Use of lung pressure-volume curves and helium-sulphur hexafluoride washout to detect emphysema in subjects with mild airflow obstruction

Mild abnormalities of peripheral lung function can be detected by simple methods, but it remains difficult to determine when these changes are the result of emphysema rather than disease of the airways. We have compared the value of measurements of lung distensibility and a multibreath test of helium (He) and sulphur hexafluoride (SF₆) washout in distinguishing between six men with mild impairment of airway function caused by asthma (group A) and six men with similar airway function but probable widespread emphysema (group E). In group E there were striking abnormalities in the static pressure-volume curve of the lungs (reduced lung recoil pressures, increased chord compliance, increased shape factor) and the relation between maximum expiratory flow and lung recoil pressure fell within the normal range. In group A there were only minor abnormalities in lung distensibility and maximum expiratory flow was reduced at a standard lung recoil pressure. In addition carbon monoxide transfer coefficient was reduced in group E but normal in group A. Normal values for He-SF₆ washout were similar to those previously described. Differences in He-SF₆ washout between group A and group E men were small and in part accounted for by differences in functional residual capacity. In subjects with lung disease, end-tidal He and SF₆ concentrations during washout were erratic and it was sometimes impossible to define a crossover point. We conclude that in our hands this technique is less useful for detecting acinar disease than are measurements of lung distensibility or carbon monoxide transfer. Considerable changes in lung distensibility may occur at an early stage in the natural history of emphysema and are readily distinguishable from the small changes that occur in mild asthma.     

Pulmonary function in children with systemic lupus erythematosus.

BACKGROUND: Abnormalities of pulmonary function have been found in children with systemic lupus erythematosus (SLE) even in the absence of clinical or radiographic evidence of pulmonary involvement. It is unknown whether these abnormalities represent an early sign of progressive lung disease or whether they are associated with disease activity. METHODS: After a mean of 4.5 years, respiratory function (forced vital capacity (FVC) and single breath gas transfer factor (TLCO)) and disease activity were reexamined in 13 of 15 previously studied children with SLE. Disease activity was assessed by a validated index of SLE activity (SLE activity measure (SLAM)). RESULTS: In spite of the high prevalence of abnormalities of respiratory function at the baseline investigation, no chest radiographic abnormalities or overt clinical signs of lung disease were found at baseline, in the interval between the two investigations, or at the re-evaluation in any patient. From baseline to the second investigation the mean value of SLAM decreased and there was a trend toward an improvement in FVC and TLCO. TLCO was more severely impaired than FVC, being found as an isolated abnormality in a high percentage of patients (45% at baseline and 35% at follow up). There was a relationship between baseline TLCO and disease activity, expressed as a SLAM score. Moreover, there was a correlation between the changes in the SLAM score from baseline to the second investigation and the corresponding changes in the TLCO value, but not with the corresponding changes in the FVC value. CONCLUSIONS: In this series of patients the decrease in SLE activity from the first to the second investigation was associated with an improvement in pulmonary function. The presence of early isolated functional abnormalities was not associated with subsequent development of lung disease.     

Type I collagen content is increased in lungs of patients with adult respiratory distress syndrome.

Collagen in lung tissue was examined from patients with adult respiratory distress syndrome, from patients who did not have this disease but required mechanical ventilation and oxygen treatment, and from patients without overt lung disease. Cyanogen bromide peptide mapping techniques were used to determine the ratio of type I to type III collagen present in these lungs. In the fibrotic lungs from patients with adult respiratory distress syndrome a shift was found in the ratio of type I to type III from the normal value of 2:1 to a mean value of 3.4:1. In patients with normal lungs and those with other lung diseases collagen type ratios were normal. Our data suggest that (i) changes in lung collagen of patients with adult respiratory distress syndrome resemble those previously described in patients with idiopathic pulmonary fibrosis, although the changes occur much more rapidly in the former; (ii) the increased content of collagen in lungs of patients with adult respiratory distress syndrome shown by others is predominantly of type I collagen; and (iii) the stimulus to the lung to produce excess type I collagen relative to type III is not solely of iatrogenic origin--that is, resulting from oxygen or ventilator treatment.     

CT evaluation of the paranasal sinuses in symptomatic and asymptomatic populations

The frequency of concha bullosa, paradoxical middle turbinate, and septal deviation on coronal computed tomographic scans evaluating sinus disease is known, but the incidence in normal subjects is unknown. We compared 100 consecutive scans performed for evaluation of sinus disease with 82 consecutive scans performed for evaluation of orbital pathology. Patients with sinus disease had significantly more frequent findings of disease in the osteomeatal complex and all sinuses. Concha bullosa was more common in patients with sinus disease (p less than 0.05), as was septal deviation (p less than 0.01). Paradoxical turbinate was equally common. Concha bullosa was associated with anterior ethmoid disease (p less than 0.04). Septal deviation was associated with osteomeatal complex disease (p less than 0.01) and with anterior (p less than 0.04) and posterior (p less than 0.04) ethmoid disease. Paradoxical turbinate was not associated with sinus abnormalities. These data imply a possible causal relationship between concha bullosa or septal deviation and sinus disease.     

Lung transplantation in the rat. A morphometric analysis of the gas exchange region

Single-lung transplantation in the rat provides a model that allows investigators to study immunologic, cellular, and morphologic changes associated with allograft rejection. We performed morphometric analysis of transplanted and nontransplanted lungs removed from recipients having received isografts, allografts, or hilus-stripping up to six months previously, and having received cyclosporine on the first postoperative day, the second postoperative day, the first five days, or not at all. When CsA was not administered, there was extensive and rapid destruction of the alveolar septa with consolidation and rejection of the transplanted lung within one week. In contrast, the allografts from rats treated with CsA were not obviously changed compared with the control lung. To evaluate whether or not these CsA-treated allografts had even subtle injury to alveolar septal cells, a morphometric analysis using transmission electron microscopy was used. There were no significant changes between control (nontransplanted or hilus-stripped) lungs and isografted or allografted lungs for most parameters measured. Exceptions included type I epithelial cell volume, which increased in rats treated with CsA on postoperative day 1 only, and the tissue component of diffusing capacity, which decreased in rats treated with CsA on postoperative day 2 only. We conclude that CsA treatment of rats given lung allografts effectively blocks the development of injury in the gas exchange region. The effect is achieved when the CsA is given during the first five days following transplantation in rats, and may be influenced by the timetable of administration and cumulative dosage.     

Endocrine cells in tumour-bearing lungs.

BACKGROUND: When hormones are detected in the serum of patients with bronchial carcinoma they are generally considered to originate from the tumour, but this may be not the only explanation. Pulmonary endocrine cells proliferate in lungs affected by non-neoplastic disease and their products are often demonstrable in the serum. The aim of this study was to examine the pulmonary endocrine systems of a series of tumour-bearing lungs to see whether any changes in them could possibly account for raised levels of pulmonary peptides in the blood. METHODS: The morphology, number, distribution, and content of pulmonary endocrine cells in 30 pairs of tumour-bearing lungs from patients coming to necropsy with bronchial carcinoma were examined. These features were related to the pathology of the tumour and to other pathological changes present in the lungs, and compared with pulmonary endocrine cells in 10 pairs of control lungs from patients without pulmonary disease. RESULTS: Increased numbers of endocrine cells, often in the form of large abnormal aggregates, were present in 17 pairs of tumour-bearing lungs where they were associated not with the tumour but with non-tumoral pathology, especially inflammation and changes associated with cardiac failure. Appropriate and inappropriate peptides were identified within them. CONCLUSION: The possibility is raised that, in some subjects with bronchial carcinoma who have raised serum hormone levels, the source of these substances might be the endocrine cells in the diseased lung around the tumour.     

Chromosome abnormalities in Peyronie's disease

Peyronie's disease is a localized and progressive fibrosis of unknown etiology that affects the tunica albuginea of the penis. We examined cytogenetically cell cultures derived from plaque, adjacent tunica, dermis and lymphocytes in patients with Peyronie's disease, and compared the results to cell cultures established from the tunica albuginea of control patients. Chromosomal abnormalities were detected in 9 plaque-derived cell cultures from 7 of 12 Peyronie's disease patients (58 per cent). Cells cultured from adjacent tunica, dermis and lymphocytes from the same patients were karyotypically normal, as were cultures derived from control (chordee and penile scar) patients. Chromosomal aberrations consisted of 5 numerical changes and 4 structural rearrangements, and included chromosomal additions (trisomy 7 and trisomy 8), deletions (45X,-Y), reciprocal translocations and inversions or markers. In 2 instances cultures derived from plaque tissue contained 2 independent chromosomal abnormalities. The apparently random chromosomal changes associated with Peyronie's disease suggests that karyotypic instability may be a common feature of cells within the plaque. It presently is unclear whether this finding represents multiple pathways for the development of Peyronie's disease or secondary consequences of Peyronie's disease.     

Vertical gradients of lung density in supine subjects with fibrosing alveolitis or pulmonary emphysema.

Computed tomography was used to determine the vertical gradient of density in the peripheral lung tissue of 12 patients with histologically proved fibrosing alveolitis and 12 patients with chronic bronchitis and evidence of pulmonary emphysema on the computed tomograms. Measurements were made at total lung capacity and at residual volume and compared with similar measurements from 12 normal subjects reported in a previous study. At residual volume the mean peripheral tissue density in the emphysematous lungs was 0.081 kg/l compared with 0.426 kg/l in the fibrotic lungs and 0.323 kg/l in the normal lungs. The observed densities in the three groups were compared with those in a theoretical model predicting the vertical changes of lung density caused by gravitational effects that would be found in lungs with differing compliance. The emphysematous lungs showed a much greater increase of density with descent down the lung than that predicted for normal lungs, and the results were explicable by an increase in compliance. The fibrotic lungs showed considerably less change in density than expected, implying loss of compliance. It is suggested that local changes of compliance are important determinants of vertical density gradients in diseased lungs.     

A comparative study of the effects of dry vs. humidified ventilation on canine lungs.

To compare the effects on canine ciliary and bronchial mucosal function of varying periods of ventilation with dry vs. humidified gas mixtures, 29 anesthetized dogs underwent 2, 4, and 6 hours of ventilation through a Carlen's double-lumen tube. Six dogs were evaluated by clearance studies, nine by differential bronchospirometry, six by surfactant studies, six by electron microscopy, and two by ventilation scanning. By means of two separate respiratory systems, dry gas (DG) was used to ventilate the right lung, and humidified gas (HG) ventilated the left lung in each dog. Serial chest roentgenograms showed more rapid clearance of inspired tantalum dust from the HG-ventilated lung in each of the six dogs, the disparity in clearance between the two lungs being more pronounced after longer periods of ventilation. The surface tension in DG-ventilated lungs increased fourfold, whereas in HG-ventilated lungs it increased only twofold as compared to preoperative values. Longer periods of ventilation did not change the surface tension appreciably in either DG- or HG-ventilated lungs. Scanning electron micrographs of bronchial mucosa from DG-ventilated lungs showed tangling and matting of cilia with a granular and stringy material attached to most cilia; these changes were much less pronounced in HG-ventilated lungs. Bronchospirometric studies showed an increase in ventilatory function in each of the lungs ventilated with the HG mixture (percent Vo2 on 100 percent oxygen increased 27.7 percent) to compensate for the decreased gas exchange provided by the contralateral DG-ventilated lung. Function in each of the lungs returned to normal within 24 hours. Ventilation scans with Xenon133 showed no apparent change in isotope uptake in the HG-ventilated lungs as compared to the DG lungs during the first 24 hours after ventilation. The observations from the present study suggest that ventilation of canine lungs with DG for 4 or more hours dries mucus and transiently retards mucociliary clearance and gas exchange. These changes may be minimized by ventilation with a humidified gas mixture. Application of these findings to patients undergoing prolonged general anesthesia and to lung preservation studies is suggested.     

Parenchymal, bronchiolar, and bronchial measurements in centrilobular emphysema: Relation to weight of right ventricle

Measurements of lung parenchyma, membranous bronchioles, and bronchial mucous gland hyperplasia were made on lungs from eight cases of pure centrilobular emphysema (CLE) and on five normal lungs. The lungs were fixed in formalin and inflated under partial vacuum at a standard transpulmonary pressure of +30 cm. H₂O. The results obtained from the upper halves and the lower halves of the lungs were compared. The circulatory effects of the disease were measured by weighing the heart ventricles, by studying the small pulmonary arteries in microscopical sections, and by post-mortem arteriography. Whereas the parenchymal and internal surface areas destroyed by the emphysematous spaces were relatively moderate and localized, right ventricular hypertrophy was noted in most of the cases. In these cases bronchiolar stenoses were found scattered throughout the whole lung and there was a reduction in the number of these bronchioles, mainly in the upper halves of the lungs. In CLE ventilatory disturbances were caused not only by the centriacinar dilated spaces delaying gas diffusion, but also by scattered bronchiolar stenoses situated at the termination of the conducting air passages. The stenoses seemed the more important cause. It was shown statistically that chronic arterial pulmonary hypertension and right ventricular hypertrophy were mainly the result of functional disturbances, especially hypoxia and abnormalities of VA/Q produced by the two structural changes situated at the end of the small airways.     

Renal sodium and water handling in hypothyroid patients: the role of renal insufficiency

The mechanism responsible for renal tubular abnormalities in sodium and water excretion in hypothyroid patients is poorly understood. To evaluate the possible contribution of the reduced glomerular filtration rate of hypothyroidism to these abnormalities, tubular function in hypothyroid patients was compared with that in patients with chronic renal failure and in normal subjects. The lithium clearance method and oral water loading were used to evaluate parameters of tubular sodium and water handling, respectively. The hypothyroid and the chronic renal failure patients were selected to have similar reductions in glomerular filtration rate. As compared to the normal subjects, the hypothyroid and chronic renal failure patients had a decrease in proximal sodium reabsorption and an increase in distal sodium reabsorption. The changes in tubular handling of sodium were not different in the hypothyroid and the chronic renal failure patients. Maximal urinary flow rate and free water clearances were similarly reduced in the hypothyroid patients and the chronic renal failure patients. For all subjects studied, proximal sodium reabsorption and maximal urinary volume were directly correlated with the glomerular filtration rate, and distal nephron sodium reabsorption was proportionate to delivery of sodium from the proximal tubule. The results suggest that the abnormalities in tubular sodium and water handling in hypothyroid patients are comparable to those present in other patients with a similar degree of renal insufficiency. Thus, the tubular abnormalities in hypothyroidism may be a consequence of the associated decrease in glomerular filtration rate.     

Multiple nodular pulmonary amyloidosis. A case report and comparison with diffuse alveolar-septal pulmonary amyloidosis.

A case of multiple nodular pulmonary amyloidosis in a 54-year-old Caucasian man is presented. Discrete symptomless radiodensities had developed in this patient's lungs within a period of three years, leading to a suspicion of a neoplastic process. The amyloid nature of these nodules was demonstrated by biopsy. In this case, as in others previously reported, there was no evidence of systemic disease, and immunoglobulins were normal. Local factors probably play an important part in the pathogenesis of this disease. This entity is to be distinguished from the diffuse type of pulmonary amyloidosis, which has a far graver prognosis. Diffuse alveolar septal amyloidosis is usually associated with primary systemic amyloidosis or multiple myeloma and leads rapidly to respiratory distress.     

胰腺炎相关性腹水诱导大鼠肺损伤的实验研究

目的研究大鼠经腹腔内注射胰腺炎相关性腹水（pancreatitis associated ascetic fluid,PAAF）诱导的急性肺损伤的动物模型,并探讨其意义。方法大鼠腹腔内注射PAAF,制作PAAF诱导的肺损伤模型,分别于7h和12h后活杀,观察胰腺及肺脏组织结构的变化,结合动脉血气分析,外周血白细胞计数及血清淀粉酶测定,评估该动物模型。结果模型制成后,肺脏出现明显的肺损伤的病理改变,镜下表现为肺问质水肿以及肺泡和间质内大量的炎性细胞浸润。而胰腺病理学改变程度轻微,仅有组织水肿及少量的炎性细胞浸润。Pan水平显著降低,外周血白细胞升高。结论胰腺炎相关性腹水诱发的肺组织损伤与临床急性出血坏死性胰腺炎（acute hemorrhage necrotizing pancreatitis,AHNP）并发的肺损伤病理过程相似,而且本模型中胰腺本身病变程度轻微,可以为研究AHNP时肺损伤的发病机制提供较为单纯的研究背景,且可以用于临床药效评估的研究。     

Need for closure of secundum atrial septal defect in infancy

OBJECTIVES: Closure of isolated secundum atrial septal defect is generally recommended at the age of 4 to 5 years. However, there are children with isolated secundum atrial septal defect in whom early closure should be performed. We aimed to assess the underlying conditions that led to earlier closure in this special patient group and to analyze the outcome. METHODS AND RESULTS: From January 1990 through August 2002, 24 infants with isolated secundum atrial septal defect underwent surgical closure within the first year of life. All children were symptomatic. Signs of pulmonary hyperperfusion, such as tachydyspnea, failure to thrive, recurrent respiratory infections, or heart failure, were present. Four infants required artificial ventilation. Ten patients had additional problems, such as prematurity with chronic lung disease, hepato-omphalocele and congenital diaphragmatic hernia, which were present in 1 patient each. Eleven patients had defined dysmorphic syndromes. All but 1 infant underwent preoperative invasive hemodynamic evaluation. Thirteen patients had pulmonary hypertension preoperatively. The follow-up time was 46 +/- 33 months (range, 4-125 months). At follow-up, pulmonary artery pressure proved to be normal in 11 of the 13 children who had pulmonary hypertension previously. One patient died of persistent pulmonary hypertension. Clinical performance, growth, and development improved in nearly all patients. All ventilator-dependent children could be weaned shortly after atrial septal defect closure. CONCLUSIONS: If lungs are compromised, even a minor left-to-right shunt might be poorly tolerated in infancy. In these children early surgical closure of an isolated secundum atrial septal defect should be performed to support thrive and growth and to prevent the onset of irreversible changes of the pulmonary vasculature.     

Bronchial artery perfusion during cardiopulmonary bypass does not prevent ischemia of the lung in piglets: assessment of bronchial artery blood flow with fluorescent microspheres.

OBJECTIVE: Blood supply of the lungs during total cardiopulmonary bypass (CPB) is limited to flow through the bronchial arteries. This study was undertaken to assess the bronchial artery blood flow during CPB with fluorescent microspheres in a piglet model. METHODS: We subjected ten piglets (mean weight 5.0+/-0.5 kg) to 120 min of normothermic, total CPB without aortic cross-clamping, followed by 60 min of post-bypass perfusion. Fluorescent microspheres were injected into the left atrium or the aortic cannula or distal to the cannula to assess bronchial artery blood flow before, during and after CPB. The reference samples were taken from the descending aorta. We compared the different sites of injection. Tissue samples of the lungs were taken before and 60 min after CPB. RESULTS: Before CPB, total bronchial artery perfusion was 43.6+/-14.1 ml/min (4.8+/-1.3% of cardiac output) as by injection distal to the aortic cannula. These values were not different when microspheres were injected into the left atrium or the aortic cannula. There was no difference in scatter or in the amount of microspheres in the reference samples among the three injections sites. During CPB, bronchial artery perfusion was significantly decreased (4.4+/-2.4 ml/min vs. 40.0+/-5.0 ml/min before CPB) and returned to baseline values 60 min after CPB. Light microscopy of the tissue samples revealed alveolar septal thickening and a decrease in alveolar surface area after 60 min of reperfusion which was associated with a decreased capacity to oxygenate blood. CONCLUSIONS: (1) Bronchial artery blood flow can quantitatively be assessed during CPB when microspheres are injected into the ascending aorta and the reference samples are taken from the descending aorta. (2) Despite adequate perfusion pressure bronchial artery blood flow is decreased substantially during CPB. (3) The decrease in blood flow and the ultrastructural changes present at the end of CPB suggest the presence of low-flow ischemia of the lung during total CPB.     

Pulmonary injury in recipients of discordant hepatic and renal xenografts in the dog-to-pig model

Abstract: Work in our lab demonstrated that the early post-operative course of discordant hepatic and renal xenotransplantation is complicated by a pulmonary injury. The aim of this study was to characterize the nature of this injury, as well as to determine whether endothelin-1 (ET-1) and inducible-nitric oxide synthase (iNOS) are present in this form of pulmonary injury. Dog-to-pig orthotopic liver and kidney xenografts were performed. Pulmonary artery pressures were monitored throughout all procedures. The lungs were stained with monoclonal antibodies for ET-1, endothelin converting enzyme-1, and iNOS. The lungs from pig recipients of hepatic or renal xenografts were compared to lungs from untreated pigs. Pulmonary artery pressures were elevated in recipients of liver xenografts when the suprahepatic caval cross clamp was placed and continued to rise to systolic levels following unclamping. The mean pulmonary artery pressures in recipients of renal and hepatic xenografts rose significantly following revascularization. Pathology in lungs from kidney and liver recipients was similar, showing congestion with peribronchial and septal edema, with diffuse adhesion of PMN to alveolar endothelium. ET-1, endothelin converting enzyme-1 (ECE-1), and iNOS staining was widespread and intense in alveolar and pulmonary arterial endothelium. Discordant xenotransplantation of livers and kidneys is associated with a significant early pulmonary injury that is associated with early PMN infiltration and expression of ET-I and iNOS.     

Clinical outcomes for the surgical treatment of sinonasal headache.

OBJECTIVE: This study was designed to explore the changes in patient-relevant clinical outcomes in a selected group undergoing surgery for nasal septal and turbinate abnormalities.Study design Seventy-nine consecutive patients with headache and correctable anatomic nasal obstruction were seen at the study institution from March 1998 to May 2000. These patients were evaluated for changes in patient-relevant clinical outcomes measures after surgical correction of their anatomic abnormalities. RESULTS: Seventy-one patients underwent surgical correction of nasal obstruction. More than half of these patients had contact points preoperatively. Statistically significant improvements were observed in the patient population with respect to 8 of the 10 clinical outcomes measures. Importantly, a decrease in the severity and frequency of headaches was noted after surgery, especially after the correction of contact points. CONCLUSION: The surgical correction of the septum and turbinates resulted in predictable improvement in headache and a majority of other important outcomes measures.Clinical significance Pain may improve after surgical correction of septal and turbinate abnormalities in a properly selected group.     

Abnormalities in von Willebrand factor and antithrombin III after cardiopulmonary bypass operations for congenital heart disease.

In patients with congenital heart disease two poorly understood postoperative complications are pulmonary hypertensive crises after repair of large atrioventricular or ventricular septal defects and right atrial and pulmonary thrombi after the Fontan operation. In this study we assessed whether cardiopulmonary bypass in these patients is associated with the release of agents that might induce platelet aggregation and vasoconstriction, such as biologically active von Willebrand factor and platelet-activating factor. In addition, we measured levels of anticoagulants such as antithrombin III and proteins C and S. Three groups of patients with congenital heart disease undergoing cardiopulmonary bypass were monitored through the perioperative period for secundum atrial septal defects, large atrioventricular or ventricular septal defects, and tricuspid atresia or univentricular heart (Fontan candidates). Control values were obtained from age-matched patients; patients requiring major noncardiac operations and those with cardiac disease not requiring cardiopulmonary bypass were also studied. After cardiopulmonary bypass in all three groups biologic activity of von Willebrand factor increased markedly in the immediate and early postoperative periods compared with preoperative values, whereas antithrombin III values were decreased. Platelet-activating factor was detected in only two patients with congenital heart disease, both in the early postoperative period. In contrast, patients who did not have cardiopulmonary bypass did not show these abnormalities. All measured parameters normalized at late follow-up (6 to 18 months after operation). Although cardiopulmonary bypass in these patients resulted in increased von Willebrand factor activity and decreased antithrombin III, changes that may predispose the patient to platelet aggregation and thrombus formation, absolute values in individual patients alone were not predictive of pulmonary hypertensive crises or detectable thrombi. This suggests that these hematologic abnormalities may contribute to but are not by themselves a cause of morbidity in the early postoperative period. Moreover, the increased von Willebrand factor biologic activity seen postoperatively in patients with congenital heart disease suggests that use of synthetic vasopressin may be ineffective and potentially detrimental.     

Early mortality after surgical repair of postinfarction ventricular septal rupture: Importance of rupture location

Background. Right ventricular (RV) dysfunction is a common but poorly understood problem associated with mechanical left heart assist (LHA). Left ventricular unloading may affect RV function even in normal hearts by altering geometry or function of the interventricular septum, although such changes have not been well defined. Accordingly, the purposes of this study were to quantify the effects of LHA on septal geometry and function in normal swine and to assess the resultant effects on RV function.

Methods. Domestic swine (50 kg, n = 10) were anesthetized and instrumented for collection of physiologic data and for open-chest LHA, which was accomplished by left atrial to subclavian artery bypass using a centrifugal pump. Both global and regional RV function data as well as two-dimensional echocardiographic data of septal geometry and function were collected at control levels and during both partial and full LHA. Short-axis echocardiographic images were obtained at the midventricular level and analyzed to quantify septal curvature (k; cm⁻¹), systolic septal thickening (%), and systolic septal excursion (cm).

Results. Partial LHA had no effect on either septal geometry or function. Full LHA resulted in decreased diastolic septal curvature (k = 0.10 ± 0.07 versus 0.42 ± 0.06 at control; p < 0.05), reduced systolic septal thickening (0.27 ± 5.23 versus 29.32 ± 8.61 at control; p < 0.05), and reversed leftward systolic septal excursion (−0.29 ± 0.11 versus 0.11 ± 0.03 at control; p < 0.05). End-diastolic septal position was shifted leftward during full LHA compared with control, but was associated with rightward systolic motion of the left ventricular mass and septum as a unit. There were no changes in global or free-wall RV function during either partial LHA or full LHA compared with control.

Conclusions. Left heart assist results in marked changes in both geometry and function of the interventricular septum in normal hearts. These changes, however, do not appear to be associated with changes in either global or regional RV function. Evaluation of the septum with echocardiography may be helpful in defining strategies for clinical application of this technology.     

Long-term fate of lung autografts charged with providing total pulmonary function. I. Light and electron microscopic studies.

Two groups of dogs underwent light and electron microscopic examination of both lungs up to five years after left lung autotransplantation. In one group of four dogs that had undergone ligation of the right pulmonary artery at the time of left lung autotransplantation, no generalized or consistent lesions were present in the transplant except for slight distension of net capillaries and slight capillary basement membrane thickening. Aside from theseminor changes which were probably of no functional significance, most areas of lung examined up to five years after transplantation were normal. In the second group of four dogs that did not have contralateral pulmonary artery ligation at the time of left lung autotransplantation, no consistent abnormality was present in either the transplanted left or nontransplanted right lung. In three animals in this group, widespread normal areas were present bilaterally up to five years after transplantation. One animal in this group had focal changes consistent with chronic pulmonary disease in both of its lungs. Thus, transplanted lungs do not necessarily develop significant late pathologic lesions.