Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transient cerebral ischemia in fetal sheep is followed by a period of delayed cerebral injury associated with cerebral vasodilation. As nitric oxide (NO) can mediate both vasodilation and neuronal death, this study investigated whether inhibition of NO synthesis would attenuate the vasodilation and decrease cerebral injury. Eleven late gestation (range 122-133 d) fetal sheep were subjected to 30 min of transient cerebral ischemia in utero. Two hours later, treatment group (n = 5) received a continuous infusion of NG-nitro-L-arginine (L-NNA) at a dose of 50 mg.h-1 for 4 h followed by 20 mg.h-1 for the subsequent study period, a competitive inhibitor of NO synthase (NOS), whereas a control group (n = 6) received PBS. Inhibition of NOS activity was confirmed in the treatment group by 1) suppression of the fall in mean arterial blood pressure (MAP) associated with acetylcholine (p < 0.01), and 2) persistent increase in MAP after commencement of L-NNA (p < 0.05). Changes in cerebral blood volume (CBV) were observed for 3 d by measuring changes in concentration of total cerebral Hb ([tHb]) using near infrared spectroscopy. The delayed increase in CBV commenced at 13.1 +/- 1.0 h postischemia in the control and 12.7 +/- 2.3 h in the treatment group. Maximum increase at 30-36 h was 0.5 +/- 0.1 mL.100 g-1 in the treatment group and 1.2 +/- 0.2 mL.100 g-1 in the control (p < 0.05). Final CBV was depressed below preischemic baseline in the treatment (-0.7 +/- 0.2 mL.100 g-1) but not the control group (-0.1 +/- 0.3 mL.100 g-1) (p < 0.05). Neuronal loss, quantified histologically 3 d postischemia, indicated that cerebral injury was increased in the treatment group (p < 0.05). The results indicate that after transient cerebral ischemia in fetal sheep, NOS inhibition attenuates the delayed rise in CBV but does not decrease the extent of cerebral injury.
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PMID:Nitric oxide synthase inhibition attenuates delayed vasodilation and increases injury after cerebral ischemia in fetal sheep. 882 65

Analysis was made of the results of 11 internal carotid reconstructions using polydioxanone (PDS) sutures 6 months after intervention performed in 10 patients. All operations on the carotid bifurcation were accomplished using 5/0 PDS continuous suture. Nine eversion carotid endarterectomies and 2 internal carotid reconstructions were performed for Kinkiking. There were no neurologic complications, thromboses, bleedings or repeated operations after interventions on the brachiocephalic arteries. Six months later the patients were examined under ambulatory conditions and were provided color duplex scanning (CDS) of the reconstructed area. Measurements were made of the diameter of the common carotid artery (CCA) right beneath the anastomosis between the CCA and the internal carotid artery (ICA), of the maximal diameter of the anastomosis between the CCA and the ICA, and of the size of the proximal ICA segment right the anastomosis. During the 6-month period following surgical intervention, all 10 patients did not demonstrate any ischemic attacks (TIA) or strokes. No cases of anastomotic aneurysms were recorded. After 9 reconstructions no ICA restenoses were marked. In one case, restenosis accounted for 40% because of atherosclerosis progression and after one operation there developed asymptomatic thrombosis of the ICA. The study has demonstrated that the use of PBS absorbable suture for autoarterial ICA reconstruction provides for anastomosis integrity minimally over the period as long as 6 months.
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PMID:The short-term results of internal carotid reconstructions by absorbable suture material. 1465 16