Complete video-assisted resection of trilobar mucormycosis.

A case of trilobar pulmonary mucormycosis in a diabetic patient with severe obstructive pulmonary disease, successfully treated with systemic antifungal therapy and complete video-assisted thoracic surgery (VATS) resection, is presented. The VATS approach permitted accurate diagnosis and definitive therapy using lung-sparing techniques in a minimally invasive manner.

Video-assisted thoracic surgery resection of chest wall en bloc for lung carcinoma.

A video-assisted thoracic surgery approach to en bloc resection of lung cancer invading the chest wall is described. Using a minimally invasive surgical approach combined with neoadjuvant external beam radiotherapy, complete resection of an upper lobe carcinoma invading two rib segments was performed in a manner that permitted complete resection with curative intent and allowed for rapid recovery.

Video-assisted thoracic surgical non-rib spreading simultaneously stapled lobectomy: a more patient-friendly oncologic resection.

OBJECTIVE: To evaluate the outcomes from a new surgical technique for lobectomy. PATIENTS: Two hundred fifty consecutive patients with an average age of 67.3 years underwent simultaneously stapled lobectomy. METHODS: Video-assisted thoracic surgical non-rib spreading lobectomy (VNSSL) is a new technique that has been evolving for approximately 6.5 years. During 1990, we began using video-assisted thoracic surgery (VATS) for simple, benign diseases. Throughout 1991, VATS was applied to malignant problems, ie, mediastinal masses, staging of lymph nodes, malignant effusions, and coin lesions. As experience was acquired, more complex procedures were attempted, such as lobectomy. On September 9, 1991, our first VATS lobectomy, using anatomic hilar dissection and lymph node sampling, was performed for primary carcinoma of the lung. One year later, we performed our first VNSSL using simultaneous stapling. RESULTS: Currently, 400 VNSSLs have been performed. In this entire series, there have been no surgical mortality, bronchopleural fistulas, port implantations, or transfusions. Bronchial stumps have averaged 4 mm in length, and all have been microscopically negative for neoplasm. In order to evaluate long-term survival for primary carcinoma of the lung in patients with an adequate duration of follow-up, the first 250 consecutive VNSSLs have been reviewed. There were 120 male and 130 female patients ranging in age from 20 to 92 years old who had 62 right upper lobe, 20 right middle lobe, 58 right lower lobe, 63 left upper lobe, and 33 left lower lobe lobectomies, and 14 bilobectomies. The lesions consisted of 214 primary carcinomas, 8 metastatic lesions, and 28 benign problems. Seven to 18 lymph nodes could be resected during staging of the primary neoplasms. The tumors ranged in size from 1 to 9 cm, and operating times averaged 78.6 min. Hospitalization averaged 2.83 days. No patient was admitted to the ICU. Intensive monitoring or narcotic analgesia were not needed. No epidural or intercostal anesthesia was used. Complications were infrequent and minor. Most patients returned to preoperative levels of physical activity within 7 to 10 days. Overall survival at a mean of 34 months, when all stages of neoplasms were combined, is 83%. For stage I, overall survival is 92%. The cost of VNSSL is approximately 50% less than the traditional open thoracotomy. CONCLUSIONS: VNSSL is an oncologic technique that has been clinically rewarding and economically beneficial for patients with malignant lesions. Long-term survival for primary carcinoma currently exceeds reports being published for the traditional open thoracotomy. Scientific reasons for this extraordinary survival are emerging. Complications, surgical mortality, pain, and length of stay have all been reduced. Patient recovery, comfort, and satisfaction have been extraordinary.

Reversal of renal failure and paraplegia after thoracoabdominal aneurysm repair.

Repair of ruptured thoracoabdominal aortic aneurysms is complicated by high rates of perioperative paraplegia, renal insufficiency, and mortality. This report describes a patient with a ruptured thoracoabdominal aortic aneurysm in whom preoperative acute renal failure was reversed with hemodialysis, aortic replacement, and renal revascularization. Prompt cerebrospinal fluid drainage reversed delayed-onset postoperative paraplegia and led to immediate, complete neurologic recovery.

Cytochrome P-450 pathway in acetylcholine-induced canine coronary microvascular vasodilation in vivo.

In the canine coronary microcirculation, acetylcholine (ACh)-induced vasodilation of large (> or = 100 microns) epicardial arterioles (LgA), but not small (< 100 microns) epicardial arterioles (SmA), is blocked by nitric oxide (NO) synthase inhibitors in vivo. We hypothesized that the ACh-induced vasodilation of SmA is mediated by a cytochrome P-450 metabolite of arachidonic acid (AA). Epicardial coronary microvascular diameters in dogs were measured at baseline and after treatment with topically applied ACh (1, 10, and 100 microM), AA (1, 5, and 10 microM), or sodium nitroprusside (SNP; 10-100 microM). Coronary microvascular diameters were compared among control dogs (group OO); dogs pretreated with N omega-nitro-L-arginine (L-NNA; 70 microM topically) (group NO); dogs pretreated with L-NNA plus clotrimazole (Clo; 1.6 microM topically) or 17-octadecynoic acid (ODYA; 2 microM topically), cytochrome P-450 monooxygenase inhibitors (groups NC and NY, respectively); dogs pretreated with Clo alone (group OC); and dogs pretreated with L-NNA plus Clo with AA as the agonist (group AA). ACh-induced vasodilation of LgA was abolished by L-NNA alone, whereas in SmA, L-NNA was without effect. Clo alone did not inhibit ACh-induced dilation in either SmA or LgA. However, the combinations of L-NNA plus either Clo or ODYA abolished ACh- and AA-induced dilation of SmA (100 microM ACh: NC, 3 +/- 5%; NY, 8 +/- 2%; 10 microM AA: 6 +/- 3%) but did not affect responses to SNP. These results suggest that the ACh-induced vasodilation of SmA is mediated in part by cytochrome P-450 metabolites of AA and provide the first evidence that the cytochrome P-450 pathway contributes to the regulation of coronary resistance vessels in vivo.

Cyclic strain increases endothelial nitric oxide synthase activity.

BACKGROUND: Endothelial nitric oxide synthase (eNOS) is an important enzyme that controls the production of a potent vascular smooth muscle relaxing factor, nitric oxide. However, the role of hemodynamic forces (blood pressure, cyclic strain, and shear stress) on the regulation of eNOS has not been fully elucidated. Recently, we showed that cyclic strain increases eNOS gene and protein in cultured bovine aortic endothelial cells (EC). Because an increase in gene transcription and protein synthesis may not necessarily translate into an increase in functional activity, the aim of this study was to determine the effects of cyclic strain on eNOS activity. METHODS: EC were seeded onto plates with flexible bottoms that can be deformed by vacuum and were then exposed to 60 cycles/minute of either 24% maximum strain (-20 kPa vacuum) or 10% maximum strain (-5 kPa vacuum) for 24 hours. eNOS activity was assessed, and nitric oxide production was determined (as nitrite) by the Greiss reaction. RESULTS: Twenty-four percent strain, at 60 cycles/min, but not 10% strain significantly increases eNOS activity compared with stationary controls. Both strain regimens increased nitric oxide (as nitrite) in culture media compared with stationary controls, although nitrite in media of EC exposed to high strain were significantly increased compared with the lower strain. CONCLUSIONS: Cyclic strain increases eNOS activity in cultured bovine aortic EC. These results may indicate the importance of hemodynamic forces in the regulation of eNOS in vivo.

Increased ambient pressure stimulates proliferation and morphologic changes in cultured endothelial cells.

Very little is known about the effects of pressure within the vascular system on EC phenotype. To study this, bovine aortic EC were seeded on rat type I collagen plates (2,000/cm2) and allowed to attach for 24 hours. The cells were exposed to either atmospheric, 40, 80, or 120 mm Hg pressure by placing them in a plexiglass pressure chamber loaded with 5% CO2/air and maintained at 37 degrees C inside an incubator. Chamber pressure was continuously monitored with an amplified voltage transducer connected to a digital monitor. EC were maintained in DMEM supplemented with 10% calf serum and substrates for up to 9 days. The results indicate that EC proliferation is influenced by their ambient pressure. EC subjected in vitro to pressures comparable to mean systemic blood pressures had a significant increase in cell number compared to EC exposed to atmospheric pressures. EC were elongated and appeared to align randomly. We hypothesize that the systemic pressure which the endothelium is exposed to in vivo may have a significant regulatory influence on the ability of the endothelium to proliferate which may affect the endothelial cell response to injury.

Lipoprotein (a): a risk factor for peripheral vascular disease.

Lipoprotein (a) [Lp(a)] is a serum protein that has been reported to be predictive of complications from coronary and cerebrovascular atherosclerotic disease. This study was designed to compare plasma levels of Lp(a) in 100 white male patients with and without peripheral vascular disease (PVD) and to determine the role of Lp(a) as a risk factor for PVD independent of known risk factors such as cigarette smoking (CIG), diabetes mellitus (DM), and coronary artery disease (CAD). Patients with PVD (mean age = 67.6 years, n = 50) had a statistically significant (p = 0.04) elevation of Lp(a) (29.8 +/- 3.9 mg/dl) as compared to patients without PVD (20.0 +/- 2.9 mg/dl (mean age = 68.3 years, n = 50). Further analysis revealed that patients with PVD had a significantly higher incidence of CIG (86% vs. 68%, p = 0.03), DM (34% vs. 14%, p = 0.02), and CAD (52% vs. 30%, p = 0.02) than those without PVD. However, there was no statistically significant difference in Lp(a) levels in patients with CIG or CAD compared to those without. Patients with DM had significantly (p = 0.04) lower levels of Lp(a) (17.8 +/- 3.5 mg/dl) than those without DM (27.1 +/- 3.0 mg/dl). Stepwise regression analysis of these various risk factors for PVD revealed that Lp(a) was the strongest significant individual predictor for the presence of PVD (R2 = 0.07) as compared to DM (R2 = 0.05) and CIG (R2 = 0.04). We conclude that there is a significant correlation of Lp(a) levels and the incidence of PVD, which is independent of other major risk factors for PVD.

Isolation and characterization of rabbit cardiac endothelial cells: response to cyclic strain and growth factors in vitro.

Studies of the cardiac endothelium have been complicated by difficulties in isolating and maintaining cardiac endothelial cells (EC) in culture. We present in this paper a method of obtaining pure EC from rabbit hearts by collagenase digestion and membrane filtration. Pure cultures of EC displaying characteristic EC morphology, uptake of di-I-acetylated LDL, and contact-inhibition of growth were successfully maintained in culture for several weeks in media supplemented with fetal bovine serum, bovine retina-derived growth factor (RDGF), and antibiotics. Since EC in vivo are exposed to a complex pattern of physical forces we also sought to determine the proliferative response of cardiac EC subjected to pulsatile strain in vitro and compared it with the response to the addition of an exogenous growth factor, RDGF. The results demonstrate that a regimen of 60 cycles per minute, 24% cyclic strain induced a significant increase in cardiac EC proliferation and suggests that physical forces may have a trophic effect on EC proliferation.

Persistent hypoglossal artery: An anomaly leading to false-positive carotid duplex sonography.

Duplex ultrasonography is becoming increasingly popular as the sole diagnostic test in the evaluation of carotid artery bifurcation disease. We present a patient with a persistent hypoglossal artery, a rare primitive internal carotid-basilar anastomosis, masquerading as an internal carotid artery stenosis on ultrasound. The operative management of this anomaly is reviewed.

Effect of cyclic stretch on endothelial cells from different vascular beds.

Endothelial cells (EC) mediate many of the organ responses to shock. Much of our knowledge of EC are obtained from cell culture studies. However, compared to the dynamic milieu in vivo, the stationary environment for large-vessel EC may be artificial and inappropriate. In this study, the morphology, growth rate, and production of prostacyclin (PGI2) by EC obtained from different vascular beds under stationary and dynamic conditions were examined. EC were harvested from the thoracic aorta (Ao), pulmonary artery (PA), and vena cava (VC) of the same calves and exposed to 0.5 sec 24% deformation alternating with 0.5 sec relaxation (i.e., 60 cycles/min). Our results show that in response to the cyclic regimen, VCEC were elongated perpendicular to the force vector and their actin filaments aligned in the same direction, while AoEC and PAEC did not exhibit any morphological changes. The growth rate of AoEC (but not PAEC or VCEC) was significantly enhanced when stimulated by cyclic stretch. In addition, AoEC demonstrated an increased PGI2 synthetic activity with cyclic stretch, while PAEC and VCEC were unaltered. We conclude that the maintenance of EC phenotype and function is dependent on the hemodynamic milieu in vivo and may be influenced by the vascular origin of the cultured EC.

Enhanced production of endothelium-derived contracting factor by endothelial cells subjected to pulsatile stretch.

The purpose of this study was to assess the role of cyclic deformation in modulating the production by endothelial cells (ECs) in culture of a recently described endothelium-derived smooth muscle cell contracting factor, endothelin. We grew bovine aortic ECs to confluence on culture plates with flexible membrane bottoms. Vacuum (-20 kPa) was applied to deform the membrane to 24% strain at 60 cycles/min for 1, 3, or 5 days. Control ECs were grown on the same membrane but without vacuum deformation. The conditioned media were collected, centrifuged at 10,000 rpm for 10 minutes to remove cells and debris, and the supernatant fluid was subjected to radioimmunoassay for endothelin. The results demonstrate that bovine aortic ECs release a basal level of endothelin under stationary conditions (107.1 +/- 14.7 pg/10(5) cells), and this production increased fivefold to sixfold with cyclic stretch. Thus physical forces exerted on ECs in culture can influence the secretion of this vasoconstrictive molecule.