Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q16637 (SMA)
 8,107 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to investigate whether local mechanisms of blood flow autoregulation mediate vasoconstriction during the early development of renal hypertension. Anesthetized rats were instrumented with Doppler flow probes on the celiac (CA), superior mesenteric (SMA), and renal arteries to measure flow velocity in these vessels. Acute two-kidney, one clip renal hypertension was produced by inflating a pneumatic occluder on the left renal artery to reduce flow velocity by 50%. Two hours after renal artery stenosis (RAS), femoral artery pressure (AP) was increased by 35%, CA resistance by 45%, and SMA resistance by 57%. No increases were observed in AP or in CA and SMA resistances for sham-operated, control rats. To determine if autoregulation contributed to the increase in SMA resistance, we protected the SMA vasculature from the increased arterial pressure by servocontrolled inflation of a pneumatic cuff implanted around the SMA. Although normalizing SMA pressure with the protective cuff significantly reduced (p less than 0.05) the increase in SMA resistance that occurred after RAS, SMA resistance remained elevated above control levels. These results suggest that (1) reduced intensity of SMA constriction produced by protection of the SMA is due to inhibition of a local autoregulatory mechanism that is contributing to the increase in SMA resistance during the acute development of renal hypertension, and (2) maintenance of elevated SMA resistance during protection from increased AP is the result of pressure-independent mechanisms that are activated subsequent to renal artery stenosis.
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PMID:Autoregulation and vasoconstriction in the intestine during acute renal hypertension. 399 21

This clinical trial aimed to prospectively investigate the morphological structure of infrarenal abdominal aortic aneurysms (AAA) to establish a valid dataset in the preoperative assessment supporting either the conventional or endovascular (TPEG) surgical approach. Regarding both the general feasibility testing and safe TPEG placing, all the anatomic AAA data must already be measured preprocedurally, due to the necessity for conversion as a frequent consequence of an intraprocedural failure. Between January 1993 and June 1995, all the patients (n = 159) admitted for elective AAA repair, were prospectively analysed. Graded on the basis of these measurements we developed a new AAA classification system supporting the kind of the surgical procedure (standard) approach vs. TPEG). Three different types of AAA were clearly defined. Due to morphological AAA criteria, 86 out of 159 patients (54.1%) might be suitable for TPEG (Type I, IIA and IIB). An infrarenal (proximal) neck < 15 mm, an infrarenal aortic diameter > 24 mm or an extension of the aneurysm to the iliac bifurcation are considered to be exclusion criteria for TPEG placement. In consideration of relevant co-morbidities (e.g. renal artery stenosis, SMA occlusion, iliac occlusive disease, simultaneous operations) only 43 out 159 patients (27.1%) were good candidates for TPEG. In general, smaller AAA are more appropriate for TPEG repair due to better proximal and distal fixation. As a consequence, indication criteria for AAA repair must not be expanded to smaller AAA.
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PMID:[Infrarenal abdominal aortic aneurysm: morphological classification as decision aid for therapeutic procedures]. 901 30