Validation of esophageal pressure occlusion test after paralysis

Measurements of respiratory mechanics are frequently made in ventilated infants and children. Esophageal pressure measurements (P_es using a balloon on a catheter have been used to partition the respiratory mechanics into lung and chest wall components. Appropriate positioning of this balloon is crucial to obtain accurate estimates of pleural pressure. Traditionally, in spontaneously breathing subjects the balloon position is assessed with an occlusion test. In ventilated subjects, it is not always possible to perform an occlusion test prior to paralysis, and even if such a test is performed it may not be relevant under conditions of positive pressure ventilation. We have assessed a positive pressure occlusion test that is suitable for paralyzed subjects. By occluding the airway opening and applying gentle pressure to the abdomen or rib cage, positive swings in pressure can be measured by both P_es and airway opening pressure (P_ao). We compared traditional occlusion tests measured in 16 spontaneously breathing puppies to the positive pressure occlusion test performed after paralysis. In 2 pups we were unable to obtain a reasonable traditional occlusion test (>15% difference between P_es and P_ao) but we obtained 10 traditional occlusion tests in each of the remaining 14 pups (2.1–14 kg). In 11 of these animals Ape, was within 10% of P_ao. This compared well to positive pressure occlusion test using abdominal pressure performed after paralysis, where Apes was within 10% of ΔP_ao in 10 animals. In 9 of these pups occlusion tests were also performed by applying pressure on the rib cage, where ΔP_es was within 10% of ΔP_ao in 6 animals. These results suggest that it is possible to perform accurate occlusion tests in paralyzed subjects by abdominal or rib cage compression with the airway occluded. Pediatr Pulmonol. 1994; 17:56–62. © 1994 Wiley-Liss, Inc.     

LONG-TERM OUABAIN ADMINISTRATION DOES NOT ALTER BLOOD PRESSURE IN CONSCIOUS SPRAGUE-DAWLEY RATS

1. We tested the ability of ouabain to cause chronic hyper tension by continuously infusing ouabain for 28 days (mini-osmotic pump implantation; i.p.). The blood pressure and metabolic effects of sham (150 mmol/L NaCI; n= 12) or ouabain infusion (10 μg/kg per day; n= 14; 100 μg/kg per day; n = 14) were examined in conscious Sprague-Dawley rats. 2. Plasma ouabain concentrations measured after 28 days of ouabain infusion were as follows: sham, not detectable (n= 11); ouabain 10 μg/kg per day, 0.60 ± 0.07 nmol/L (n= 14); and ouabain 100 μg/kg per day, 7.17 ± 0.57 nmol/L (n= 14; P < 0.001). 3. Sham or ouabain infusion did not alter food intake, bodyweight, water intake or urine output in conscious rats. 4. Blood pressure was not altered by sham treatment. Ouabain at 10 μg/kg per day or 100 μg/kg per day did not produce consistent rises in blood pressure. Ouabain at 10 μg/kg per day increased blood pressure on treatment day 12 only (+ 6mmHg; P < 0.05), while at 100μg/kg per day blood pres sure increased on treatment days 16 (+ 9 mmHg; P < 0.05) and day 18 (+ 8mmHg; P < 0.05) only. There was no significant difference in blood pressure between sham and ouabain groups. 5. Renal blood flow was decreased in rats infused with ouabain at 10 μg/kg per day (2.0 ± 0.3 mL/min per 100 g body-weight; n= 5; P < 0.01) and 100 μg/kg per day (2.2 ± 0.4 mL/ min per 100 g bodyweight; n= 7; P < 0.05) compared with sham treatment (3.5 ± 0.2 mL/min per 100 g bodyweight; n= 6). Renal vascular resistance was increased in rats treated with ouabain at 10 μg/kg per day (65.5 ± 12.6 mmHg/mL per min per 100 g bodyweight; n= 5; P < 0.01) and 100 μg/kg per day (66.0 ± 15.6 mmHg/mL per min per 100 g bodyweight; n= 7; P < 0.05) compared with sham treatment (32.6 ± 2.5 mmHg/mL per min per 100 g bodyweight; n= 6). 6. High plasma concentrations of ouabain do not cause consistent increases in blood pressure in conscious Sprague-Dawley rats.     

Activation of the langendorff perfused rat heart depolarized by increased external potassium concentration

Myocardial activation under depolarized conditions was studied in spontaneously beating Langendorff perfused hearts from albino rats. Depolarization was obtained by increasing external potassium concentration in steps (5.4, 7.4, 10, 10.5, 11 and 11.5 mM) in the perfusing solution with or without adrenaline (Adr). Left ventricle isovolumic systolic pressure and coronary flow did not change as external potassium increased, albeit being larger with Adr in the perfusing solution. Atrial and ventricular rates decreased, the latter showing a larger decline. The same behaviour was displayed by perfused hearts, with higher rates being developed by the group with Adr. PR interval and QRS complex duration increased as a function of external potassium. PR intervals were the same in both groups but QRS duration was larger in the Adr group, indicating that AV conduction was not changed in presence of Adr but intraventricular conduction was delayed in that situation. It was also observed that in the great majority of perfused hearts, differing from isolated preparations, ventricular mechanical activity ceased at around 11.5 mM external potassium.     

Aptitude for physical exercise in a population of female hospital workers

Summary The aim of this study was to evaluate the level of physical capacity in a female hospital population of Paris and its suburbs. A total of 1505 women working in the selected departments filled in a questionnaire concerning their working conditions, life habits and health and also attended a medical examination. The effort test performed consisted in flexing the legs 20 times with the chest held straigt, in 40 s. The heart rates were measured for the first, the second and the third minutes of recovery (first 15 s multiplied by 4). The blood pressure was measured just after the heart rate, for the first and the third minute. Recovery indices have been constituted from the results. The respective weights of anthropometric and sociodemographic risk factors for recovery indices were studied in multiple logistic regression models. The classification enables us to consider about 25%–30% of our population as having a satisfactory physical capacity, about 26%–27% as having an acceptable capacit, and about 24%–27% as having a weak capacity. About 21% of the population presented an excessive pressure reaction and 44% a questionable pressure reaction. Our results concerning the level of physical capacity of the female nursing staff should be taken into account especially in the future planning of work loads and architectural choices, which must avoid excessive physical burdens in relation to this level. An improvement in the level of physical capacity could be envisaged as well.     

正常人眼筛板的结缔组织纤维结构

采用组化特染，透射电镜和图象分析仪观察了３５只正常人眼筛板结缔组织的纤维成分和结构形态，根据生物力学原理分析了筛束的力学性质和筛板的结构特征，探讨了筛板的损害形式和在眼压与视神经损害间的中介作用及其影响因素。结果显示，筛束含有细胞间质所有三种纤维，具有弹性、塑性和刚性三重复合性质，筛板纵向椭圆、筛束行径和密度象限性差异及筛板厚度个体性差异等与筛板抗损害性能有关。眼压对筛板作用有两种途径，筛板损害是     

A review of the effects of external pressure on skin blood flow

The human foot is a complex mechanical structure consisting of bones, ligaments and joints. They act together to provide a robust system capable of absorbing and dissipating the intermitted pressure that is subjected to its plantar surface during walking to prevent soft tissue breakdown. Current studies suggest that plantar foot pressure may lead to soft tissue breakdown (e.g. neuropathic ulceration) and hence research has so far concentrated on investigating the mechanical effects of plantar foot pressure on the foot’s integrity. This has been possible through the widely available pressure and force platforms as well as in-shoe pressure systems. However, to understand how plantar foot pressure causes soft tissue breakdown it is vital to investigate both the physiological–mechanical interactions between the skin and plantar foot pressure. This review suggests that with the current advances in technology, the physiological response of skin blood flow to mechanical plantar foot pressure should be investigated and correlated further, both during static and dynamic loading, by developing a new system capable of either measuring both variables simultaneously or by synchronising two systems in real time.     

Hydrodynamic aspects of pyelocalyceal peristalsis

This study was undertaken to determine the nature of pressure changes in manometric studies of renal pelvis and calyces. In previous studies in pigs it has been assumed that pressure increases occur in the contracting segments of the renal pelvis and calyces, but our observations suggested that these increases were actually due to distension of noncontracted segments. Pressures were recorded with two catheters introduced percutaneously into the pyelocalyceal system with simultaneous video recording of the fluoroscopic image. There was no pressure rise in the calyces or the renal pelvis when these segments contracted; however, pressure rose when the noncontracted calyces were distended by a remote contraction ring. These findings confirmed the observations at kinetic urography. They agreed with the hydrodynamic experience that the pressure in a ring-shaped contracted segment is lower than upstream and downstream of that segment. It was concluded that if the porcine pyelocalyceal system is a valid model of the human, the pressure increases, assumed to be contractions, were actually caused by the injection and distension of the noncontracted segments.     

Captopril and time dependent changes in post- to pre-glomerular resistance ratios in remnant kidneys of pre-hypertensive rats

Wilke , W. Lee & Person , A. E. G. 1992. Captopril and time dependent changes in post- to pre-glomerular resistance ratios in remnant kidneys of pre-hypertensive rats. Acta Physiol Scand 144 , 253–261. Received 26 June 1991, accepted 8 October 1991. ISSN 0001–6772. Department of Physiology, Colorado State University, Fort Collins, Colorado, USA and Department of Physiology and Biophysics, University of Lund, Sweden. Micropuncture experiments were performed on intact and remnant kidneys of male Sprague-Dawley rats before and after angiotensin converting enzyme inhibition with captopril (0.5 mg kg^-1 iv). Partially nephrectomized rats were studied at 2 and 8 weeks post-surgery before the development of systemic hypertension. At 2 weeks, nephrectomized rats had a numerically higher tubular stop-flow pressure than controls (43 ± 2 mmHg vs. 38 ± 2 mmHg; P = 0.08) and a higher post- to pre-glomerular resistance ratio (Re/Ra) (0.40 ± 0.03 vs. 0.31± 0.03; P = 0.08). At 8 weeks, stop-flow pressure and post- to pre-glomerular resistance ratios were similar in remnant and intact kidneys. Captopril had no effect on stop-flow pressure in 2 week post-surgery nephrectomized rats or either control group, but it increased stop-flow pressure in 8 week post-surgery nephrectomized rats (40 ± 2 to 44 ± 2 mmHg, P= 0.04). This increase in stop-flow pressure was associated with an increase in the post- to pre-glomerular resistance ratio (0.33 ± 0.02–0.42 ±0.02, P = 0.009). Stop-flow pressure was positively correlated with the post- to pre-glomerular resistance ratio in 2-week post-surgery nephrectomized rats and their respective controls when combined (r = 0.89, P= 0.0001) and 8-week post-surgery nephrectomized rats and their respective controls combined (r= 0.78, P = 0.0001). Stop-flow pressure was not significantly correlated with mean arterial pressures or welling-point pressures in these groups. We conclude that stop-flow pressure in remnant kidneys of pre-hypertensive rats is primarily determined by the post- to pre-glomerular resistance ratio, and increases in stop-flow pressure and post- to pre-glomerular resistance ratios in remnant kidneys are transient in the absence of systemic hypertension. The role of the renin-angiotensin system in determining the ratio and stop-flow pressure is dependent on time post-nephrectomy. Captopril-induced increases in stop-flow pressure and post- to pre-glomerular resistance ratio at 8 weeks, suggests that its primary effect at that time is not a preferential post-gIomerular vasodilation subsequent to reductions in intrarenal angiotensin II.