电刺激膈神经中枢端引起降压反应的外周机理

电刺激麻醉家兔膈神经中枢端呆引起动脉血压下降，此降压反应不能被剪断双侧迷走神经所阻断；但可被静脉注射心得１．０ｍｇ／ｋｇ部分阻断；也可被静注射酚妥拉明２．０ｍｇ／ｋｇ部分阻断，去除缓冲神经后其降压效应更为明显。     

大鼠延髓腹外侧区在可乐定心血管效应中的作用

目的：探讨大鼠延髓腹外侧区（VLM）在介导可乐定心血管效应中的作用。方法：氨基甲酸乙酯麻醉SD大鼠，应用微量注射和细胞外记录等方法观察尾端延髓腹外侧区（CVLM）和头端延髓腹外侧区（RVLM）内局部给予可乐定导致的心血管活动变化。结果：单侧CVLM微量注射可乐定（5nmol/100nl,n=10)不仅能明显升主动脉血压（AP）和增加心率（HR）（P＜0．01），而且能增加同侧RVLM压力敏感性神经元（n=80)的放电频率（P＜0．01），而单侧RVLM微量注射可乐定（5nmol/100nl,n=9)，明显降低AP和HR（P＜0．01）。结论：RVLM和CVLM在介导可乐定的心血管效应中具有不同的作用。     

A role of insular cortex in cardiovascular function

We sought to determine whether the insular cortex contributes to the regulation of arterial blood pressure (AP). Responses to electrical and chemical stimulation of the cortex were studied in the anesthetized, paralyzed, and artificially ventilated Sprague-Dawley rat. The insular cortex was initially defined, anatomically, by the distributions of retrogradely labeled perikarya following injections of wheat germ agglutinin-horseradish peroxidase (WGA-HRP) into the nucleus tractus solitarii (NTS). Injections of WGA-HRP into the insular cortex anterogradely labeled terminals in cardiopulmonary and other divisions of the NTS and confirmed projections revealed by retrograde tracing experiments. Electrical stimulation of the insular cortex elicited elevations of AP (less than or equal to 50 mm Hg) and cardioacceleration (less than or equal to 40 bpm). The locations of the most active pressor sites corresponded closely to the locations of retrogradely labeled cells in layer V of granular and posterior agranular areas of the insular cortex (areas 14 and 13) and the extreme capsule. Maximal pressor responses were obtained at a stimulus intensity of three to five times threshold current of 20-30 microA. Responses elicited mostly with higher-threshold currents were also mapped in areas 2a and 5lb and the claustrum and within the corpus callosum. Unilateral injections into the insular pressor area of the excitatory amino acid monosodium glutamate (L-Glu; 0.05 nmol to 10 nmol) or the rigid structural analogue of L-Glu, kainic acid (KA) (0.4 nmol) (which specifically excite perikarya), caused topographically specific elevations in AP and tachycardia. During the course of the anatomical transport studies, new findings were obtained on the organization and characteristics of the cortical innervation of the NTS and the nucleus reticularis parvocellularis. Topographic relationships between the cortex and the NTS were organized in a more complex manner than previously thought. Cells projecting to caudal cardiopulmonary segments of the NTS were fewer and generally located ventrally and caudally and in a more restricted area than cells projecting rostrally or to the parvicellular reticular formation. Anterograde transport data revealed new presumptive terminal fields in dorsolateral, ventral, periventricular, and commissural regions of the NTS, including an area overlapping the terminal field of the aortic baroreceptor nerve. We conclude that neurons within an area of the insular cortex projecting to multiple brainstem autonomic nuclei, including a region of the NTS innervated by baroreceptor afferents, increase arterial blood pressure and heart rate.(ABSTRACT TRUNCATED AT 400 WORDS)     

动脉顺应性及其影响因素

动脉顺应性又称动脉弹性，反映血管内皮功能。已成为预测心血管疾病的重要危险因素。无创测量动脉弹性的方法在临床上已有一定程度的应用。各种方法具有其各自适用范围及局限性。多种干预手段可以影响动脉弹性。合理测量及维持正常的动脉弹性可延缓多种心血管疾病的发生及发展。     

磁场对家兔急性实验性高血压的影响

目的 :探讨内关穴敷磁的降压效应。方法 :40只清醒家兔和 40只麻醉家兔 (其中 2 0只去减压神经 ) ,静脉注射去甲肾上腺素或苯肾上腺素引起急性实验性高血压 ,并于内关穴敷磁 (0 .1～ 0 .2T) ,记录血压、心率和敷磁前及 1h后的血液粘度的变化。结果 :敷磁 1h后各实验组平均动脉压 (MAP)显著下降 (P <0 .0 1)。麻醉和清醒家兔MAP降幅无差异 (P >0 .0 5 ) ,但显著高于去减压神经家兔MAP的降幅 (P <0 .0 1或 0 .0 5 ) ,各实验组全血比粘度显著下降 (P <0 .0 1或 0 .0 5 ) ,实验组与各自对照组心率敷磁前后无差异 (P >0 .0 5 )。结论 :磁场具有降压作用 ,但对心率无影响 ,其降压效应与减压神经的抑制和全血粘度的降低有关 ,与化学感受性升压反射无关     

Technetium-99m sestamibi scintigraphy for the assessment of lower extremity ischaemia in peripheral arterial disease

Technetium-99m sestamibi was used for functional investigation of the muscle perfusion of lower extremities in 35 patients with peripheral vascular disease. The aim was to test what useful information could be obtained by additional imaging of the legs in patients referred for risk stratification with dipyridamole myocardial scanning. Posterior images were acquired over the thighs and calves after postocclusive reactive hyperaemia and at rest. Inter- and intraextremity ratios and differences between the stress and rest data were used for the assessment of abnormal circulation. Arteriography was performed in every case, and surgical procedures or transluminal angioplasty in 31 patients. To estimate diagnostic accuracy, the results of^99mTc-sestamibi scintigraphy were compared with those of angiography and the functional consequences of revascularization procedures. The sensitivity and specificity of^99mTc-sestamibi scintigraphy were 55% and 25%, respectively, with an overall accuracy of 50%. Apparently methodological error was not responsible for these poor results. Instead, a paradoxically high uptake of the radiopharmaceutical in muscles supplied by significantly stenosed vessels was identified as the main source of both false-negative and false-positive results. This phenomenon resembles the findings of a previous study involving delayed administration of thallium-201 after exercise. In conclusion,^99mTc-sestamibi scintigraphy has not proved sufficiently reliable to help in the management strategy for patients with peripheral vascular disease.     

Specific response to adrenaline in arterial hypertension induced by exogenous calcium deficiency

Injection of a synthetic analog of parathyroid hypertensive factor to WKY rats considerably increases and prolongs pressor response to adrenaline. Synthetic analog injected after adrenaline induces a short-term (3–4 min) and potent (to 250%) rise of arterial pressure. Each subsequent injection of the synthetic analog induces a less pronounced in the amplitude and duration pressor response. The α-adrenoblocker phentolamine completely abolishes the effects of the parathyroid hypertensive factor analog. Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, Vol. 124, No. 8, pp. 148–150, August, 1997     

Diving physiology and pathophysiology

Summary. Divers have worked at 500 m depth in the sea and have reached 700 m in simulated chamber dives. A prerequisite for this has been extensive physiological studies of the body's reactions to pressure and pressure changes. This paper reviews such physiological and pathophysiological studies with emphasis on recent developments.