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Time to occlusion

Time to occlusion of the tube by the thrombus establishes a definite end point in this system. [Pg.258]

Time to occlusion (min) the time between onset of the electrical current and the time at which blood flow decreases under 0.3 ml/min... [Pg.284]

Compoimd Arteriovenous shunt EDi5 mg/kg Injury and stasis in vena cava minimum dose to achieve patency mg/kg FeCls-mediated injury to carotid artery bolus dose (mg/kg) + infusion (pg/kg/min) Mean time to occlusion (minutes)... [Pg.279]

While rMTT can depict changes in cerebral hemodynamics, which are due to vessel occlusion of cerebral arteries and the respective compensation mechanisms, the time to arrival of contrast (TTA) is sensitive to vessel diseases, which are more upstream of the arterial flow, most commonly high grade stenoses or occlusions of the carotid arteries. In such patients, blood flow in the hemisphere ipsilateral to the stenosis is mainly supplied by the contralateral carotid artery via the circle of Willis. Due to this detour, TTA is prolonged in the ipsilateral hemisphere (Reith et al. 1997). At the same time, rMTT may be prolonged in the ipsilateral hemisphere resulting from decreased blood flow (Dorfler et al. 2001). If TTP is calculated instead of MTT, the effect of the bolus delay cannot be separated from that of the perfusion decrease, because TTP is influenced by both rMTT and TTA. [Pg.110]

Teng MM, Cheng HC, Kao YH et al (2001) MR perfusion studies of brain for patients with unilateral carotid stenosis or occlusion evaluation of maps of time to peak and percentage of baseline at peak . J Comput Assist Tomogr 25 121-125... [Pg.115]

Fig. 15.1 la-d. A 62-year-old patient with symptomatic left internal carotid artery occlusion and progressive stroke. Initial DWI shows only punctuate small lesions in the deep borderzone of the left hemisphere (a), while the hypoperfused area on the time-to-peak maps affects the complete left middle cerebral artery territory and is most pronounced in the deep borderzone area (b). On day 3, the acute lesion has grown considerably larger, paralleling progression of symptoms (c). Contrast-enhanced MRA shows proximal occlusion of the left internal carotid artery (d)... [Pg.235]

Fig. 15.12. An asymptomatic 54-year-old patient suffering from left internal carotid artery occlusion (left) shows excellent collateralization via the posterior communicating artery and a sufficient filling of the ipsilateral middle cerebral artery (middle). As a consequence, perfusion MRI (time-to-peak) detects only a slight asymmetry and delay of contrast agent arrival in the parietal parts of the middle cerebral artery territory (right)... Fig. 15.12. An asymptomatic 54-year-old patient suffering from left internal carotid artery occlusion (left) shows excellent collateralization via the posterior communicating artery and a sufficient filling of the ipsilateral middle cerebral artery (middle). As a consequence, perfusion MRI (time-to-peak) detects only a slight asymmetry and delay of contrast agent arrival in the parietal parts of the middle cerebral artery territory (right)...
Occlusion time (min) = time to zero blood flow... [Pg.280]

In a study using spontaneously hypertensive rats, a dose of 12 mg kg-1 of compound X was also neuroprotective [these rats were subjected to 2h of focal ischemia by occlusion of the right middle cerebral artery (MCA), followed by 22 h of reperfusion]. With the assumption of 100% systemic absorption, the expected plasma Cmax at this dose was 2000ng ml In this model, there was a significant reduction (greater than 30%) in cortical infarct volume, compared with saline controls, when the drug was given at the time of occlusion and at 0, 0.5, 1 and 1.5 h post-MCA occlusion. [Pg.87]

Figure 8.41 (A) ECG of a 35-year-old multiparous woman with a very serious ACS due to occlusion of LAD proximal to D1 and S1. Observe the morphology of the advanced RBBB + SAH together with evident ST-segment changes (ST elevation in precordials - occlusion in LAD), with ST-segment depression in II, III and VF (occlusion proximal to D1), and ST-segment elevation in VR and V1 with ST-segment depression in V6 (occlusion proximal to S1). (B) The ECG patterns of the evolution through time (V1). Figure 8.41 (A) ECG of a 35-year-old multiparous woman with a very serious ACS due to occlusion of LAD proximal to D1 and S1. Observe the morphology of the advanced RBBB + SAH together with evident ST-segment changes (ST elevation in precordials - occlusion in LAD), with ST-segment depression in II, III and VF (occlusion proximal to D1), and ST-segment elevation in VR and V1 with ST-segment depression in V6 (occlusion proximal to S1). (B) The ECG patterns of the evolution through time (V1).
An occlusive dressing applied quickly after phenol helps it macerate and deepens its action. An occlusive dressing applied immediately after TCA creates a barrier to epidermal water evaporation and to the water in the solution itself. Under occlusion, this water accumulates in the uppermost layers of the skin, where it dilutes the TCA fairly rapidly. With phenol, this slight dilution enhances its penetration. An occlusive dressing applied 30 minutes after TCA does not dilute the acid, as it has had enough time to coagulate the proteins in the skin and neutralize itself by combining with the proteins before occlusion can dilute it. [Pg.92]

When phenol is applied to healthy skin, occlusion slows down the absorption rate but does not alter the total quantity absorbed. The Kver therefore has more time to detoxify the phenol and the kidneys have more time to eliminate it. This increases the peel s safety margin. [Pg.284]

In contrast, the relationship between time-to-treatment and clinical outcomes has been the subject of intense debate for patients undergoing mechanical reperfusion. This controversy has been fueled, in part, by the discordant results of clinical studies (104-110). Some reports have identified an association between time-to-reperfusion and survival, while others have found no clear relationship. Difficulty in interpretation of these observational data is further compounded by our inability to account for the dynamic nature of coronary occlusion in humans, failure to examine the importance of collateral circulation, differences in study design and analysis, and marked patient heterogeneity... [Pg.99]

Figure 6.3 Effect of two structurally distinct thromboxane A2/prostaglandin endoperoxide receptor antagonists, L636,499 and SQ29,548, on the time to coronary occlusion in the canine model of coronary thrombosis following electrically-induced endothelial injury... Figure 6.3 Effect of two structurally distinct thromboxane A2/prostaglandin endoperoxide receptor antagonists, L636,499 and SQ29,548, on the time to coronary occlusion in the canine model of coronary thrombosis following electrically-induced endothelial injury...

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