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1.
V Allen PhD DW Ryan MB FRCA A Murray PhD FIPSM 《International journal of clinical practice》1994,48(3):125-129
SUMMARY Four specialised air mattresses had interface pressure measured under six body sites prone to pressure sores in 10 subjects, supine and sitting. The mattresses were the Clinirest (SSI) and FirstStep (KCI) continuous airflow mattress overlays, and Airwave (Pegasus) and Nimbus (Huntleigh) alternating pressure air mattresses. On the mattress overlays, average supine interface pressures were 2.33 kPa (scapula), 4.15 kPa (elbow), 1.94 kPa (sacrum) and 2.79 kPa (buttock), although they were higher at the occiput (7.97 kPa) and heel (11.7 kPa). The alternating pressure air mattresses had an average minimum interface pressure close to zero for three sites, rising to 4.28 kPa under the heel. Average maximum interface pressures were 8.61 kPa (occiput), 5.21 kPa (scapula), 4.90 (elbow), 4.85 kPa (sacrum), 4.61 kPa (buttock) and 13.2 kPa (heel). No accepted scientific method exists for comparing the two types of mattress. Our data suggest a clinical benefit at the occiput and heel (supine) in using an alternating pressure air mattress and a benefit in using a continuous airflow mattress overlay at other sites. 相似文献
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Kitzman DW 《国外医学:老年医学分册》2002,23(1):45
众所周知,充血性心衰(CHF)为老年人较为常见的临床综合征之一.迄今关于左室收缩功能正常的CHF老人的相关临床特点远未清楚,本文特此进行了大样本分析. 对象与方法 4842例老年人,男1922例,女2920例,年龄66~103岁.尔后人均随访1年.旨在分析老年CHF年发病率,以及左室收缩功能正常的CHF老人相关临床特点. 结果随访期内,罹发1次或以上CHF者共425例次(8.8%/年).与未患发CHF老人相比,CHF老人平均年龄更大(79±6岁:77±5岁,P<0.001),女性居多,尤以高龄女性更多,如85岁以上的高龄女性CHF年发病率约较65~69岁女性高2倍(14%∶6.6%,P<0.001),AMI史、房颤、高血压、糖尿病、慢性阻塞型肺病、吸烟者均多,血脂及血肌酐亦高.多变量分析表明,罹患CHF与下列因素有关:老年尤其是高龄[年龄每增加5岁的患病奇数率(OR)女性1.2,男性1.1],AMI史(OR7.3),房颤者(OR3.0),糖尿病(OR2.1),肾功能不全(血肌酐≥1.5mg/dl的OR2.0),慢性阻塞肺病(仅老年女性的OR为1.8),以及左房、左室内径增大(内径每递增1cm的OR为2.0),和左室重量增加、左室收缩末期室壁张力增高、早期跨心房血流增多.超声心动图检测结果显示,CHF老人中,左室收缩功能正常者达55%,而仅有左室舒张功能不全,且左室收缩功能正常或轻度减退者高达80%.其中女性左室收缩功能正常者尤较男性多见(67%∶42%,P<0.001),表现为单纯左室舒张功能不良.而在左室收缩功能正常的CHF老人,常伴有左室内径较小、左室收缩末期室壁张力较低、左室重量较轻、左室收缩末期室壁厚度增加,而左室射血分数正常或仅轻度降低. 讨论以上结果提示,在老年人群中,CHF年发病率相对较高,且随年龄而增加,多数左室收缩功能正常,仅有左室舒张功能障碍,尤其是在高龄女性,亦即高龄女性左室舒张功能不全性CHF更为常见.对此,临床上更应拟出合理的防范措施,来正确诊治老年CHF综合征. (袁志敏摘) 相似文献
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Packham MA; Perry DW; Kinlough-Rathbone RL; Rand ML; Guccione MA; Evans RM; Mustard JF 《Blood》1985,65(3):564-570
Rabbit platelets were aggregated by adenosine diphosphate (ADP), allowed to deaggregate and then separated into density subpopulations by centrifugation through discontinuous Stractan density gradients. Although ADP causes little or no release of the contents of the amine storage granules of rabbit platelets, ADP caused a decrease in platelet density as compared with control platelets subjected to the same procedures except for exposure to ADP. The density change persisted for at least four hours. The apparent size of platelets stimulated with ADP increased initially, but returned to control values during a one-hour period. A similar decrease in platelet density was observed with an albumin density gradient. Under conditions in which aggregation did not occur in response to ADP with ethylenediaminetetraacetic acid (EDTA) in the medium, little or no decrease in platelet density was observed. Agglutination with polylysine did not change platelet density. Thus, not only agents such as thrombin and plasmin that cause the release of the contents of the platelet granules decrease platelet density, but ADP also has this effect. Platelets would be exposed to all of these stimuli during thromboembolic processes, and their effect on platelets may account for the decrease in platelet density observed previously in experiments with rabbits with indwelling aortic catheters. Agents that increase the concentration of cyclic AMP (cAMP) in platelets (PGE1, adenosine, dibutyryl cAMP, forskolin, and papaverine) also decreased platelet density. This effect persisted when the platelets were washed and resuspended in fresh medium and was also demonstrable in plasma. Platelet size was gradually increased by prostaglandin E1 (PGE1) which maintains platelets in a disc shape and does not cause the release of granule contents, indicating that the decrease in platelet density caused by PGE1 may be attributable to platelet swelling. 相似文献