Technical failure of desflurane vaporizer Tec-6.
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Biomedical subjects
S Abdi
Publications and source records attributed to S Abdi.
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↗
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↗
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↗
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↗
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↗
Determination of pulmonary microvascular reflection coefficient in sheep by venous occlusion.
We devised a technique that permitted elevation of pulmonary pressures in unanesthetized sheep by occluding their pulmonary veins. Using this technique, we raised pulmonary capillary pressure from a baseline of 13.2 +/- 2.2 to 35.3 +/- 5.1 mmHg. This increased lung lymph flow (from 8.8 +/- 2.7 to 53.1 +/- 13.9 ml/h). We estimated the pulmonary microvascular oncotic reflection coefficient and found it to be 0.82 +/- 0.05 (SD). The filtration coefficient was 0.019 +/- 0.005 ml.mmHg-1.min-1. During the period of increased pressure, the animals had stable arterial pressures and cardiac outputs. None of the animals developed blood coagulation problems. These data illustrate the usefulness of pulmonary venous occlusion to elevate pulmonary microvascular pressure to obtain plasma-to-lymph protein concentration ratios independent of flow, allowing for the calculation of the oncotic reflection coefficient.
Animals↗
Inhalation injury to tracheal epithelium in an ovine model of cotton smoke exposure. Early phase (30 minutes).
The purpose of this study was to evaluate lung cell injury during the acute phase of smoke inhalation injury. A group of 10 sheep were anesthetized with halothane and pancuronium followed by endotracheal intubation. In the first experiment 5 sheep were given air (sham group) and 5 were insufflated with cooled cotton smoke with a modified bee smoker. In the second part of our study (Experiment 2) the animals were insufflated with the following number of smoke breaths: 1 x 12 (n = 3); 2 x 12 (n = 4); 3 x 12 (n = 4) 4 x 12 (n = 4); and sham control (n = 1). After 30 min the animals were killed with KCl and the trachea prepared for scanning, transmission electron, and light microscopy. Our initial observation with scanning electron microscopy revealed a large amount of mucus on the surface of the epithelia. Numerous ciliated cells had been sloughed from the epithelium and were observed on the surface of the remaining ciliated cells. The sloughed cells were intact, and the cilia remained on the apical cell surface. Light and transmission electron microscopy revealed that most goblet cells were in the process of extruding mucus. The cytoplasm of goblet and basal cells appeared normal. Ciliated cells had a slightly vesiculated cytoplasm, and many were in the process of being sloughed from the epithelial surface. In these cells desmosomal attachment had been separated. The light microscope evaluation of the tracheal epithelium showed there was no dose-dependent effect between the four treatment groups.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Time course of alterations in lung lymph and bronchial blood flows after inhalation injury.
The effects of inhalation injury on the pulmonary microvascular fluid flux and bronchial blood flow were examined in a long-term study of sheep (N = 13). They were insufflated with either 48 breaths of cotton smoke (n = 8) or air (n = 5) while they were deeply anesthetized with halothane. After injury, anesthesia was discontinued and the animals were mechanically ventilated throughout the experimental period (24 hours). Bronchial blood flow increased significantly at all time points recorded and reached its peak 20 minutes after the inhalation trauma (11 +/- 1 ml/hr to 106 +/- 18 ml/hr; p less than 0.05). Thereafter, bronchial blood flow decreased to a value that was six to eight times above the baseline measurement for the remainder of the study period. With these changes in blood flow, there was a concomitant increase in lung lymph flow. This variable gradually increased and was 633% of the baseline value (6 +/- 1 ml/hr to 44 +/- 8 ml/hr) 24 hours after the challenge with smoke. The control animals showed little or no change in cardiopulmonary function during the experimental period. There is no correlation between the increase in bronchial blood flow and lung lymph flow patterns after cotton smoke inhalation injury.
Animals↗
[Mixed cryoglobulinemia with monoclonal IgA and biclonal IgM during hepatitis C virus infection].
Cryoglobulins are immunoglobulins that precipitate at low temperature and dissolve when warmed. According to Brouet, their classification relies upon the immunochemical study: type I comprises monoclonal immunoglobulins (IGG), when types II and III include both monoclonal and polyclonal components. During C hepatitis, the presence of a cryoglobulin, essentially made of mixed G-IGG and M-IGG, is a common feature with a prevalence of 40 to 80%. The authors report a case of a 63-year patient who presented with a vascular purpura and a peripheral polyneuropathy in a context of C hepatitis infection. The cryoglobulin found was composed of a monoclonal kappa A-IgG associated with a biclonal kappa and lambda M-IgG. No decrease of normal IgGs was found. This type of cryoglobulin does not belong to Brouet's classification, and argues for a new and more pertinent classification to be proposed.
Antibodies, Monoclonal↗