[On the effect of colloidal blood substitutes on blood proteins and blood sedimentation].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
BACKGROUND: It is unclear whether hypertension should be treated after acute stroke, and some have hypothesised that blood pressure should be increased to improve cerebral perfusion. OBJECTIVES: The objective of this review was to assess the effect of lowering or elevating blood pressure in people with acute stroke, and the effect of different vasoactive drugs on blood pressure in acute stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group trials register, the Ottawa Stroke Trials Registry (1994), Medline (from 1965), Embase (from 1981), ISI, and existing review articles. We contacted researchers in the field and pharmaceutical companies. SELECTION CRITERIA: Randomised trials of interventions that aimed to alter blood pressure in patients within two weeks of acute ischaemic or haemorrhagic stroke. DATA COLLECTION AND ANALYSIS: Two reviewers independently applied the inclusion criteria and assessed trial quality. Two reviewers extracted the data. MAIN RESULTS: Three trials involving 133 people were included. The trials tested the following vasodilators: nimodipine (66 people), nicardipine (five people), captopril (three people) and clonidine (two people). Oral calcium channel blockers (nimodipine, nicardipine) reduced systolic blood pressure (weighted mean difference 10.9mmHg, 95% confidence interval 2.0 to 19.7), diastolic blood pressure (weighted mean difference 9.5mmHg, 95% confidence interval 4.0 to 15.1) and heart rate (weighted mean difference 4.7 beats per minute, 95% confidence interval 0.2 to 9.2) at 48 hours. The greatest fall in blood pressure over the first 24 hours was shown in patients given the highest dose of nimodipine. The relationship between change in blood pressure and clinical outcome was not clear. There was not enough information to assess the effect of drugs other than calcium channel blockers. No studies of interventions to raise blood pressure were found. REVIEWER'S CONCLUSIONS: There is not enough evidence to evaluate the effect of altering blood pressure after acute stroke. Although oral calcium channel blockers appear to reduce blood pressure following acute stroke, the balance of benefit and risk remains unclear.
Paired arterial and venous cord blood samples were obtained from 42 normal newborns (24 males and 18 females). T4 was determined in all paired samples. In addition, other indices were determined: T3 in 40, RT3 in 29, TBG in 29, thyroglobulin (Tg) in 14, and TSH in 11. Gender difference in any of the thyroid indices was not found. Arterial and venous cord serum thyroid indices correlated positively (T4, r = 0.743; T3, r = .907, rT3, r = .920; TBG, r = .752; Tg, r = .934, and TSH, r = .989; P less than 0.005). The difference between the means +/- SD of arterial and venous levels was significant (P less than 0.01) only for rT3 (191 +/- 43.2 v 224 +/- 55.8 ng/dL). Arterial (T4 v T3, r = .453, P less than .005; T4 v RT3, r = .660, P less than 0.005) and venous (T4 v T3, r = .620, P less than 0.005; T4 v rT3, r = .612, P less than 0.005); T3 and rT3 levels correlated positively with T4 levels. In contrast, T3 and rT3 levels for arterial (r = .216, P greater than 0.1) and venous (r = .216, P greater than 0.1) samples did not show a significant correlation. These data are in keeping with earlier reports for animal placental models studied in vitro, suggesting that placental inner ring deiodination of maternal thyroxine is a source of fetal RT3.