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Biomedical subjects

C A Henke

Publications and source records attributed to C A Henke.

8 recordsLinked to original sources
PubMed1992

Obliterative bronchiolitis after lung transplantation: a fibroproliferative disorder associated with platelet-derived growth factor.

Fibroproliferative disorders are characterized by accumulations of mesenchymal cells and connective tissue in critical locations, leading to organ dysfunction. We examined the role of platelet-derived growth factor (PDGF) in the pathogenesis of obliterative bronchiolitis, a fibroproliferative process that occurs after lung transplantation and results in small airway occlusion. Bronchoalveolar lavage fluid from obliterative bronchiolitis patients significantly stimulated fibroblast migration, whereas fluid from patient controls did not. Quantitation by radioligand binding assay demonstrated increased concentrations of PDGF in lavage fluid from obliterative bronchiolitis patients (patients, 104 +/- 26.9 pM; controls, 8.4 +/- 6.9 pM; P < 0.01). Heparin affinity, gel filtration, and Western blot analysis confirmed the presence of PDGF in lavage fluid. Immunohistochemical and in situ hybridization studies of histologic sections and bronchoalveolar lavage cells suggest that alveolar macrophages are one cellular source. Prospective evaluation of sequential bronchoalveolar lavage samples from a patient who developed obliterative bronchiolitis demonstrated markedly increased PDGF concentrations before the onset of irreversible airflow obstruction. These findings are consistent with a role for PDGF in the fibroproliferative changes observed in obliterative bronchiolitis.

Adult↗
PubMed1992

Intrapleurally administered streptokinase in the treatment of acute loculated nonpurulent parapneumonic effusions.

Adequate pleural drainage is believed to be an essential component of the management of low pH-low glucose parapneumonic effusion. Parapneumonic effusions may become loculated rapidly, preventing adequate drainage with a single chest tube. Administration of intrapleural streptokinase may be effective in promoting drainage for loculated, nonpurulent low pH-low glucose parapneumonic effusions when fibrin adhesions may not yet be organized. Intrapleural streptokinase was used in 12 patients with relatively large, symptomatic, loculated, nonpurulent parapneumonic effusions in whom the initial thoracentesis demonstrated a pH less than or equal to 7.0 and/or glucose less than or equal to 40 mg/dl, and when inadequate drainage was demonstrated roentgenographically despite tube thoracostomy. Mean pleural fluid WBC was 9,750/mm3 (range, 1 to 27 K), and pleural fluid glucose and pH were 33 +/- 21 mg/dl and 6.95 +/- 0.19, respectively. A solution of streptokinase, 250,000 units in normal saline, was given intrapleurally via the chest tube. Effectiveness of intrapleural streptokinase was assessed radiographically and by monitoring the volume of fluid drained from the chest tube after streptokinase instillation. A greater than 50% improvement in the CXR was seen in nine of 12 patients after intrapleural administration of streptokinase. The volume of fluid out in the first 48 h post-streptokinase was 849 +/- 836 ml (range, 100 to 3,000). In addition, clinical improvement (decreased chest discomfort, less dyspnea, or reduced fever) was noted in eight of 12 patients after streptokinase treatment. We conclude that intrapleural administration of streptokinase is an effective adjunct to the management of nonpurulent, loculated parapneumonic effusions that may reduce the need for multiple chest tubes or surgical drainage.

Acute Disease↗
PubMed1991

Lung transplant pathology. A comparative study of pulmonary acute rejection and cytomegaloviral infection.

This article describes a comparative study performed to determine the histologic features of pulmonary rejection and cytomegaloviral (CMV) infection following lung transplantation. Rejection was defined clinically by findings of new pulmonary symptoms or radiographic changes or decreased oxygenation in the absence of documented infection in patients who were treated for rejection and improved. These patients also had negative CMV cultures. CMV infection was studied in a group of non-lung and non-bone marrow transplant patients and was defined by the presence of characteristic nuclear inclusions in lung biopsies. Ten rejection biopsies and nine CMV biopsies were examined. No histologic feature was unique to rejection, however; perivascular lymphocytic infiltrates occurred more frequently and more intensely in rejection than in CMV infection (p = 0.0029). Endothelialitis also occurred more frequently in rejection (p = 0.0331), but it was always seen in association with perivascular lymphocytic inflammation. In rejection, the inflammatory infiltrate was primarily perivascular, with extension into the interstitium in several cases. In contrast, CMV infection was characterized predominantly by interstitial inflammation with involvement of associated vessels. We conclude that although overlapping features are present in both processes, pulmonary rejection can be distinguished from CMV infection on the basis of histology.

Adolescent↗
PubMed1991

Acute lung injury. Pathogenesis of intraalveolar fibrosis.

In patients dying with acute lung injury, interstitial mesenchymal cells migrate into the airspace where they replicate and deposit connective tissue. We therefore hypothesized that peptides capable of promoting mesenchymal cell migration and replication would be present in the alveolar airspace. To examine this hypothesis, patients with severe acute diffuse lung injury (n = 26) underwent bronchoalveolar lavage. Acutely ill patients without lung injury served as controls (n = 12). Recovered effluent was examined for mesenchymal cell growth-promoting and migration-promoting activity. Lavage cell supernates from both patients and controls were devoid of bioactivity. However, substantial growth-promoting and migration-promoting activity was present in lavage fluid from nearly every patient, whereas little or none was present in fluid from controls. Characterization of the bioactivity indicated a significant proportion consisted of three peptides related to PDGF: (a) a 14-kD peptide that shared with PDGF several biophysical, biochemical, receptor-binding, and antigenic properties; (b) a 29-kD peptide that appeared identical to PDGF of platelet origin; and (c) a 38-kD peptide that was biophysically and antigenically similar to PDGF. These data indicate that peptide moieties are present in the airspace of patients after acute lung injury that can signal mesenchymal cell migration and replication.

Adolescent↗
PubMed1990

Mechanisms of alveolar fibrosis after acute lung injury.

In patients who die after severe acute lung injury, a dramatic fibroproliferative response occurs within the alveolar air space, interstitium, and microvessels. Profound shunt physiology, dead space ventilation, and pulmonary hypertension are the physiologic consequences of this fibroproliferative response. The anatomic pattern of the response is unique within each alveolar compartment. For example, the air space is obliterated by granulation tissue, with replicating mesenchymal cells, their connective tissue products, and an expanding network of intra-alveolar capillaries. In contrast, the vascular fibroproliferative response is dominated by mesenchymal cell replication and connective tissue deposition within the walls of microvessels. Despite the unique anatomic features of these fibroproliferative processes, the regulatory signals involved are likely to be similar. Although our current understanding of the signals regulating the fibroproliferative response to acute lung injury is limited, inferences can be made from in vitro studies of mesenchymal cell behavior and several better understood fibroproliferative processes, including wound healing and chronic fibrotic lung diseases. As clinicians, our future ability to enhance effective lung repair will likely utilize therapeutic strategies specifically targeted to the signals that regulate the fibroproliferative process within the alveolar microenvironment.

Acute Disease↗
PubMedDate not supplied

Single lung transplantation for severe emphysema.

UNLABELLED: Lung transplantation is effective therapy for patients with severe obstructive lung disease. We reviewed seven patients with severe emphysema (age, 48 +/- 5 years; forced expiratory volume in 1 second [FEV1] 0.76 +/- 0.26 liters) who received single-lung transplants (SLT) at our institution between August 1989 and September 1990. Studies to assess the adequacy of cardiac function before transplantation showed moderately reduced right ventricular function (by multiple gated acquisition, 34 +/- 6%), moderately elevated pulmonary artery pressure (25 +/- 3 mm Hg), and normal left ventricular function (by multiple gated acquisition 65% +/- 12%) and coronary arteriograms. Time on the waiting list before transplantation was reduced compared with heart-lung transplant (HLT) recipients (waiting time, 2.9 +/- 1.5 months for SLT, 9.6 +/- 10.2 months for HLT). Six of the SLT recipients are currently alive (after transplantation interval, 17 +/- 5 months); the remaining recipient died of pulmonary embolism 21 days after SLT. Number of ventilator days, intensive care unit days, and days to hospital discharge after transplantation did not differ significantly from HLT recipients. Cardiopulmonary bypass was necessary in four SLT recipients. Pulmonary function was markedly improved after SLT (FEV1, 1.78 +/- 0.73 L/min after SLT versus 0.75 +/- 0.3 L/min before SLT; p less than 0.01), and functional status is correspondingly improved. CONCLUSIONS: SLT constitutes effective therapy for patients with severe emphysema, including those with moderate reduction of right ventricular function; and SLT offers distinct advantages over HLT, including decreased waiting time before transplantation, improved donor organ utilization, and less frequent need for cardiopulmonary bypass.

Female↗