Biomedical subjects

D L Traber

Publications and source records attributed to D L Traber.

At least 145 records · Page 8Linked to original sources

PubMed1991

[The effect of halothane anesthesia on pulmonary circulation regulation during unilateral hypoxic ventilation].

Controversies exist over the influence of inhalation anaesthesia on blood flow regulation in response to local alveolar hypoxia. This study investigates the blood flow diversion from a hypoxic to an oxygenated lung in anaesthetized and ventilated animals in comparison to unanaesthetized animals. Chronically instrumented adult ewes (n = 14, 32-45 kg) were intubated one week after surgery with a modified Carlen's tube, allowing separate ventilation of the left and right lung. In the awake state (n = 7) or after one hour of constant anaesthetic conditions (n = 7, halothane 1.6% and 2.4%), cardiac output (thermodilution) and left pulmonary blood flow (ultrasonic transit time) were evaluated. Then, under identical ventilatory conditions, the left or right lung, alternately, was rendered hypoxic for 10 min by ventilation with nitrogen. The contralateral lung was ventilated with oxygen. After 10 min, haemodynamics were again recorded. The changes in left pulmonary blood flow under unilateral lung hypoxia were similar either in the awake or the anaesthetized state. Thus, we conclude that, under these experimental conditions, halothane anaesthesia and mechanical ventilation have no influence on blood flow regulation under unilateral lung hypoxia.

Anesthesia, Inhalation↗

PubMed1991

Inhibition of thromboxane synthesis reduces endotoxin-induced right ventricular failure in sheep.

BACKGROUND AND METHODS: There is a marked decrease of the right ventricular ejection fraction after the administration of a bolus of endotoxin to sheep. This hemodynamic response may be the result of thromboxane-mediated pulmonary hypertension. Right ventricular function was studied in an ovine model after the administration of endotoxin (1 microgram/kg Escherichia coli) with and without pretreatment with OKY-046, a selective thromboxane synthetase inhibitor. RESULTS: OKY-046 attenuated the endotoxin-induced increase in pulmonary arterial pressure and prevented the early decreases in right ventricular ejection fraction and cardiac output. However, thromboxane synthetase inhibition failed to prevent endotoxin-induced hypoxemia. The marked increase in plasma thromboxane concentrations, which is usually seen after the administration of endotoxin, was prevented by pretreating the animals with OKY-046. On the other hand, increased plasma prostacyclin concentrations were observed in sheep treated with the thromboxane synthetase inhibitor. CONCLUSION: This series of experiments shows that the early endotoxin-induced decrease in right ventricular ejection fraction can be alleviated by the application of OKY-046.

Animals↗

PubMed1991

Derived pulmonary capillary pressure changes after smoke inhalation in sheep.

BACKGROUND AND METHODS: We determined derived pulmonary capillary pressure and the longitudinal distribution of pulmonary vascular resistance in chronically instrumented sheep with inhalation injury by using analysis of pressure decay curves after pulmonary artery occlusion. RESULTS: There was an increase in derived pulmonary capillary pressure and an increase in the lung lymph flow after smoke inhalation. The pulmonary vascular, arterial, and venous resistances increased significantly in the inhalation group. Pulmonary venous resistance increased proportionately more than pulmonary arterial resistance in the inhalation group. The plasma osmotic pressure-derived pulmonary capillary pressure gradient decreased to a greater extent in the inhalation group than in the control group. CONCLUSIONS: The present experiments suggest that the estimates of derived pulmonary capillary pressure can predict filtration pressure better than pulmonary artery occlusion pressure. The derived pulmonary capillary pressure can be measured easily in man with a pulmonary arterial catheter.

Analysis of Variance↗

PubMed1991

Effects of anesthesia, surgery, fluid resuscitation, and endotoxin administration on postburn bacterial translocation.

The aim of the study reported here was to assess the effects of some clinically relevant factors on the incidence and outcome of postburn bacterial translocation. Miniature pigs in 8 groups (n = 6 in each) underwent: (1) general anesthesia (GA); (2) operation (insertion of Swan-Ganz, arterial, and portal catheters) under GA; (3) burn (40% total body surface area, third degree, under GA); (4) burn and operation; (5) burn, operation, and resuscitation (Parkland); (6) burn, operation, and resuscitation plus endotoxin (100 micrograms/kg IV bolus, 2nd day). Groups 1-6 were killed at 48 hours and tissue samples were harvested for bacteriologic culture. Groups 7 and 8 were the same as 2 and 5, respectively, but were killed at 96 hours. Resuscitation and endotoxin increased postburn bacterial translocation but only endotoxin promoted systemic sepsis. In the absence of additional trauma, translocated bacteria were cleared by 96 hours postburn.

Anesthesia, General↗

PubMed1991

Cardiac dysfunction after acute endotoxin administration in conscious sheep.

We evaluated cardiac function in an unanesthetized ovine model of hyperdynamic endotoxemia. The animals were instrumented for crystallographic dimension analysis of the left ventricle (LV) and measurement of LV, aortic, atrial, central venous, and pulmonary arterial pressures, and cardiac output. Seven sheep received 1.5 micrograms/kg of Escherichia coli endotoxin [lipopolysaccharide (LPS) LPS-P group] and were compared to a sham group. The sham group demonstrated no significant change in any of the variables. In the LPS-P group, the cardiac index increased (5.7 +/- 0.4 to 7.9 +/- 0.6 l.min-1.m-2) between 8 and 12 h after LPS. Concomitantly, the maximum elastance of LV end-systolic pressure-volume relations significantly decreased (2.88 +/- 0.27 mmHg/ml) compared with baseline (3.89 +/- 0.50 mmHg/ml). Other indexes of the LV contractility (maximum pressure development and ejection fraction) were also reduced. There was a simultaneous increase in the LV end-systolic and diastolic volumes. These findings confirm the hypothesis that there is a myocardial depression during LPS in the ovine model.

Animals↗

PubMed1991

Time course of hypoxic pulmonary vasoconstriction after endotoxin infusion in unanesthetized sheep.

Endotoxin [lipopolysaccharide (LPS)] has been reported to reduce hypoxic pulmonary vasoconstriction and thus increases venous admixture. The time course of this failure of pulmonary blood flow regulation was investigated in six chronically instrumented unanesthetized sheep after infusion of Escherichia coli LPS (1 microgram/kg). The change in left pulmonary arterial blood flow (LPBF, ultrasonic transit time) in response to unilateral lung hypoxia (10 min of N2 alternately to the left and right lungs) was compared before and at various time intervals after the administration of LPS. During baseline conditions, LPBF was 33% of total cardiac output and decreased to 15% when the left lung was ventilated with a hypoxic gas mixture. One hour after endotoxin infusion, LPBF remained at 33% of total cardiac output yet only decreased to 28% during the hypoxic challenge. The response to one-lung hypoxia was still significantly depressed 10 h post-LPS administration. It is concluded that hypoxic pulmonary vasoconstriction is almost completely abolished for a prolonged time period after a small dose of LPS.

Animals↗

PubMed1991

Lung edema formation following inhalation injury: role of the bronchial blood flow.

We investigated the contribution of the bronchial blood flow to the lung lymph flow (QL) and lung edema formation after inhalation injury in sheep (n = 18). The animals were equally divided into three groups and chronically prepared by implantation of cardiopulmonary catheters and a flow probe on the common bronchial artery. Groups 1 and 2 sheep were insufflated with 48 breaths of cotton smoke while group 3 received only room air. Just before injury, the bronchial artery of group 2 animals was occluded. The occlusion was maintained for the duration of the 24-h study period. At the end of the investigation, samples of lung were taken for determination of blood-free wet weight-to-dry weight ratio (W/D). Inhalation injury induced a sevenfold increase in QL in group 1 (7 +/- 1 to 50 +/- 9 ml/h; P less than 0.05) but only a threefold increase in group 2 (10 +/- 2 to 28 +/- 7 ml/h; P less than 0.05). The mean W/D value of group 1 animals was 23% higher than that of group 2 (5.1 +/- 0.4 vs. 3.9 +/- 0.2; P less than 0.05). Our data suggest that the bronchial circulation contributes to edema formation in the lung that is often seen after the acute lung injury with smoke inhalation.

Animals↗

PubMed1991

Thromboxane synthase inhibition and cardiopulmonary function during endotoxemia in sheep.

We studied the cardiopulmonary response to endotoxin (lipopolysaccharide, LPS) in sheep with and without the administration of a thromboxane synthase inhibitor, OKY-046. The animals were instrumented for crystalographic dimension analysis of the left ventricle (LV) and for measurement of LV, aortic, left atrial, and pulmonary arterial pressures and cardiac index, as well as lung lymph flow. They received 1.0 micrograms/kg of Escherichia coli LPS with (n = 8) and without (n = 8) OKY-046 (10 mg/kg bolus, then 10 micrograms.kg-1.min-1). OKY-046 prevented the increase of pulmonary arterial pressure and the decrease of cardiac index that occurred during the early phase of endotoxemia. Between 8 and 12 h after LPS, cardiac index increased from 6.8 +/- 0.7 to 8.9 +/- 0.51.min-1.m-2. Concomitantly, the end-systolic pressure-diameter relationship (ESPDR, sensitive myocardial contractility index) significantly decreased from 14.7 +/- 0.6 to 7.7 +/- 0.7. Other indexes of the LV contractility (+dP/dtmax) were also reduced. OKY-046 prevented the decreases of ESPDR and +dP/dtmax. OKY-046 also attenuated the increased lung lymph flow changes seen with LPS.

6-Ketoprostaglandin F1 alpha↗

PubMed1991

Analysis of pulmonary microvascular permeability after smoke inhalation.

We estimated the reflection (sigma) and filtration coefficients (Kf) in a chronic sheep lung lymphatic preparation after smoke inhalation. Group I (n = 7) sheep were insufflated with cotton smoke and group II animals (n = 5) with room air. After inhalation injury, the lung lymph flow increased nearly four times the baseline value by 24 h after injury. There was a concomitant reduction of sigma (0.81 +/- 0.02 to 0.64 +/- 0.02) and elevation of Kf (0.020 +/- 0.002 to 0.042 +/- 0.009 ml.min-1.mmHg-1); pulmonary capillary pressure was also elevated (13 +/- 1 to 17 +/- 1 mmHg). By 48 h postinjury, sigma and Kf returned toward baseline but pulmonary capillary pressure was still elevated. We determined that 34% of the increase in capillary filtration was attributable to increased capillary pressure and 66% to increased permeability 24 h after inhalation, but 48 h after injury, 75% of the increase in capillary filtration was attributable to increased capillary pressure and 25% to increased permeability. We conclude that the lung edema formation following smoke inhalation is the result of marked increases in both capillary pressure and permeability.

Anesthesia↗

PubMed1991

Cardiac function in an ovine model of endotoxemia.

Eight awake sheep were monitored with ultrasonic crystals, positioned at the anterior and posterior left ventricular wall. A left-sided intraventricular pressure transducer and a right ventricular ejection fraction catheter were positioned in the right and left hearts, respectively. After administration of endotoxin (Escherichia coli, LPS 1.5 micrograms/kg in 30 min), the hemodynamic variables showed a triphasic course. Phase I, (0-1 hr post LPS) was characterized by an increased pulmonary artery pressure and a decreased right ventricular ejection fraction. The inability of the right ventricle to compensate for the increased preload resulted in a fall of the left ventricular preload, stroke volume, and cardiac output. Three hours after LPS administration a second drop of the cardiac output was noted (phase II). This occurred as a result of a fall in preload. Eight hours post LPS a hyperdynamic phase (phase III) was distinguished, with a high cardiac output and a low systemic vascular resistance. During this time there was evidence of probable reduced myocardial contractility.

Animals↗

PubMed1991

Role of bradykinin in ovine endotoxemia.

We determined if the cardiopulmonary response to endotoxin (LPS) is mediated by bradykinin (BK). Sheep (n = 30) were prepared for chronic study with cardiopulmonary catheters, and chronic lung lymph fistulae. They were divided into the following study groups: A) BK infusion; B) LPS; C) LPS with angiotensin converting enzyme inhibitor (ACEI); D) ACEI alone; E) LPS with BK antagonist. Cardiac index and mean arterial pressure fell (6.9 +/- 0.4 to 5.3 +/- 0.3 L/min/m2 and 93 +/- 4 to 72 +/- 3 mmHg, respectively), and pulmonary lymph flow increased (10.5 +/- 3.0 to 17.8 +/- 4.3 ml/hr) during BK infusion. Addition of ACEI during BK infusion reduced the amount of BK necessary to induce a comparable response (125 to 2 micrograms/kg/hr). Administration of ACEI to LPS animals did not significantly alter their cardiopulmonary responses. BK antagonist did not change the response to LPS. Although the kallikrein-kinin pathway is believed to be activated during the septic response, our data do not lend support for the hypothesis that bradykinin is an important mediator of the cardiopulmonary changes.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed1990

Monitoring patients during helicopter flight.

In 11 patients being transported via helicopter we monitored heart rate, arterial oxygen saturation, and systolic blood pressure with a pulse oximeter. We were able to obtain vital signs in 10 of 11 patients. The pulse oximeter was a useful tool in monitoring vital signs intraflight.

Adolescent↗

PubMed1990

Does measurement of systolic blood pressure with a pulse oximeter correlate with conventional methods?

The pulse oximeter is commonly used in the operating room. We evaluated the use of a pulse oximeter to monitor systolic blood pressure in 20 healthy volunteers and 42 anesthetized patients. We compared the pulse oximeter method of measuring systolic blood pressure with the cuff methods using Korotkoff sounds and Doppler ultrasound as well as with direct pressure measurement through an intraarterial cannula. Systolic blood pressure values obtained by pulse oximeter correlated well with values obtained by other conventional methods. The best correlation was found with Doppler ultrasound (r = 0.996) and the worst with arterial cannulation (r = 0.880). We conclude that this method can be used intraoperatively to measure systolic blood pressure.

Adolescent↗

PubMed1990

Bronchial blood flow reduction with positive end-expiratory pressure after acute lung injury in sheep.

Smoke inhalation increases bronchial blood flow (Qbr) and produces edema of the airway system. This study investigates whether the increased Qbr seen 24 h after inhalation injury can be affected by mechanical ventilation with PEEP (5, 10, 15 cm H2O). Sheep (n = 8) previously prepared with cardiopulmonary catheters and ultrasonic transit time flow probes mounted around their bronchial arteries were insufflated with four sets of 12 breaths each of cotton smoke. Different levels of PEEP were added to the mechanical ventilation 24 h after injury; each PEEP level was applied for 45 min. There were significant increases in Qbr and lung lymph flow (QL) associated with a marked decrease in bronchial vascular resistance (BVR) 24 h after injury. However, no change was observed in mean arterial pressure (MAP) or cardiac index (CI). There was a substantial reduction in PaO2/FIO2 (P/F), which indicated a deterioration in arterial oxygenation. The application of varying levels of PEEP decreased Qbr (p less than .05) while BVR increased (p less than .05), but QL and P/F did not. CI and MAP were recorded. After removal of PEEP, none of the cardiopulmonary variables were significantly different from their postsmoke control values. These findings suggest that mechanical ventilation with PEEP markedly decreases the smoke-induced hyperemia edema frequently seen after inhalation injury without any significant alterations in MAP or CI.

Animals↗

PubMed1990

Endotoxin (LPS) increases mesenteric vascular resistance (MVR) and bacterial translocation (BT).

Endotoxemia is responsible for many of the pathophysiologic alterations that occur with Gram-negative sepsis. We utilized a chronic ovine model to determine the hemodynamic disturbances in the gastrointestinal tract during endotoxemia. Sheep with indwelling arterial, venous, and pulmonary arterial catheters were used. An ultrasonic flow probe was placed on the cephalic mesenteric artery. The animals were subjected to: 1) Ringer's lactate infusion (sham n = 6); or 2) 1.5 mcg/kg E. coli endotoxin (n = 6) over over a period of one half hour and were monitored for 48 hours. They were then sacrificed and specimens of mesenteric lymph node, liver, spleen, kidney, and lung obtained for bacteriologic cultures and histologic analysis. Sheep receiving endotoxin showed more than 50% reduction in the mesenteric blood flow. Mesenteric vascular resistance increased while non-mesenteric systemic vascular resistance decreased. The increase in the total systemic vascular resistance, noted during endotoxemia, was thus likely due to the increase in the mesenteric vascular resistance. At autopsy there were positive cultures for microorganism in the mesenteric lymph nodes in six out of six sheep with endotoxemia as compared to one out of six of control. Thus the vasoconstriction in the mesenteric areas may have resulted in bacterial translocation from the GI tract.

Animals↗

PubMed1990

Hydroxyethyl starch pretreatment in bacteremic sheep.

Live bacteria were infused in a chronic ovine lung lymph model to determine if a preceding infusion of the colloid, hydroxyethyl starch (HES), exaggerated the cardiopulmonary dysfunction or impaired removal of bacteria by macrophages in the pulmonary circulation. HES was infused (3 mL/kg/hr; n = 6) from 24 to 12 hr before the bacteria and decreased plasma protein content and increased pulmonary lymph to plasma protein concentration because of its oncotic properties. Ringer's lactate (2 mL/kg/hr) was given after stopping HES and also to the control group (n = 6). Infusion of live Ps. aeruginosa (2.5 x 10(8) Ps./min for approximately 30 min) induced equivalent pulmonary hypertension, increased pulmonary microvascular permeability, and cardiovascular depression in the two groups. The removal of bacteria in the lungs was not affected, indicating that this measurement of the function of the mononuclear phagocytic system was not impaired by the preceding HES.

Animals↗

PubMed1990

Pulmonary circulation and burns and trauma.

The lung is a critical organ in victims of thermal injury or multiple trauma since the blood that drains injured organs circulates through the pulmonary circulation before passing through any other organ. The lung therefore will receive the first volley of cytotoxins released postinjury. In addition to being a target of injury, the lung may also contribute to the injury of systemic organs. This injury may be the result of a reduced delivery of oxygenated blood or the direct release of cytotoxins into the systemic circulation. The injury to the lung may be to the pulmonary microvasculature or the airway. The bronchial circulation responds to injury by a marked elevation in its blood flow and microvascular permeability. These latter effects may be important in mediating the changes which occur in the lung parenchyma.

Animals↗

PubMed1990

Effects of allopurinol on smoke inhalation in the ovine model.

We hypothesized that the pulmonary damage induced by smoke inhalation is the result of ischemic reperfusion injury. We determined the effect of allopurinol (xanthine oxidase inhibitor) on the pulmonary microvascular fluid flux in an ovine model after inhalation of cotton smoke (n = 13) and compared these data with those from untreated similarly smoke-injured (n = 7), as well as sham- (air, n = 9) smoked, animals and sheep given an equivalent dose of CO (n = 7). Smoke injury resulted in an increased lung lymph flow, lymph-to-plasma protein ratio, lung content of polymorphonuclear cells, and extravascular lung water (gravametric), in addition to histological evidence of tissue (pulmonary) edema and destruction. No significant difference was found in these variables between the sheep that were injured with smoke whether or not they were pretreated with allopurinol. The sham-smoked and CO-insufflated animals showed no significant changes in cardiopulmonary function or morphology. We conclude that there are few data to support a role of ischemic reperfusion injury in the pulmonary damage seen after smoke inhalation.

Allopurinol↗