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.

Use of the biceps femoris following failed inferior gluteal flap transfer. Case report.

Considering the high recurrence rate of pressure ulceration in paraplegic patients, flap procedures to reconstruct a defect should not be at the expense of another possible future flap. The posterior thigh fasciocutaneous flap is useful for the coverage of ischial and trochanteric pressure sores; the biceps femoris musculocutaneous flap is a useful choice for deep ischial defects. However, the cutaneous portions of these two flaps is nearly identical. The previous transfer of the biceps flap excludes the further use of the posterior thigh flap. In contrast, use of the posterior thigh flap still permits the employment of a biceps V-Y advancement flap. Even if the donor site of the previous posterior thigh flap must be skin-grafted, the graft will remain viable on its muscular bed and function as the cutaneous portion of the flap; thus stable coverage is provided, despite previous use of 'first line' flaps. We demonstrate how careful planning of the stages of flap procedures can allow the most economic use of donor areas in this difficult patient group.

Bronchial blood flow during changes in inhaled oxygen and carbon dioxide concentrations in conscious sheep.

Bronchial artery blood flow index (BFI) was measured in an unanesthetized sheep model using a chronically implanted ultrasonic flow probe. The bronchial circulation was monitored during changes of the concentrations of oxygen and carbon dioxide in inhaled air. Control BFI was 15.9 +/- 3.8 ml/min/m2 during normoxic breathing with 0% CO2 (n = 6) and 18.0 +/- 1.6 ml/min/m2 while breathing 28% O2 and 0% carbon dioxide (n = 6). Hypoxia (FIO2 = 0.10) significantly increased BFI to 25.8 +/- 4.9 ml/min/m2 with a decrease in the bronchovascular resistance index (BVRI) from a baseline of 7.85 +/- 1.73 to 4.75 +/- 0.86 mm Hg/(ml/min)/m2. Hyperoxia (FIO2 = 1.0) raised BFI to 30.5 +/- 10.1 ml/min/m2 without a significant decrease in BVRI. Changing the inhaled carbon dioxide concentration from 0 to 10% resulted in a significant increase in BFI from 18.0 +/- 1.6 to 43.6 +/- 10.3 ml/min/m2 and a decrease in BVRI from 5.56 +/- 0.44 to 4.63 +/- 2.18 mmHg/(ml/min)/m2 (not significant). The change in BFI varies directly with lymph flow for hypoxia and hypercarbia. This is consistent with changes in cardiac index, indicating probable changes in surface area being perfused in the lung. Changes in BFI with hyperoxia did not follow changes in systemic vascular resistance or cardiac index. Similarly, lymph flow elevation did not occur during hyperoxia. These data suggest that BFI changes with hyperoxia are not related to changes in total systemic vascular resistance, or cardiac index, and a different mechanism may control bronchovascular flow for this condition.

Indications for surgical débridement in 125 human bites to the hand.

Indications for operative intervention following human bites to the hand were determined based on physical examination and time elapsed since injury. One hundred twenty-four patients admitted to Charity Hospital of New Orleans, La, were stratified according to time elapsed from injury to treatment (early, less than 24 hours; delayed, 1 to 7 days; and late, greater than 7 days). Patients in the early group were mainly treated with conservative wound care, consisting of local wound exploration and irrigation in the emergency department, while those in the late group underwent surgical débridement. Patients in the delayed group either received conservative wound care or underwent débridement in the operating room. The early and late groups recovered excellent hand function while results within the delayed group were variable with improved results depending on rapid surgical débridement or drainage.

Selective permeability changes in the lungs and airways of sheep after toxic smoke inhalation.

The effect of toxic smoke inhalation on selective microvascular sieving of macro-molecules and lymph protein flux was assessed in adult sheep to determine whether the time course of microvascular dysfunction differs between the lung and trachea. Protein flux across the lung increased sixfold 48 h after inhalation of the products of incomplete cotton combustion, whereas tracheal protein flux increased fivefold 8 h after exposure and returned to near base line 48 h after exposure. The lung and trachea selectively retained some sieving to three different protein macromolecules with molecular radii of 36, 54, and 123 A. In the lungs the sieving selectivity for these macromolecules was least 48 h after injury, and in the trachea molecular selectivity was least 8 h after injury. These data suggest that the time course of microvascular injury differs for the trachea and the lung; microvascular changes are detected earlier in the trachea than in the lung. The inhalation injury described thus permits the characterization of the time course of airway and lung microvascular changes.

Airway aspiration of hydrochloric acid in sheep.

We have compared the effects of aspiration of 2.5 ml/kg of 0.1 N hydrochloric acid (HCl) on groups undergoing normal saline aspiration (2.5 ml/kg) and a sham control in unanesthetized sheep with chronic lung lymph fistula for up to 148 hr. Significant changes in pulmonary lymph flow and cardiopulmonary variables occurred in the airway acid group within the first 48 hr, as compared to saline and sham control. In the HCl group lymph flow increased from a baseline of 8.5 +/- 1.5 to 21.8 +/- 3.0 ml/hr (mean +/- SEM) at 2 hr. Pulmonary vasoconstriction occurred at this time with significant elevations of lymph thromboxane B2 from a baseline of 400 +/- 11 to 2,090 +/- 690 pg/ml. During the early acid aspiration phase products of lipid peroxidation were noted to increase from 0.29 +/- 0.03 to 0.81 +/- 0.17 absorbance units. Associated with elevated lymph flow was a significant drop in cardiac index in the airway-acid-aspirated group (6.59 +/- 0.52 to 5.53 +/- 0.36 L/min/m2) and a rise in bronchial blood flow from 9.8 +/- 1.7 to 63.7 +/- 8.9 ml/min. These data suggest that a moderate airway acid injury created by 2.5 ml/kg of HCl results in acute pulmonary damage with the release of several potential mediators which may be responsible for the observed effects. The long-term acid-injured animals survived for up to 1 week following the aspiration procedure with evidence of resolution of lung damage by wet-weight dry-weight evaluation of lung (normal lab control = 4.0 +/- 0.2, and 148 hr after acid = 4.5 +/- 0.3) and microscopic evidence of minimal persistent injury. These data document the pulmonary damage and repair resulting from airway acid instillation.

Effect of antibody-mediated neutropenia on the cardiopulmonary response to endotoxemia.

An ovine anti-neutrophil antibody has been produced by immunizing rabbits with purified sheep neutrophils. Serial intraarterial infusions of anti-neutrophil antibody in awake instrumented sheep produced selective and profound neutropenia. Intravascular infusion of endotoxin (Escherichia coli, 1.5 micrograms/kg/30 min) resulted in significant and equivalent increases in pulmonary artery pressure, peripheral vascular resistance, and protein-rich pulmonary lymph flow in an endotoxin group (n = 9) and a depletion + endotoxin group (n = 4). Changes in cardiopulmonary parameters were most pronounced 2 to 8 hr after endotoxin administration in both groups. Cardiac index (CI) showed a precipitous and transient fall in both experimental groups at 0.5 to 1 hr after endotoxin infusion; however, by 8 hr CI rose significantly in the endotoxin group, while it remained unchanged in the depletion + endotoxin group. A significant rise in the peripheral neutrophil count was associated with the increase in CI in the endotoxin group. Plasma and pulmonary lymph levels of thromboxane-B2 were unchanged during the depletion period with a significant increase 1 hr after endotoxin infusion. In this study questions arise regarding the exclusive role of circulating neutrophils in the microvascular permeability changes seen in sepsis-mediated adult respiratory distress syndrome.

The effect of leukocyte depletion on smoke inhalation injury in sheep.

Leukocytes and the production of oxygen radicals and proteolytic enzymes have been implicated in the pathogenesis of lung injury after smoke inhalation. We investigated the mechanism responsible for this form of pulmonary damage in chronically prepared sheep previously made leukopenic with intra-arterial infusions of nitrogen mustard (mechlorethamine hydrochloride). A control air insufflated group (sham: n = 6), a cotton smoke insufflated group (smoke: n = 12), and a leukopenic cotton smoke insufflation group (smoked + depleted: n = 6) were compared. Although both smoke insufflation groups had equivalent smoke exposure, which was indexed by carboxyhemoglobin, the smoked + depleted group had significant attenuation in the increases in pulmonary artery pressure, pulmonary vascular resistance, and pulmonary lymph flow. The PaO2 to FiO2 ratio (P:F) did not fall to the same extent, nor was there a fall in PaO2. The production of oxygen radicals, which was measured as plasma-conjugated dienes, and the consumption of antiprotease, as measured by alpha 2-macroglobulin levels in lung lymph, were not changed in the smoked + depleted group, whereas it was elevated in the smoked group. We conclude that circulating leukocytes and the release of oxygen radicals and proteolytic enzymes contribute to the lung injury, pulmonary microvascular permeability increase, and pulmonary edema seen after smoke inhalation.