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Biomedical subjects

R G Spragg

Publications and source records attributed to R G Spragg.

67 records · Page 4Linked to original sources
PubMed1982

Studies on the pathogenesis of the adult respiratory distress syndrome.

Bronchoalveolar lavage (BAL) fluid was obtained from 24 sequentially studied patients with adult respiratory distress syndrome (ARDS) for assessment of potential activating and mediating factors. Proteolytic activity of the fluids was observed by measuring cleavage of radiolabeled proteins of the contact (Hageman factor) and complement systems. Proteolytic activity was observed in 17 of 24 (71%) patients with ARDS, and BAL fluid of the 7 ARDS patients without demonstrable, active, enzyme exhibited inhibitory activity for the proteolytic activity. The enzymes cleaved Hageman factor, prekallikrein, plasminogen, high molecular weight kininogen, C4, C3, C5, and Factor B of the complement system. Cleavage of the contact system proteins producted fragments similar or identical in size to the fragments observed during activation of these molecules, although continued incubation invariably reduced the protein to small peptide fragments. None of 7 normal individuals, and 29 of 99 patients (29%) with other forms of pulmonary disease contained measurable enzymes. The proteolytic activity in BAL fluid of ARDS patients was blocked by diisopropylphosphofluoridate (0.1 mM), Trasylol, soybean trypsin inhibitor, and normal plasma, or plasma deficient in inhibition of the first component of complement. Alpha(1)-proteinase inhibitor (alpha1-PI)-deficient plasma failed to inhibit the proteolytic activity and addition of alpha1-PI to the deficient plasma reconstituted the inhibition. MUCH OF THE PROTEOLYTIC ACTIVITY OF THE BAL FLUID FROM ARDS PATIENTS WAS IDENTIFIED AS NEUTROPHIL ELASTASE: the fluids cleaved elastin and synthetic peptide substrate of neutrophil elastase, neutrophil elastase antigen was present in the BAL fluids as determined immunologically using antineutrophil elastase, alpha1-PI was the major inhibitor in plasma, and the enzyme was inhibited by diisopropylphosphofluoridate but not chelation. In addition, purified neutrophil elastase produced cleavage fragments of proteins of the contact system similar to those of the BAL fluids. In each of the seven BAL fluids of ARDS patients that did not reveal active elastase, alpha1-PI was present in active form (as determined by (125)I-trypsin binding). In 9 of the 17 patients with active elastase in the BAL fluid, alpha1-PI antigen was present in the fluid, but was inactive (no binding of (125)I-trypsin). Immunoelectrophoretic analysis of elastase and alpha1-PI throughout proteins in these BAL fluids revealed the presence of both elastase and alpha1-PI that migrated with the same R(f), suggesting the presence of an enzyme-inhibitor complex. Free, inactive alpha1-PI was also observed in these fluids. The data reveal that in BAL fluids from all 24 patients with ARDS, leukocytic elastase and/or alpha1-PI exist. A complex of elastase and alpha1-PI was observed in BAL fluids, and in some cases where active enzyme and alpha1-PI coexisted, free, but inactive alpha1-PI was present.

Adult↗
PubMed1982

Pulmonary endarterectomy for chronic thromboembolic obstruction: recent surgical experience.

Pulmonary thromboendarterectomy for chronic pulmonary emboli was performed on ten patients, ages 20 to 67 years, between July 1977 and June 1981. Five patients each were assigned to New York Heart Association functional classes III and IV. All patients had pulmonary hypertension and increased pulmonary vascular resistance. Obstruction beginning in the lobar arteries and involving more than 50% of the sequential arteries was present in all patients. Five patients had complete obstruction of a pulmonary artery. All patients had obstructive disease in both lungs. Pulmonary thromboendarterectomy was performed through central pulmonary arteriotomies and by use of deep hypothermia and circulatory arrest. Circulatory arrest was employed in one to four periods totaling up to 60 minutes. No neurologic deficit was observed. All patients developed reperfusion edema in the lungs. All patients had improvement in pulmonary hypertension and pulmonary vascular resistance. One patient died of lung failure in the late postoperative period. All survivors had improved lung function, with two functional classes in seven patients. Improvement in one equaled three functional classes and in one, by one functional class.

Adult↗
PubMed1981

Deep venous thrombosis and pulmonary embolism. Frequency in a respiratory intensive care unit.

Radiofibrinogen leg scans were performed in 34 patients admitted to a respiratory intensive care unit (ICU) for treatment of acute respiratory failure. In 23 patients, the leg scans were performed during the first ICU week, and abnormal leg scans developed in three (13%). In 11 patients, leg scans were done beyond the first week; all were normal. Autopsy incidence of embolism was 20%. No patient died of embolism. The low frequency of fatal embolism had led us to discontinue the routine use of low-dose heparin prophylaxis in these patients in our respiratory ICU. In its place, we have substituted an ongoing investigation of noninvasive monitoring with both radioactive fibrinogen leg scanning and impedance plethysmography. From such investigations should emerge more definitive strategies for dealing with venous thromboembolism in this complex patient population.

Acute Disease↗
PubMed1981

Massive pulmonary infarction during total cardiopulmonary bypass in unanesthetized spontaneously breathing lambs.

We provided total cardiopulmonary support for 1-18 hours in unanesthetized tethered lambs by peripheral vascular cannulation, using a roller pump and the spiral membrane lung. Respirations were allowed to remain spontaneous and unaided. A Swan-Ganz catheter was placed for retrograde pulmonary artery blood flow sampling. Within a few minutes following induced ventricular fibrillation the PCO2 of sampled blood flowing retrograde through the lungs fell below 10 mm Hg, the PO2 rose to near 150 mm Hg, the pH rose to above 7.8, and the glucose level fell to less than 20 mg %. All of these values later gradually shifted, approaching mixed venous blood values within minutes. After 1-18 hrs of perfusion the animals went into shock and were sacrificed. At autopsy, the lungs of animals breathing room air were beefy and hemorrhagic. In lambs that were "breathing" CO2 enriched air the retrograde pulmonary artery blood pH and PCO2 was usually maintained close to the mixed venous blood values. The observed pulmonary changes were considerably less abnormal, and the microscopic abnormalities were at times nonexistent. We believe the integrity of pulmonary blood flow is vital to the survival of the lungs as a functioning organ. Cessation of total forward pulmonary blood flow (unlike partial cardiopulmonary bypass), combined with spontaneous pulmonary ventilation, rapidly leads to massive, pulmonary infarctions, shock, and death.

Alkalosis, Respiratory↗
PubMed1980

Cardiopulmonary consequences of decompression stress.

Clinically undetectable venous gas emboli (VGE) can be routinely demonstrated in both animals and men undergoing clinically uneventful decompression from hyperbaric environments. The effect of VGE on gas exchange and pulmonary hemodynamics in this setting is unclear. We therefore have studied the cardiopulmonary effects of clinically uneventful decompression on unanesthetized sheep. Sheep were instrumented with a femoral arterial catheter, Swan-Ganz catheter, chronic tracheostomy, and were loosely restrained in the prone position. Following baseline measurements of pulmonary artery pressure (pPA), mean pulmonary artery wedge pressure (pPAw), cardiac output (CO), arterial and mixed venous blood gases, Doppler ultrasonic bubble detection, and V/Q scans using 133Xe, the animals were exposed to: (a) a 15-min exposure to 6.03 ATA (n = 8), (b) a 17.5-min exposure to 6.03 ATA, or (c) a 15-min control period at 1 ATA (n = 7). All measured parameters remained unchanged in the control group. VGE were detected in all animals exposed to pressure. In both exposure groups CO fell 20% (P < 0.05) and pulmonary vascular resistance (PVR) rose 60% (P < 0.05) compared to the control group. This rise in PVR was significantly in excess of that predicted for the observed fall in CO. Analysis of pPA and pPAw suggested neither right nor left ventricular failure. No significant abnormalities of gas exchange were detected. V/Q scans remained unchanged in all animals. We conclude that CO and PVR are altered by clinically uneventful decompression stress.

Animals↗
PubMed1980

Distribution of ventilation in the turtle Pseudemys scripta.

Spontaneously ventilating turtles, Pseudemys scripta, were allowed to rebreathe 133Xe to equilibrium. Frequent gamma camera images were obtained and processed to allow regional evaluation of ventilation. The distribution of ventilation was markedly inhomogeneous, with washin to equilibrium most rapid in anterior lung compartments and slowest in posterior lung compartments. Similarly washout from equilibrium was most rapid in anterior compartments and slowest in posterior compartments. During apnea intercompartmental gas exchange occurred rapidly during spontaneous activity of the limbs or, more slowly, during episodes ascribed to regional contraction of lung smooth muscle. Despite inhomogeneous ventilation, overall washout of 133Xe could be monoexponential. A simple series model of the turtle lung is consistent with the inhomogeneous ventilation observed.

Animals↗
PubMed1980

Study of factors that may condition scintigraphic detection of venous thrombi and pulmonary emboli with indium-111-labeled platelets.

Incorporation of indium-111-labeled platelets (In-111-P) into venous thrombi and pulmonary emboli may permit rapid detection of these thromboemboli by gamma imaging. In a series of dogs in which femoral-vein thromboses and/or pulmonary embolism were induced experimentally by stasis and small amounts of thrombin, we addressed several questions pertinent to the sensitivity, specificity, and potential applicability of this approach. We found that when In-111-P were injected intravenously before thrombus induction or embolus release, femoral-thrombus images were consistently detectable within 15 min, whereas control femoral-vein images were unremarkable. Pulmonary emboli were also promptly imaged, and such In-111-P images agreed well with defects on Tc-99m MAA perfusion scans. When thrombi were aged in vivo for up to 10 hr after formation, they could still be imaged within 20-90 min after In-111-P injection. Administration of heparin, as an initial bolus followed by constant infusion, blocked platelet deposition on femoral-vein thrombi as assessed by both thrombus-to-blood ratios and failure to image. Injection of protamine at 6 hr, however, resulted in prompt thrombus imaging. These data indicate that this approach may well have applicability to the detection of thromboemboli in humans, since imaging remains possible in canine thrombi aged in vivo for 10 hr so long as heparin therapy has not been instituted. The dose of heparin required to inhibit imaging is not known. However, if these data prove comparable in humans, they suggest that imaging of thromboemboli could be achieved so promptly that only modest delay in the institution of heparin therapy would be required.

Animals↗