Attenuation of pain on injection of propofol--an unexpected benefit of co-induction with midazolam.
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Biomedical subjects
Publications and source records attributed to J W Mackenzie.
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BACKGROUND: This study was performed to evaluate and determine the validity and benefits of video-assisted thoracic surgical simultaneously stapled pulmonary lobectomy without rib spreading. METHODS: Between September 1992 and August 1995, 100 consecutive video-assisted thoracic surgical simultaneously stapled lobectomies without rib spreading were performed. RESULTS: Forty-five male and 55 female patients had 24 right upper, 8 right middle, 29 right lower, 24 left upper, 15 left lower lobectomies for 66 adenocarcinomas, 20 squamous cell carcinomas, 4 large cell carcinomas, 8 benign lesions, and 2 metastatic lesions. Seventy-six patients had negative nodes. Nine patients had positive nodes. Every bronchoscopy was visually and cytologically negative. Forty-nine cervical mediastinoscopies were negative. Operating time for the series averaged 90.3 minutes. Hospitalization averaged 3.5 days for the entire group, but was 2.6 days for the last 20 patients. Lesions ranged from 1.5 to 8 cm, averaging 3.4 cm. There was no surgical mortality, no hemorrhage, no transfusion, and no urgent conversion to an open procedure. No bronchial fistula, vascular fistula, or bronchovascular fistula has occurred. Complications included 6 air leaks, 2 cerebrovascular accidents, 1 infected chest tube site, 2 cases of pneumonitis, and 1 subcutaneous emphysema. CONCLUSIONS: Video-assisted thoracic surgical simultaneously stapled lobectomy without rib spreading is a safe operation that can be combined with lymph node sampling. At this early stage, therapeutic outcomes (survival) for resected neoplasms appear similar to results obtained from traditional open techniques.
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This experimental study was undertaken to evaluate the hypothesis that cardioplegic arrest at 37 degrees C is superior to 10 degrees C cardioplegic arrest in the myocardial protection of an acutely injured heart. The hypothesis was tested using Sprague-Dawley rat hearts that were excised and retroperfused with Krebs-Henseleit buffer as isolated, isovolumic heart preparations. After 15 min of equilibration and baseline readings, ischemic injury of the myocardium was established by cessation of perfusion for 20 min, followed by 30 min of reperfusion to obtain cardiac measurements and verify uniformity of ventricular dysfunction. All hearts were then arrested for 30 min with continuous cardioplegia (oxygenated crystalloid cardioplegia, 4 ml/min) followed by 30 min of reperfusion. In one group (N = 12), temperature of cardioplegia was 10 degrees C. In the second group (N = 12), cardioplegia temperature was 37 degrees C. The experiments showed that in acutely injured hearts, cardioplegic arrest at 10 degrees C resulted in further deterioration in ventricular dysfunction (P < 0.01). In contrast, similarly injured hearts which underwent cardioplegic arrest at 37 degrees C showed a modest deterioration in ventricular dysfunction which did not reach statistical significance (P > 0.05). The experimental findings suggest that in the presence of acute myocardial injury, cardioplegic arrest at normothermia may provide better myocardial protection.
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Pseudoaneurysm of the left ventricle most often occurs after transmural myocardial infarction but may also follow cardiac operations, trauma, inflammation, or infection. In contrast to patients with true ventricular aneurysm, those with false aneurysm most commonly die of hemorrhage. Review of the reported surgical experience and of our 14 cases confirms that standard chest radiographs with an abnormal cardiac silhouette and rapidly expanding size may alert the physician to this sometimes overlooked diagnosis. Noninvasive tests such as color-flow Doppler echocardiography, 2-dimensional echocardiography, cineangiographic computed tomography, and transesophageal echocardiography allow relatively easy recognition of these apparently rare lesions with increasing frequency. Cardiac catheterization, however, is usually still necessary for a clear picture of the location and anatomy of the aneurysm and the state of the coronary arteries. Finally, a new classification is proposed, consisting of true aneurysm, false aneurysm, pseudo-false aneurysm, and mixed aneurysm.
The synthesis of type I and III collagens in cultured skin fibroblasts from normal skin, normal scar, hypertrophic scar, and keloids was examined. The ratio of type I/III collagen was significantly elevated in keloids compared to that in the other groups. When mRNA steady-state levels coding for alpha 1(I) procollagen were determined, it was apparent that this increase in the type I/III collagen ratio in keloids was paralleled by a specific increase in alpha 1(I) procollagen mRNA. This specific increase in alpha 1(I) procollagen mRNA in keloids was the result of increased gene expression because the transcription rate of the alpha 1(I) procollagen gene was significantly elevated in keloids, as determined by nuclear runoff transcription. The rate of transcription of the alpha 1(I) procollagen gene was also elevated in hypertrophic scars, although no concomitant increase in alpha 1(I) procollagen mRNA levels or alteration in the type I/III collagen ratio was observed. These data indicate that the rate of gene transcription of alpha 1(I) procollagen is increased in both hypertrophic scars and keloids, but only keloids exhibit increased steady-state levels of alpha 1(I) procollagen mRNA and concurrent increases in type I collagen. These results suggest that at least two distinct mechanisms, one pretranscriptional and one post-transcriptional, regulate type I collagen synthesis. It is possible, therefore, that in keloids, neither mechanism functions efficiently to down-regulate type I collagen. In hypertrophic scars, however, the post-transcriptional mechanisms are able to decrease elevated levels of mRNA coding for alpha 1(I) procollagen that result from increased transcription of the alpha 1(I) procollagen gene.
To assess the early and late valve-related events, 340 consecutive patients undergoing mitral valve repair from 1969 to 1988 were evaluated. Follow-up was complete, with a mean of 7.5% years and range from 2 to 22 years (cumulative 2456 patient-years). There were 221 (65%) female patients. Rheumatic valvular disease was present in 246 (68%) patients. The remaining patients had ischemic or congenital valve disease, floppy valve or infective endocarditis. At surgery, 47% of the patients had pure mitral incompetence, 43% had mixed mitral stenosis and incompetence and 10% had predominant mitral stenosis. Seventy-three percent of the patients were in functional class III or IV. Twelve percent had had prior heart surgery. Concomitant valve procedures including coronary revascularization were performed in 62.3%. There were 23 hospital deaths (6.8%) but only 3 of these (0.8%) were valve-related in patients who died at reoperation for valve repair failure. There were 4 other early repair failures who survived early reoperation. Of the 317 hospital survivors, there were 127 late deaths, and an actuarial survival of 44 +/- 3.7% (70% CL) at 14 years. Of these, 13 were valve-related or 0.5% patient-year. Late events included thromboembolism (TE) 1% patient-year, anticoagulant bleeding 0.4% patient-year, infective endocarditis (IE) 0.2% patient-year and late reoperation for mitral valve repair failure in 63 patients or 2.8% patient-year. At the late follow-up, 88% of the hospital survivors were in functional class I or II.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: The aim of this study was to determine if alterations in fibrillar collagen synthesis were associated with the development of inguinal hernias. SUMMARY BACKGROUND DATA: Previous work has suggested that alterations in connective tissue accumulation may play a functional role in the development of inguinal hernias. In particular, several investigators have suggested that alterations in collagen synthesis, causally related to connective disorders such as osteogenesis imperfecta, may also be responsible for the inguinal herniation that is markedly increased in such patients. This study was undertaken therefore to study collagen synthesis in patients with inguinal hernia in the absence of any other connective tissue disease. METHODS: Skin fibroblasts from 9 patients with hernias and 15 control individuals were radiolabeled with 3H-proline. Trypsin-chymotrypsin-resistant type I and III collagens were isolated and analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis, and recovery was quantified by laser densitometry. Steady-state levels of alpha 1(I) and alpha 1(III) procollagen mRNAs were also determined by northern and slot-blot hybridization analysis. RESULTS: The alpha 1(I)/alpha 1(III) collagen ratios were shown to be 6.3 +/- 0.34 in fibroblasts from control individuals and 3.0 +/- 0.25 in fibroblasts from patients with inguinal hernias. This statistically significant difference (p < 0.0001) was caused by an increase in the secretion of alpha 1(III) procollagen from the fibroblasts of patients with hernias. A concomitant increase in the steady-state levels of alpha 1(III) procollagen mRNA was observed in total RNA isolated from the patients' fibroblasts. CONCLUSIONS: A constitutive and systemic increase in type III collagen synthesis may result in reduced collagen fibril assembly in the abdominal wall, eventually leading to the development of herniation. Although it is not yet clear what genetic factors are responsible for the elevation in type III collagen synthesis in patients with hernias, this study represents the first attempt to define individuals with an abnormality in collagen production that may be specifically related to herniation. A clearer understanding of the possible genetic factors that influence the pathophysiology of this disease will be important to improve the treatment of patients in whom inguinal hernias develop.
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Video-assisted thoracic surgery is a new modality that allows visualization of and access to the intrathoracic organs without making a thoracotomy incision. One hundred consecutive patients underwent 113 thoracic procedures using this technique. Eight wedge resections for metastatic lesions, 6 pericardial windows, 1 bronchogenic cystectomy, 4 explorations of the aortopulmonary window, 1 decortication, 5 pleural scleroses, 8 bullous ablations, 25 lung biopsies, 19 wedge resections for carcinoma, 9 explorations of the thorax, 3 lobectomies, 1 esophageal cystectomy, 14 wedge resections for benign lesions, 4 pleurectomies, 1 excision of a neurogenic tumor, 3 mediastinal explorations, and 1 imaged axillary dissection were performed. There was no mortality. Ten patients had complications from which they recovered completely. Patients undergoing video-assisted thoracic operations seem to have reduced postoperative pain, shorter hospitalization, and quicker recovery times. Currently, this new modality appears to have beneficial value for patients; however, only further experience will determine its true merits.
From a very heterogeneous group of 340 patients undergoing mitral valve reconstruction from 1969 through 1988, 313 hospital survivors were analyzed for factors affecting the occurrence of reoperative mitral valve procedures related to native mitral valve dysfunction. Follow-up was 100% and extended from 1 year to 20 years (mean follow-up, 7.2 years). Sixty-three patients (18.5% of the 340) required mitral valve reoperation at a mean postoperative interval of 6 years (range, 1 to 15 years). Incremental risk factors analyzed for the event late mitral valve failure included age, sex, preoperative New York Heart Association class, cause of valvular disease, pathophysiology of the mitral valve, previous mitral valve operation, mitral valve pathology, and estimation of mitral valve function at operation after repair. Mitral valve pathophysiology affected the actuarial freedom from mitral valve replacement (p = 0.023 [log-rank]). Actuarial freedom from mitral valve reoperation was 90% at 5 years and 80% at 8 years in patients who had either pure mitral regurgitation or isolated mitral stenosis compared with 80% and 72% at 5 and 10 years, respectively, in patients who had mixed mitral stenosis and regurgitation (p = 0.023). Patients undergoing late reoperation were younger (51.7 +/- 1.56 years [+/- the standard error of the mean]) than those not having reoperation (p less than 0.0003). Durability of the repair was less in patients with rheumatic heart disease (p less than 0.025) and greater in patients with ischemic heart disease (p less than 0.004). Seventy-three percent of patients undergoing reoperation had concomitant operations compared with 68% of those not having reoperation (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)