation of lung lymph. Proof that the lymph drainage of the lung comes from the pulmonary circuit has been based on the finding of an elevation of lymph flow when the pulmonary venous pressure is elevated. This proof is wanting since recent work demonstrates that the venous drainage of the intrapulmonary bronchi flows into the pulmonary vascular system at the precapillary level. The administration of endotoxin induces an elevation of lung lymph. The bronchial circuit may play a role in this response since it is likewise exposed to the high pulmonary pressures induced by endotoxin, and there is evidence that ischemia/reperfusion injury to the airway occurs with endotoxin administration. After acute lung injury from smoke inhalation, lung lymph flow is markedly elevated. The lymph drainage from the airway may play an important role in this response. Bronchial blood flow is markedly increased after inhalation injury and there is airway edema. The increases in lung lymph flow and extravascular lung water are markedly reduced by occlusion of the bronchial artery. These data support the need for additional study of the role of the bronchial circulation in the formation of lung lymph.

Animals↗
PubMed1992

Comparison of the pulmonary lymphatic and hemodynamic changes of near-drowning in a sheep model.

The hemodynamic and lung lymph changes following near-drowning (ND) were studied in sheep. Experimental ND was by transtracheal aspiration of 10 ml/kg body weight of either seawater (SW) or freshwater (FW). Extravascular lung water and lung lymph protein flux were significantly increased, but cardiac index was depressed in both groups following ND. Systemic and pulmonary vascular resistances were markedly elevated with FW compared to only a slight rise with SW. Lung lymph oncotic pressure decreased with SW ND from baseline of 9.7 +/- 0.4 to 6.8 +/- 0.63 mm Hg (P < 0.05). In contrast, FW ND increased lung lymph oncotic pressure from 12.8 +/- 0.9 to 16.6 +/- 1.3 mm Hg (P < 0.05). These data suggest that the changes in lung lymph and hemodynamic response to SW and FW ND differ in sheep. The changes are immediate and profound with SW, but slower in onset and less severe with FW. FW ND is associated with hemolysis, which is absent in SW ND.

Animals↗
PubMed1992

Pentafraction reduces the lung lymph response after endotoxin administration in the ovine model.

For the past half-century, several high molecular weight compounds have been used for volume expansion during cardiopulmonary resuscitation. However, the effectiveness and side effects of these different expanders are varied. We have compared plasma, pentastarch, and a new product, pentafraction, for effective plasma volume expansion before and after tissue injury with endotoxin administration. In each group, eight range ewes instrumented with a Swan-Ganz, arterial, and venous catheters, and lung and flank lymphatic cannulas were compared. Each group received 15 ml/kg of either 6% pentafraction, 6% pentastarch, or plasma followed two hours later by 1.5 micrograms/kg/0.5 hr E. Coli endotoxin over 30 min. Data were collected for an additional 24 hr after endotoxin administration. Our results indicated a plasma volume expansion in all three groups. However, the prior administration of pentafraction significantly attenuated the increase in the lung lymph flow and early evaluation of systemic vascular resistance noted with endotoxin in comparison to the other two groups.

6-Ketoprostaglandin F1 alpha↗
PubMed1992

Mechanism of immunoreactive atrial natriuretic factor release in an ovine model of endotoxemia.

We have previously reported an increase in plasma levels of atrial natriuretic factor (ANF) in an ovine model of endotoxemia. The purpose of this study was to determine if this IR-ANF release was mediated by the increase of right atrial pressure (RAP) and right heart volumes concomitantly observed following endotoxin (LPS) administration. We studied right ventricular function, renal blood flow (RBF), urinary output (UO), urinary clearance of free water (CH20), urinary osmolality (UOSM), sodium excretion (UENA), and the plasma IR-ANF concentration (radioimmunoassay), following the administration of an E. coli LPS bolus (1 microgram/kg) with (group O, n = 8) and without (group E, n = 10) pretreatment with OKY-046, a selective thromboxane synthetase inhibitor. LPS induced early increases in RAP, right ventricular end-systolic (RVESV) and end-diastolic (RVEDV) volumes, heart rate (HR), and IR-ANF, and delayed increases in RBF, UO, and CH20. OKY-046 prevented the elevation of RAP, RVEDV, and RVESV; however, both groups showed virtually identical increases in IR-ANF (E: 20.03 +/- 3.8 to 192.33 +/- 35.47 pg/ml, O: 17.9 +/- 4.1 to 159.5 +/- 23 pg/ml) as well as an increase of HR, RBF, UO, and CH20. The increase in IR-ANF release noted following the administration of LPS in an ovine model does not appear to be related to the early elevations in right heart volumes or atrial distension.

Animals↗
PubMed1992

Effects of thromboxane synthetase inhibition on postburn mesenteric vascular resistance and the rate of bacterial translocation in a chronic porcine model.

It is known that thromboxane (TX)B2, the metabolite of the potent vasoconstrictor TXA2, is elevated markedly in the serum of the patients immediately postburn. We had shown that extensive thermal injury causes a reduction in mesenteric blood flow that can lead to bacterial translocation from the intestine. In this study, we tested the hypothesis that the TX synthetase inhibitor, OKY-046, prevents increased mesenteric vascular resistance (MVR) and decreases the rate of translocation of bacteria seen after extensive thermal injury. Pigs in groups 1 (n = 6) and 2 (n = 6) had third degree burns of 40 per cent total body surface area under general anesthesia and were resuscitated according to the Parkland formula. Pigs in group 2 received 10 milligrams per kilogram of OKY-046 as a bolus just before the burn and 10 grams per kilogram per minute for 16 hours as a continuous infusion. Pigs in group 3 (control, n = 6) underwent general anesthesia only and received daily maintenance fluids of lactated Ringer's solution, 2 milliliters per kilogram per hour. OKY-046 prevented the significant increase in MVR seen during the first eight hours after burn. The total peripheral resistance (TPR) showed an early increase and a late decrease in the burn group, while the cardiac index (CI) and temperature (T) significantly increased after 24 hours. Administration of OKY-046 kept TPR, Cl, and T remarkably stable. OKY-046 reduced the rate of translocation of bacteria seen in the burn group from 67 to 17 per cent. Our results show that the blockade of thromboxane synthesis by OKY-046 prevented the early mesenteric vasoconstriction and the late hyperdynamic response seen after thermal injury and was useful in reducing the incidence of postburn translocation of bacteria.

Animals↗
PubMed1991

Halothane markedly reduces mesenteric blood flow but does not impair gut mucosal oxygenation in pigs.

We investigated the effect of halothane on in mesenteric blood flow and gut mucosal oxygenation. Pittman-Moore mini-pigs (n = 6) were chronically instrumented with aortic, pulmonary arterial (Swan-Ganz), and mesenteric venous catheters and an intestinal tonometer. Blood flow in the superior mesenteric artery was measured with an ultrasonic flow probe. On the day of the experiment, data were obtained before and during halothane administration (1.5% end-tidal). Halothane caused a marked decrease in mesenteric blood flow, associated with an increase in mesenteric vascular resistance. Likewise mesenteric oxygen delivery and consumption were significantly decreased under halothane, while the oxygen extraction rate of the intestine was not significantly changed. There was no significant change in intramucosal gut pH after halothane administration, which indicates that an adequate mucosal tissue oxygenation was maintained. We conclude that the marked halothane-induced reduction in mesenteric blood flow did not seem to impair the oxygenation of the gut mucosa in our experimental model.

Animals↗
PubMed1991

Ibuprofen therapy in experimental porcine gram-negative septic shock.

To evaluate the effects of ibuprofen on gram-negative septic shock, immature piglets were subjected to fecal-Escherichia coli peritonitis. Group I (n = 5) received a 12.5 mg/kg bolus of ibuprofen in 0.9% benzyl alcohol, followed by a continuous infusion of 6.25 mg/kg/h. Group II (n = 5) received the vehicle, benzyl alcohol, and Group III (n = 5) received lactated Ringer's solution. Mean survival times among the three groups were not significantly different. Ibuprofen-treated animals had a mean survival time (+/- S.E.M.) of 17.1 +/- 2 h vs. 19.2 +/- 2.4 h in the benzyl alcohol group and 15.7 +/- 2.7 h in the animals receiving lactated Ringer's solution. Thromboxane B2 levels were not significantly different in the treatment vs. non-treatment groups while 6-keto-PGF1a levels were significantly lower in the ibuprofen-treated animals. Neutropenia and thrombocytopenia were not prevented by treatment with ibuprofen.

6-Ketoprostaglandin F1 alpha↗