Biomedical subjects
Publications and source records attributed to W L Bailey.
Taxol is a relatively new antineoplastic agent whose classification as either vesicant, non-vesicant, or irritant remains under debate. This case study is presented to follow a large-volume Taxol extravasation. The article illustrates assessment, follow-up, intervention and outcome of this situation. This case suggests the drug is a vesicant with the potential to cause moderate soft tissue injury.
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Matrix production by smooth muscle cells (SMC) appears to play a major role in the intimal thickening process. Proteoglycans (PG) are the predominant extracellular matrix component of early restenotic lesions. As angiotensin II (A II) has been proposed as a mediator of restenotic process, we hypothesized that A II may directly affect PG synthesis by SMC. SMC were cultured in the presence of [35S]sulfate and angiotensin II, and both the secreted and membrane-bound proteoglycans were analyzed. A II (1 to 100 nM) evoked a dose- and time-dependent increase in both cell- and media-associated PG production, an effect abrogated by the A II receptor antagonist, saralasin. SMC constitutively synthesize small amounts of PG with a molecular mass of 170-250 kDa. After treatment with A II, the abundance of PG is increased, as well as its molecular mass (230-300 kDa). Selective degradation by chondroitinases and heparinase identified chondroitin and dermatan sulfate PG as the predominant form being induced. These results demonstrate that the effect of A II is not general and is specific to certain classes of PGs. In order to further examine the specificity of the A II effect, we compared the synthesis of PG induced by A II with that induced by platelet-derived growth factors AA and BB (PDGF-AA and -BB), insulin-like growth factor I (IGF-I), and tumor necrosis factor alpha (TNF alpha). This comparison demonstrated that the profile of PG induced by A II is different from the other factors examined. Taken together, these data indicate that A II may not only function as a hypertrophic factor for SMC, but in addition may also be a potent modulator of specific PG synthesis by these same cells, which could significantly contribute to the formation of atherosclerotic and restenotic lesions.
Primary angioplasty (direct angioplasty without antecedent thrombolytic therapy) has remained an exclusive and consistent method of infarct intervention at our institution over the past 13 years. A total of 1,000 consecutive patients were prospectively enrolled in our primary angioplasty database. Of patients presenting to our group with an acute myocardial infarction, 96% of those eligible received immediate angioplasty. Cardiogenic shock was noted in 79 patients (7.9%). The mean time from pain onset to reperfusion was 5.4 +/- 4.0 hours. Infarct-vessel recanalization was accomplished in 94% of patients. Recanalization rates were similar among the 3 native epicardial coronary systems but were lower in bypass grafts (86%; p < 0.0001). Overall in-hospital mortality was 7.8%; mortality with cardiogenic shock was 44%. Global ejection fraction increased from 49.7% preangioplasty to 57.4% at the time of dismissal. The amount of myocardial salvage was highly dependent on the size of the initial infarction (the largest infarctions benefiting the most). Patients reperfused in < 2 hours experienced a very low mortality (4%) and impressive myocardial salvage. Complications included stroke in 0.5%, significant bleeding in 2.8%, and early reocclusion of the infarct vessel in 13%. Primary angioplasty is broadly applicable to patients presenting with acute myocardial infarction and results in a very high rate of infarct vessel recanalization, with a mortality rate of 7.8%. This strategy may be uniquely effective in patients presenting with cardiogenic shock, large infarctions, contraindications to thrombolytic therapy, and prior bypass surgery.
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Explore the source record for details and available documents.
Explore the source record for details and available documents.