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Biomedical subjects

J Archibald

Publications and source records attributed to J Archibald.

At least 19 recordsLinked to original sources
PubMed1994

Combined use of cerebral spinal fluid drainage and naloxone reduces the risk of paraplegia in thoracoabdominal aneurysm repair.

PURPOSE: This report summarizes our experience with the use of cerebral spinal fluid drainage (CSFD) and naloxone for prevention of postoperative neurologic deficit (paraplegia or paraparesis). METHODS: We reviewed 110 consecutive patients with 86 thoracoabdominal aneurysms and 24 thoracic aneurysms. The status of 47 patients (43%) was acute (rupture or dissection), and the status of 52 (47%) was Crawford type I or II. None of the patients had intercostal artery reimplantation. There were two patient groups for analysis of neurologic deficit risk. Group A (61 patients) received naloxone and CSFD, and group B (49 patients) did not. RESULTS: One deficit occurred in group A and 11 deficits occurred in group B (p = 0.001). By multiple logistic regression analysis, the variables acute status, Crawford type II, or group B classification were significant factors for deficit risk. Use of the same logistic regression analysis on the subgroup of 47 patients with acute aneurysms and 33 patients with Crawford type 2 aneurysms confirmed the protective effect of combined CSFD and naloxone (group A) and that clinical presentation and extent of aorta replaced are the primary risk factors for development of deficit. To test this conclusion we developed a highly predictive model (correlation coefficient 0.997 with 16 series of thoracoabdominal aneurysms) for neurologic deficit. We applied our data to this model. Group B had the predicted number of deficits, and group A had substantially fewer deficits than predicted. CONCLUSIONS: We conclude that the combined use of CSFD and naloxone offers significant protection from neurologic deficits in patients undergoing thoracoabdominal and thoracic aortic replacement.

Adolescent↗
PubMed1991

Differential T cell hyporesponsiveness induced by in vivo administration of intact or F(ab')2 fragments of anti-CD3 monoclonal antibody. F(ab')2 fragments induce a selective T helper dysfunction.

Induction of peripheral T cell anergy associated with stimulation through the TCR complex in vivo has been described in mice using chemically modified APC, staphylococcal enterotoxin B, and intact anti-CD3 mAb. In the latter two models, T cell proliferation, IL-2R expression, and lymphokine production have been demonstrated before subsequent induction of hyporesponsiveness, whereas in the former model, these events have not been observed. To further investigate the relationship between mitogenicity and induction of peripheral hyporesponsiveness, mice were treated with either mitogenic intact anti-CD3 mAb or nonmitogenic F(ab')2 fragments of anti-CD3 mAb. T cells from F(ab')2-treated mice demonstrated a selective decrease in helper functions, with minimal effect on CTL function. Specifically, a marked reduction in ability of Th cells to secrete IL-2 when challenged in vitro with mitogen or alloantigen was observed, which persisted for at least 2 mo after mAb administration and which was independent of T cell depletion. Proliferative function was decreased in CD4+ T cells and could not be fully restored with addition of exogenous IL-2. A helper defect was also evident in vivo, in that F(ab')2-treated mice were deficient in their ability to reject MHC-disparate skin grafts, and in vivo administration of IL-2 reconstituted their ability to reject skin grafts normally. In contrast, T cells from mice treated with intact mAb demonstrated a significant decrease in both CTL and helper functions. A long term reduction in TCR expression on CD4+ cells from F(ab')2-treated mice, and on both CD4+ and CD8+ cells from intact mAb-treated mice was observed. These findings demonstrate that peripheral T cell hyporesponsiveness can be induced in vivo by binding an identical epitope on the TCR complex in the presence or absence of initial proliferation, lymphokine secretion, or IL-2R expression, and that binding to the same epitope can result in varying long term effects on T cell function.

Animals↗
PubMed1990

Naloxone and spinal fluid drainage as adjuncts in the surgical treatment of thoracoabdominal and thoracic aneurysms.

Forty-seven patients who were treated for thoracoabdominal or thoracic aneurysms over a 5 1/2-year period were analyzed for neurologic deficit risk. Patients were divided into two groups for analysis. Twenty-four patients, who were treated from January 1984 to December 1986, did not undergo spinal fluid drainage or naloxone administration (group A). Twenty-three patients, who were treated from January 1987 to August 1989, had spinal fluid drainage (group B); 12 patients in this group also received naloxone as an intravenous drip at 1 microgram/kg/hr for 48 hours after surgery. Permanent neurologic deficits occurred in seven (29%) group A patients but in only one (4%) group B patient, who did not receive naloxone (p less than 0.03). The first two group B patients to receive naloxone showed complete reversal of neurologic deficits on waking from anesthesia. This significant reduction in neurologic deficit was associated with an increased 1-year survival rate (72% in group A, 91% in group B). We conclude that the use of naloxone and spinal fluid drainage reduces the incidence of neurologic deficit that is associated with repair of thoracoabdominal and thoracic aortic aneurysms. This reduction in neurologic deficit is associated with improved survival in the long term. The observed reversal of postoperative neurologic deficits with naloxone implicates opiates as a major factor in the pathophysiology of spinal cord ischemia.

Adult↗