Biomedical subjects
Publications and source records attributed to A R Cale.
A 69-year-old man with unstable angina and impaired left ventricular function who was admitted for emergency coronary artery bypass grafting had echocardiographic findings suggestive of a left ventricular thrombus. A transmital cardioscopy was successfully performed at surgery, without video assistance, to confirm the diagnosis. We discuss our approach and the advantages.
OBJECTIVES: During cardiac surgery it is sometimes necessary to examine heart chambers remote from the site of surgery. Similarly visualization of the pulmonary arterial tree will enable assessment for the completeness of pulmonary embolectomy. There are no standard adjunctive procedures to accomplish this. Left ventriculotomy used to examine the left ventricle, and maneuvers used to ensure complete pulmonary embolectomy can have serious complications. Impelled by the need to obviate the complications, we adopted and, herein describe a simple method of examining the cardiopulmonary system with an endoscope. Our early experience is also presented. METHOD: Transmitral cardioscopy was performed in two patients, and pulmonary angioscopy in one. One patient had the combined procedure. The indications for transmitral cardioscopy were; suspected left ventricular thrombus and a right atrial thrombus propagating into the left atrium through a patent foramen ovale. The indications for pulmonary angioscopy were pulmonary embolectomy and right atrial thrombus. SSURGICAL TECHNIQUE Cardiopulmonary endoscopy was performed on cardiopulmonary bypass, at an appropriate stage of the primary procedure. For transmitral cardioscopy, a flexible fibreoptic endoscope was passed into the left ventricle through the right superior pulmonary vein, or the right atrium. For pulmonary endoscopy, the flexible endoscope was introduced through a pulmonary arteriotomy. At the end of the procedure, the port of entry of the endoscope was closed and cardiopulmonary bypass terminated. RESULTS: A good visualization of the cardiac chambers and the pulmonary artery was obtained in all the patients. One patient was found to have an endocardial scarring, and a left ventricular thrombus was excluded in another. Visual guidance facilitated pulmonary emboli retrieval. There were no complications in these patients. CONCLUSION: Cardiopulmonary endoscopy is simple, safe and effective in examining the cardiac chambers and the pulmonary arterial system. It can be performed with a sterilized flexible fibreoptic endoscope. It facilitates pulmonary embolectomy, and precludes procedures and maneuvers that can cause serious complications. It adds a visual advantage to pulmonary embolectomy, which is otherwise blind. Cardiopulmonary endoscopy has the potential for a wider applicability, possibly in minimally invasive and robotic cardiac surgery.
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Circulating leukocytes activated during rejection of organ allografts could potentially have generalized effects on systemic blood vessels of the transplant recipient. Experiments were designed, therefore, to determine the function of the endothelium and smooth muscle of arteries from nontransplanted organs in dogs who received single lung transplants. Dogs underwent single lung allotransplantation and were immunosuppressed for 5 days. Immunosuppression was then withheld for 3 days, allowing rejection to occur. Dogs were studied at this time (rejecting) or following treatment for rejection for an additional 6-8 days (treated). Arteries from unoperated, untreated dogs also were studied to provide baseline responses of healthy tissue. Rings cut from left circumflex coronary, nonoperated native pulmonary, and renal arteries were suspended in organ chambers for measurement of isometric force. Endothelium-dependent relaxations to the calcium ionophore A23187 were not affected by rejection in any of the arteries. Contractions to angiotensin I were reduced significantly only in native pulmonary arteries. Contractions to KCI and endothelin-1 increased in renal arteries with endothelium during rejection. These contractions in renal arteries were reduced following treatment of rejection. None of the responses of the coronary arteries were affected significantly by rejection of the lung allograft. These results demonstrate that contractions of arteries in the transplant recipient's native organs are altered during rejection of lung allografts. The effects are organ specific, may include production of endothelium-derived contractile factors in renal arteries, and can be partially reversed by treatment of rejection.
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PURPOSE: Experiments were designed to determine whether or not leukocytes activated by acute pulmonary rejection cause contractions of isolated pulmonary arteries. METHODS AND RESULTS: Separate suspensions of (a) polymorphonuclear cells (> 95%) and (b) mononuclear cells (85% lymphocytes/10% monocytes/5% polymorphonuclear cells), respectively, were obtained from the arterial blood of four groups of adult male mongrel dogs: unoperated dogs (controls), dogs with single-lung autotransplants, dogs with rejecting single-lung allotransplants, and unoperated dogs treated with the same immunosuppressants as allotransplanted dogs. These suspensions were added to rings of control intralobar pulmonary arteries suspended in organ chambers for measurement of isometric force. The endothelium was removed mechanically from selected rings. No significant change in basal tension of pulmonary arterial rings occurred by adding suspensions of polymorphonuclear cells from any of the four groups of dogs. Significant cell-number-dependent increases in tension occurred with suspensions of mononuclear cells from unoperated dogs, autotransplanted dogs, and unoperated, medicated dogs. These increases in tension were less in rings with compared to those without endothelium. Addition of a synthetic analogue of L-arginine abolished this difference. Suspensions of mononuclear cells from rejecting allotransplanted dogs caused significantly greater contractions in rings with endothelium than those observed with suspended cells from either unoperated, autotransplanted dogs or unoperated, medicated dogs. Addition of superoxide dismutase plus catalase or an antagonist of endothelin-A receptors (BQ-123) reduced contractions in rings with endothelium but not in those without endothelium to suspensions of mononuclear cells from rejecting allotransplanted dogs. CONCLUSIONS: The results of this study suggest that mononuclear cells cause contraction of pulmonary arteries, which can be partially inhibited by endothelium-derived nitric oxide. However, if the mononuclear cells are activated by acute pulmonary rejection, contractions are no longer inhibited by the endothelium. Under conditions of rejection, contractions are mediated in part by oxygen radicals and endothelin(s).
In 1953 Hufnagel and Harvey reported their successful treatment of aortic valve insufficiency by the implantation of a ball-valve prosthesis into the descending thoracic aorta. Since then, great advances in technology, surgery, and anesthesia have made aortic valve replacement a more common procedure with relatively low mortality. This remains true for the vast majority of prosthetic valve replacements. However, cases requiring reoperation can be difficult, leading to a much higher degree of morbidity and mortality. In selected patients who require repeated approaches to the aortic root we propose that Hufnagel's original idea may still be of value to reduce the severity of aortic insufficiency. We report our experience in 4 cases of aortic prosthetic incompetence, all of which were improved by two New York Heart Association functional classes after a modification of Hufnagel's procedure.
A prospective study of 248 patients admitted consecutively under the care of a single surgeon was performed and data on a variety of patient details were collected daily during the period of their hospitalization. Analysis of the data identified four quantifiable indices of morbidity, namely duration of hospitalization, duration of intravenous infusion, analgesic requirement and antibiotic administration, which can be combined arithmetically and used to produce a morbidity profile. The use of such a profile may allow comparisons to be made between different units if applied to specific conditions and permit a more accurate assessment of overall patient morbidity than can be presently done using mortality rates.
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Monoclonal antibodies against leukocyte adhesion molecules reduce the severity of reperfusion injury and, in some cases, prevent acute allograft rejection. These effects are assumed to be due to prevention of leukocyte-endothelial adhesion. Experiments were designed to study activation of polymorphonuclear leukocytes during acute rejection of canine single lung allografts and to test the ability of an anti-beta 2-integrin monoclonal antibody (R15.7/H4) to regulate leukocyte metabolism independent of leukocyte-endothelial adhesion. Peripheral blood polymorphonuclear leukocytes were obtained by Ficoll-Hypaque centrifugation from unoperated control dogs (n = 10), from dogs with a single lung autotransplant (n = 4), and from dogs after single lung allotransplantation during unmodified rejection (n = 12). Oxygen radicals were measured with luminal-enhanced chemiluminescence of unstimulated polymorphonuclear leukocytes, polymorphonuclear leukocytes stimulated by opsonized-zymosan, and polymorphonuclear leukocytes incubated with anti-beta 2-integrin beta-chain (CD18) monoclonal antibodies before exposure to opsonized zymosan. Polymorphonuclear leukocyte viability was unaffected by the monoclonal antibodies. Polymorphonuclear leukocytes from unoperated and autotransplant dogs did not produce oxygen radicals unless stimulated by opsonized zymosan. Polymorphonuclear leukocytes from rejecting animals produced oxygen radicals in the absence of zymosan, and when stimulated, production of oxygen radicals was significantly greater than that of polymorphonuclear leukocytes from unoperated and autotransplant dogs. Production of oxygen radicals was inhibited significantly by the monoclonal antibodies in polymorphonuclear leukocytes from all three groups. This study shows that rejection activates polymorphonuclear leukocytes and increases the potential to produce activated oxygen species. In addition to inhibiting leukocyte adhesion to endothelial cells, anti-beta 2-integrin monoclonal antibodies appears to suppress production of oxygen radicals by polymorphonuclear leukocytes.