Local blood flow and metabolism of the tongue before and during panting in the dog

Summary The effects of hyperthermia on blood flow and oxygen consumption of the tongue were investigated in anesthetized dogs. For comparison, blood flow through the skin and deep muscle of the hind leg was also measured in some animals. Increasing blood temperature revealed a biphasic response of lingual blood flow. At 41°C blood temperature respiratory frequency was twice that of control and there was a reduction of lingual blood flow, while resistance of the lingual bed was increased significantly. The arterio-venous oxygen difference (AVDO₂) of lingual blood was markedly increased at this level and the of the tongue was like-wise significantly greater than control. At 41.9°C, the steep increase of respiratory frequency was accompanied by a marked fall in lingual resistance as evidenced by a four-fold increase of lingual blood flow. The systemic AVDO₂ rose at this temperature, while the lingual AVDO₂ fell dramatically. There was no further increase of lingual . At both temperature levels the blood flow through the skin did not change substantially, while the deep muscle blood flow slightly increased. The mean arterial pressure showed a progressive fall during hyperthermia. It is assumed that the decrease of lingual blood flow at elevated blood temperature without panting is due to a redistribution of cardiac output to areas other than the tongue. The increase of lingual blood flow without an additional increase of lingual during panting may be explained solely as a mechanism for heat dissipation. The fact that the decrease of lingual resistance was demonstrated in immobilized animals concomitant with high frequency phrenic burst activity suggests that the decrease of lingual resistance and panting may be induced by a common central integrating mechanism.     

Priming effect of RANTES on eosinophil oxidative metabolism

Background RANTES has been shown to possess chemotactic activity for eosinophils, which have also been considered to play a role in allergic inflammation through reactive oxygen species. Thus, in this study, we examined the effect of RANTES on radical oxygen products from eosinophils.
Methods Purified eosinophils by CD16-negative selection or an eosinophilic cell line (EoL-1) were incubated with or without RANTES (2.5 x 10⁻⁶). To the mixture of eosinophils and luminol, calcium ionophore (A23187) or opsonized zymosan (OZ) was added, and radical oxygen products were determined by luminol-dependent chemiluminescence for 600 s.
Results Eosinophil-mediated radical oxygen products of untreated eosinophils produced with A23187 gave a peak value of 14.09 + 2.40 (mean±SE, n = 12) relative light units (RLU) and an integrated value of 3232.20 + 513.09 RLU. However, with treatment with RANTES, a peak value of 18.66 + 2.40 RLU and an integrated value of 5301.05 ±561.02 RLU were obtained. Eosinophil oxidative metabolism-induced A23187 or OZ was apparently augmented by the preincubation with RANTES. In addition, the radical oxygen products of EoL-1 showed similar results.
Conclusions Thus, we concluded that RANTES may play an important role the pathogenesis of allergic inflammation through its involvement in eosinophil activation, as evidenced by oxygen products, as well as in selective eosinophil infiltration as selective eosinophil chemoattractant.     

Identification of vascular sphincters at the junction between alveolar capillaries and pulmonary venules of the mouse lung

Background: A peculiar feature of lung circulation in the lung is the pronounced variations in blood volume observed in alveolar capillaries that occur because of the changes in the conformation of the alveolar wall that are associated with the respiratory movements. This phenomenon has led to the postulate that mechanisms of postcapillary control of blood flow are to be present in the lung vessels. In the present study we searched for microanatomical evidence of vascular sphincters in the deep lung tissue of mice, namely in alveolar capillaries and pulmonary veins. Methods: We have used scanning electron microscopy (SEM) to examine two types of samples of normal lung tissue of CD-1 mice: 1) vascular corrosion casts made by vascular perfusion with Mercox® resin, and 2) routinely made gold/platinum-coated replicas of sectioned lung tissue. Results: Careful scrutiny of the vessels of the deep lung tissue led to the identification of sphincters in alveolar capillaries. These sphincters were located at the junction between capillary and pulmonary veins. They corresponded to areas to the vascular wall showing circular swellings where a radial organization was observed, since they were made up of alternating grooves and bulges. Transmission electron microscopy showed that smooth muscle cells participated in the formation of the sphincters. Conclusions: Our data reveal a new location for vascular sphincters in pulmonary vessels and, because these novel sphincters are located at the capillary-vein junction, they offer a structural setting for the existence of postcapillary control of blood flow in the pulmonary circulation of mice. © 1995 Wiley-Liss, Inc.     

脐带血清对骨髓粒—巨噬细胞集落形成的影响

在骨髓细胞半固体琼脂培养体系中，研究脐带血清（ＣＢｓ）对骨髓粒—巨噬细胞集落形成单位（ＣＦＵ－ＧＭ）的影响，单纯应用ＣＢｓ培养可使骨髓ＣＦＵ－ＧＭ（ｘ±ｓ为２６．０３７５±１０．２３２７）显著的高于正常成人外周血清（ＰＢｓ）组（ｘ±ｓ为１１．５９１７±３．６０４７；Ｐ＜０．００１）。ＣＢｓ加粒－巨噬细胞刺激因子，ＧＭ－ＣＳＦ组ＣＦＵ－ＧＭ（ｘ±ｓ为１１９．０７９２±３５．０９９１）是单纯ＣＢｓ组的４．５７倍；而ＰＢｓ加ＧＭＣ－ＳＦ组（ｘ±ｓ为９７．１２５±２６．７５５９）是单纯ＰＢｓ组的８．３８倍。有白细胞介素－６（ＩＬ－６）存在的ＣＢｓ组，ＣＦＵ－ＧＭ（ｘ±ｓ为３１．９３３３±１０．９１４４）明显的高于单纯ＣＢｓ组（Ｐ＜０．０２）。提示ＣＢｓ中含有较高水平的内源性ＧＭ－ＣＳＦ。     

Noninvasive,automatic 24-h ambulatory blood pressure monitoring in normotensive subjects

Summary The reliability of noninvasive, automatic blood pressure monitoring is not yet clearly established. A 24-h ambulatory blood pressure profile was obtained in 9 healthy, normotensive subjects with an automatic, noninvasive device. The blood pressure profile showed the typical circadian pattern with lower systolic and diastolic values during sleep, although pulse pressure was fairly constant (about 40 mm Hg). The systolic blood pressure rose steeply in the early morning hours — before waking up. The results were compared with simultaneous hourly readings using the auscultatory method. There were no statistically significant differences between the automatic and auscultatory readings, 13 of the 18 mean values at. different time points being within 2 mm Hg of each other. All the auscultatory means fell within the 95% confidence limits of those measured hourly by the automatic method. Although the automatic method seemed to be reliable compared with the auscultatory method, its sensitivity to motion artifacts is a disadvantage in a truly ambulatory setting.     

Tumor necrosis factor-alpha in the placenta is not elevated in pre-eclamptic patients despite its elevation in peripheral blood

PROBLEM: Tumor necrosis factor-alpha (TNF-alpha) is present in human placental and uterine cells at the early and late stages of gestation and promotes the regulation of trophoblast growth and invasion. We evaluated whether TNF-alpha levels in the placenta and blood of pre-eclamptic women differed from those with normal pregnancies. METHOD OF STUDY: The subjects were 39 pregnant women carrying single fetuses (21 normal-pregnant and 18 pre-eclamptic patients). Their average gestational age at entry was 38-39 weeks. Peripheral blood was collected before the onset of labor and separated serum was stored at -20 degrees C. A tissue segment of the placenta was cut and frozen in liquid nitrogen immediately after delivery at -80 degrees C. The frozen placental tissue was added to phosphate-buffered saline. The tissue was fully homogenized and centrifuged. Separated supernatant was stored at -80 degrees C. TNF-alpha levels in separated serum and TNF-alpha and total protein (TP) levels in separated supernatant were measured. The presence of TNF-alpha in the placenta was evaluated by immunohistochemistry in five pre-eclamptic and five normal-pregnant patients. RESULTS: Serum TNF-alpha levels were higher in pre-eclampsia than in normal pregnancies. However, TNF-alpha/TP levels in the placenta did not differ significantly between the two groups. As for TNF-alpha immunostaining of trophoblastic cells in the placenta, it was weak in three and moderate in two of the normal pregnancies, while it was absent in two, weak in one, and moderate in two in the pre-eclampsia group. CONCLUSIONS: We demonstrated no significant increase in TNF-alpha/TP levels in the placenta in pre-eclampsia despite a significant increase in serum TNF-alpha levels. There was no strong immunostaining for TNF-alpha detected by immunohistochemistry in the pre-eclampsia group. These findings suggest that TNF-alpha in the placenta is not a key cytokine to interfere with normal trophoblast invasion into the myometrium in pre-eclampsia, and that sources other than the placenta may contribute to the elevated levels of TNF-alpha found in the circulation of pre-eclamptic patients.     

优化原理与小动脉血流量─管径关系

作者假设血液为符合幂定律的非牛顿流体，对小动脉血管系统进行了详细的优化分析。导出了血流量与管径立方成正比的结论以及壁面切变率与管径无关的推论。此结果既包含了前人对于牛顿血流的研究成果，又能克服后者的不足，而与近期的生理测定一致。     

高血压急诊患者降压前后脑电图变化及临床意义

目的:观察高血压急诊快速降血压对大脑功能的影响情况。方法:监测56例病人含服 降压药前后的脑电活动和血压情况,并对所获资料进行分析。结果:2 h内收缩压(SBP)下降>5.33 kPa (40 mmHg)或舒张压(DBP)下降>4.00 kPa(30 mmHg)时,脑电图异常程度增加,θ及δ频段功率值明 显升高(P<0.01)。结论:降压急骤,可能会造成大脑功能损害     

Contribution of adrenomedullin to homeostatic response to cold stress in rat model

Acute stress known to stimulate sympathetic activity as well as the hypothalamo-pituitary–adrenal (HPA) axis, produces a significant increase in adrenomedullin (ADM) levels in the pituitary gland, plasma and adrenal glands, all of which are key components of HPA axis, suggesting a regulatory or protective role for ADM in countering HPA activation following a variety of physiological and psychological stressors. This study was conducted to assess a rat model for in depth investigation of biochemical mechanisms and consequences of cold stress. Four groups of Sprague–Dawley rats were observed for their serum total protein, glucose, trigliceride and cholesterol levels as well as their blood pressures after housing at room temperature, administration of ADM (1.0 nm/kg), exposing to cold stress (8 °C for 48 h) and exposing to ADM injection in addition to cold stress. The results suggest that application of ADM in addition to cold stress may act via receptors on different end-organs and causes altered metabolic regulation taking partial or total occupation of ADM receptors, stimulated in response to cold application induced physiologic ADM release before pharmacological ADM administration.     

Hemodynamic and hormonal responses to lower body negative pressure in men with varying profiles of strength and aerobic power

Hemodynamic, cardiac, and hormonal responses to lower-body negative pressure (LBNP) were examined in 24 healthy men to test the hypothesis that responsiveness of reflex control of blood pressure during orthostatic challenge is associated with interactions between strength and aerobic power. Subjects underwent treadmill tests to determine peak oxygen uptake ( O_2max) and isokinetic dynamometer tests to determine knee extensor strength. Based on predetermined criteria, subjects were classified into one of four fitness profiles of six subjects each, matched for age, height, and body mass: (a) low strength/average aerobic fitness, (b) low strength/high aerobic fitness, (c) high strength/average aerobic fitness, and (d) high strength/high aerobic fitness. Following 90 min of 0.11 rad (6°) head-down tilt (HDT), each subject underwent graded LBNP to –6.7 kPa or presyncope, with maximal duration 15 min, while hemodynamic, cardiac, and hormonal responses were measured. All groups exhibited typical hemodynamic, hormonal, and fluid shift responses during LBNP, with no intergroup differences between high and low strength characteristics. Subjects with high aerobic power exhibited greater (P < 0.05) stroke volume and lower (P < 0.05) heart rate, vascular peripheral resistance, and mean arterial pressure during rest, HDT, and LBNP. Seven subjects, distributed among the four fitness profiles, became presyncopal. These subjects showed greatest reduction in mean arterial pressure during LBNP, had greater elevations in vasopressin, and lesser increases in heart rate and peripheral resistance. Neither O_2max nor leg strength were associated with fall in arterial pressure or with syncopal episodes. We conclude that interactions between aerobic and strength fitness characteristics do not influence responses to LBNP challenge.