Mapping of neurons in the central nervous system of the guinea pig by use of antisera specific to the molluscan neuropeptide FMRFamide

Summary Immunoreactive neurons were mapped in the central nervous system of colchicine-treated and untreated guinea pigs with the use of two antisera to the molluscan neuropeptide FMRFamide ¹. These antisera were especially selected for their incapability to react with peptides of the pancreatic polypeptide family. Only one group of perikarya was stained by both antisera; this group was mainly located in the nucleus dorsomedialis hypothalami and extended to the nucleus paraventricularis and nucleus periventricularis hypothalami. The perikarya were found to project fibers to all regions of the hypothalamus, to the septum, nucleus proprius striae terminalis, nucleus paraventricularis thalami, nucleus centralis thalami, nucleus reuniens, medial, central and basal amygdala, area praetectalis, area tegmentalis ventralis of Tsai, substantia grisea centralis mesencephali, formatio reticularis mesencephali, nucleus centralis superior, locus coeruleus, nuclei parabrachiales, nucleus raphe magnus, A 5-region, vagus-solitarius complex, ventral medulla, nucleus spinalis nervi trigemini, and substantia gelatinosa of the spinal cord. In many brain regions FMRFamide-immunoreactive processes were found in close contact with blood vessels.Abbreviations of Amino Acids D aspartic acid - F phenylalanine - G glycine - H histidine - L leucine - M methionine - P proline - R arginine - V valine - W tryptophan - Y tyrosine     

Social status,social context,and arterial blood pressure

As social change and economic development have proceeded, the prevalence of chronic diseases, especially cardiovascular diseases, has increased in the developing world. In part this is due to the adoption of diets and other health behaviors characteristic of industrialized nations; in part it is a function of changing social and economic circumstances. In this paper, we describe the development and testing of a model designed to account for social and economic effects on cardiovascular disease risk. The model incorporates the fact that global economic processes have made a lifestyle characterized by the consumption of Euroamerican material goods and information a basis for the assignment of social status in local communities. But economic change at the local level is rarely sufficient to provide a foundation for individuals' status aspirations. Hence, many individuals attempt to maintain a lifestyle inconsistent with their economic standing, a variable we term lifestyle incongruity. Here we describe how this factor is associated with higher blood pressure in a variety of settings and also how the effects of lifestyle incongruity can be modified in local contexts by social class and social role processes. This latter process, contextual modification, is illustrated by data from American Samoa. In this example, the association of lifestyle incongruity with blood pressure is examined in 30 male household heads and 26 spouses. After an examination of Samoan ethnography focused attention on the importance of age and gender differences as defining social contexts of intracultural variation, the model was modified to assess interactions between age and gender as they affect the association of lifestyle incongruity and blood pressure. Lifestyle incongruity is strongly associated with higher systolic and diastolic blood pressure for the younger household heads, minimally associated with blood pressure for older household heads, and only slightly associated with the blood pressure of their spouses. The regression coefficients for the lifestyle incongruity by age by sex interaction term was significant at P ≤ 0.01 for both systolic and diastolic blood pressure. The consistency of these results with expectations based on the ethnographic record is emphasized in the interpretation. We feel that the lifestyle incongruity model represents an empirically successful attempt to link global political-economic processes, local social structure, and biological outcomes. Am J Phys Anthropol 102:55–66, 1997. © 1997 Wiley-Liss, Inc.     

Role of zinc in regulation of arterial blood pressure and in the etiopathogenesis of arterial hypertension

Increased gastrointestinal absorption and urinary excretion of zinc has been confirmed in experimental and clinical studies on primary arterial hypertension as a result from changes of intracellular and extracellular zinc content. In arterial hypertension, the levels of zinc in serum, lymphocyte, and bone decrease while increasing in heart, erythrocytes, kidney, liver, suprarenal glands and spleen. These changes result in the loss of zinc homeostasis that leads to various degrees of deficiency, not entirely compensated by nutritional factors or increased absorption in the gastrointestinal tract. Loss of zinc homeostasis can be both cause and effect of high blood pressure. In the present review, the role of zinc metabolism changes and its mechanisms in arterial hypertension are discussed.     

Cardiorespiratory fitness influences the blood pressure response to experimental weight gain

Objective: We tested the hypothesis that with similar weight gain the increase in blood pressure (BP) would be smaller in men with higher cardiorespiratory fitness (HCRF) than in men with lower cardiorespiratory fitness (LCRF). Research Methods and Procedures: Thirteen men (age = 23 ± 1, BMI = 24 ± 1) were overfed by ～1000 kcal/d over ～8 weeks to achieve a 5‐kg weight gain. Resting BP and 24‐hour ambulatory BP, body composition, and fat distribution were measured. Results: Cardiorespiratory fitness (CRF) was higher in the HCRF group compared with the LCRF group (49.9 ± 1.2 vs. 38.1 ± 1.4 mL/kg per minute, p < 0.001). At baseline, body weight was similar in the HCRF and LCRF groups, whereas the HCRF group displayed lower levels of total body fat (13.0 ± 1.7 vs. 16.9 ± 1.3 kg, p = 0.049) and abdominal visceral fat (49 ± 6 vs. 80 ± 14 cm², p = 0.032). Resting BP and 24‐hour ambulatory BP were similar in the two groups at baseline. After weight gain, body weight increased ～5 kg (p < 0.05) in both groups; the changes in body composition and regional fat distribution were similar. As hypothesized, the increases in resting systolic (1 ± 2 vs. 7 ± 2 mm Hg; p = 0.008) and diastolic (?1 ± 4 vs. 5 ± 1 mm Hg; p = 0.005) BP were smaller in the HCRF group. CRF was correlated with the increases in resting systolic (r = ?0.64; p = 0.009) and diastolic BP (r = ?0.80; p < 0.001). Furthermore, the relationship between CRF and BP remained significant after adjusting for the changes in the proportion of total abdominal fat gained as visceral fat. Discussion: These findings suggest that higher levels of CRF are associated with a smaller increase in BP with weight gain, independently of changes in abdominal visceral fat.     

Physiological role of a novel neuropeptide, apelin, and its receptor in the rat brain

Apelin, a peptide recently isolated from bovine stomach tissue extracts, has been identified as the endogenous ligand of the human orphan APJ receptor. We established a stable Chinese hamster ovary (CHO) cell line expressing a gene encoding the rat apelin receptor fused to the enhanced green fluorescent protein, to investigate internalization and the pharmacological profile of the apelin receptor. Stimulation of this receptor by the apelin fragments K17F (Lys1-Phe-Arg-Arg-Gln-Arg-Pro-Arg-Leu-Ser-His-Lys-Gly-Pro-Met-Pro-Phe17) and pE13F (pGlu5-Arg-Pro-Arg-Leu-Ser-His-Lys-Gly-Pro-Met-Pro-Phe17) resulted in a dose-dependent inhibition of forskolin-induced cAMP production and promoted its internalization. In contrast, the apelin fragments R10F (Arg8-Leu-Ser-His-Lys-Gly-Pro-Met-Pro-Phe17) and G5F (Gly13-Pro-Met-Pro-Phe17) were inactive. The physiological role of apelin and its receptor was then investigated by showing for the first time in rodent brain: (i) detection of apelin neurons in the supraoptic and paraventricular nuclei by immunohistochemistry with a specific polyclonal anti-apelin K17F antibody; (ii) detection of apelin receptor mRNA in supraoptic vasopressinergic neurons by in situ hybridization and immunohistochemistry; and (iii) a decrease in vasopressin release following intracerebroventricular injection of K17F, or pE13F, but not R10F. Thus, apelin locally synthesized in the supraoptic nucleus could exert a direct inhibitory action on vasopressinergic neuron activity via the apelin receptors synthesized in these cells. Furthermore, central injection of pE13F significantly decreased water intake in dehydrated normotensive rats but did not affect blood pressure. Together, these results suggest that neuronal apelin plays an important role in the central control of body fluid homeostasis.     

Innervation of human omental arteries and veins and vasomotor response to noradrenaline, neuropeptide Y, substance P and vasoactive intestinal peptide

Human omental arteries and veins are supplied with nerve fibers containing noradrenaline (NA) and neuropeptide Y (NPY); these two agents probably co-exist in perivascular sympathetic nerve fibers. Substance P (SP)- or vasoactive intestinal peptide (VIP)-containing fibers could not be detected. In studies on isolated omental vessels NA produced constriction. The results of blockade experiments suggest that human omental arteries are equipped predominantly with alpha 1-adrenoceptors and omental veins with a mixture of alpha 1- and alpha 2-adrenoceptors. NPY at a concentration of 10(-7) M or higher had a weak contractile effect on veins and virtually no effect on arteries. NPY at a concentration of 3 X 10(-8) M shifted the NA concentration response curve to the left in arteries (pD2 = 5.8 for NA versus 6.6. for NA in the presence of NPY; P less than 0.001) but not in veins. Both SP and VIP relaxed arteries precontracted with NA or prostaglandin F2 alpha (PGF2 alpha). The potency of SP as a relaxant agent was similar in arteries and veins; the effect of VIP was elicited at lower concentrations in veins than in arteries.     

Spinal and peripheral modulation of gastric acid secretion and arterial pressure by neuropeptide Y, peptide YY, and pancreatic polypeptide in rats

Spinal and peripheral modulation of pentagastrin-stimulated gastric acid secretion by the pancreatic polypeptide-fold (PP-fold) peptides, neuropeptide Y (NPY), peptide YY (PYY), and pancreatic polypeptide (PP), in urethane-anesthetized rats was evaluated. Neuropeptide Y, PYY, and PP (400 pmol) were administered via intravenous (IV) and intrathecal (IT) injections. The ₂ antagonist, yohimbine, was used to evaluate the role of the ₂ adrenergic receptors in the modulation of pentagastrin-stimulated gastric acid secretion by NPY, PYY, and PP. Peptide YY and PP (IV) rapidly increased pentagastrin-stimulated gastric acid secretion. Peptide YY and PP (IT) increased pentagastrin-stimulated gastric acid secretion following administration into the thoracic (T8–T10) region of the spinal cord. The ₂ adrenergic receptor antagonist, yohimbine, did not modify the increases in pentagastrin-stimulated gastric acid secretion following PYY and PP (IV or IT) administration. Neuropeptide Y (IT) decreased pentagastrin-stimulated gastric acid secretion. However, in the presence of ₂ adrenergic receptor blockade, pentagastrin-stimulated gastric acid secretion was potentiated by NPY (IT) administration. Therefore, the inhibitory effect of NPY (IT) on pentagastrin-stimulated gastric acid secretion required the activation of ₂ adrenergic receptors in the spinal cord of rats. Mean arterial blood pressure (MAP) was increased immediately following NPY and PYY (IV) administration. During the same time period, PP (IV) decreased MAP in anesthetized rats. Mean arterial blood pressure was rapidly increased by NPY and PYY (IT) in anesthetized rats. The increase in MAP following PYY (IT) was partially attenuated in the presence of yohimbine. The modulation of MAP and gastric acid secretion by the PP-fold peptides occurred by independent mechanisms at spinal and peripheral sites in the rat. The modulation of pentagastrin-stimulated gastric acid secretion by PYY and PP in rats differed from that of the third member of the PP-fold family, NPY, following spinal and peripheral administration.     

Increase in the sensitivity of the vascular smooth muscle to constrictor factors after denervation and with a decrease in blood pressure

The effect of denervation on the contractile activity of the saphenous artery in normotensive rats and rats with regional hypotension was studied. Hypotension was caused by partial occlusion of the abdominal aorta distally from the renal arteries, and then, in four weeks, to denervate the saphenous artery, a portion of the femoral nerve in one of the limbs was resected. In two more weeks, the contractile responses of ring preparations of the saphenous artery (after removal of the endothelium and block of neuronal uptake and β-adrenoreceptors) were investigated under isometric conditions. In normotensive rats, the denervation led to an increase in the vascular sensitivity to norepinephrine, phenylephrine, serotonin, and KCl. Similar changes in contraction were caused by chronic hypotension; however, rats with hypotension exhibited no additional denervation-induced increase in the vascular sensitivity. After treatment with glyoxylic acid, the fluorescence intensity of the vascular adrenergic fibers adapted to a reduced pressure was lower than that in the norm. It was assumed that the vascular hypersensitivity in hypotension is caused by impairment of sympathetic innervation.     

新一代动物无创血压测定仪的研制及性能检验

目的：研制新一代“动物无创血压测定仪”。方法：本研究利用与人血压测定相似的原理,以自行开发、拥有自主知识产权的专用软件克服了动物舒张压的测定点较难精确标定的困难,成功研制出新一代“动物无创血压测定仪”。并与经典的动物有创血压测定法行同步比较。结果：在正常血压、高血压、低血压等不同情况下,两法测值极为相近,相关系数皆大于0．9。结论：本研制的新一代“动物无创血压测定仪”可作为家兔、大鼠血压无创测定的可靠方法。     

Identical immunoreactivity of afferents to the rat suprachiasmatic nucleus with antisera against avian pancreatic polypeptide,molluscan cardioexcitatory peptide and neuropeptide Y

Summary Avian pancreatic polypeptide (APP)-like, molluscan cardioexcitatory peptide (FMRF)-like and neuropeptide Y (NPY)-like immunoreactivities were studied in a secondary visual pathway in rat brain. The cell bodies of this pathway are located in the lateral geniculate nucleus and its terminal plexus is found in the suprachiasmatic hypothalamic nucleus (SCN). The neurons and terminal plexus demonstrated by antiserum to each peptide are identical, and immunoreactivity is blocked by preabsorption of each antiserum with a low concentration of the antigen against which it was raised. Immunoreactivity is also blocked by preabsorption of each antiserum with either NPY or APP. In contrast, APP- and NPY-like immunoreactivities are blocked only partially when these antisera are preabsorbed with concentrations of FMRF as high as 100 M. Since NPY is the only one of these peptides that has been isolated from mammalian brain, we conclude that NPY is the endogenous CNS peptide produced by neurons of the lateral geniculate-SCN projection.     

慢性动脉血压监测模型在惊恐条件反射中的应用

目的：探索一种新的、可靠的模型,用于惊恐条件反射的相关研究。方法：通过使用条件刺激(声音)和非条件刺激(足部电击)相结合的方法,可使动物对条件刺激产生惊恐反应。同时对动脉血压进行长期监测并测定利多卡因阻断杏仁基底外侧核群前后的血压变化。结果：该惊恐条件反射建立后(需经4d训练),单独给予动物条件刺激即可引起血压明显升高。我们将它作为条件反射已形成的标志。此时,用利多卡因阻断杏仁基底外侧核群的作用,单独给予动物条件刺激不再引起血压明显升高。结论：慢性动脉血压监测模型在惊恐条件反射的研究中是一种可靠的动物模型。     

Expression of a novel neuropeptide, NVGTLARDFQLPIPNamide, in the larval and adult brain of Drosophila melanogaster

Advances in mass spectrometry and the availability of genomic databases made it possible to determine the peptidome or peptide content of a specific tissue. Peptidomics by nanoflow capillary liquid chromatography tandem mass spectrometry of an extract of 50 larval Drosophila brains, yielded 28 neuropeptides. Eight were entirely novel and encoded by five not yet annotated genes; only two genes had a homologue in the Anopheles gambiae genome. Seven of the eight peptides did not show relevant sequence homology to any known peptide. Therefore, no evidence towards the physiological role of these 'orphan' peptides was available. We identified one of the eight peptides, IPNamide, in an extract of the Drosophila adult brain as well. Next, specific antisera were raised to reveal the distribution pattern of IPNamide and other peptides from the same precursor, in larval and adult brains by means of whole-mount immunocytochemistry and confocal microscopy. IPNamide immunoreactivity is abundantly present in both stages and a striking similarity was found between the distribution patterns of IPNamide and TPAEDFMRFamide, a member of the FMRFamide peptide family. Based on this distribution pattern, IPNamide might be involved in phototransduction, in processing sensory stimuli, as well as in controlling the activity of the oesophagus.     

大鼠侧脑室注射神经降压素对血压的作用

雄性Ｓｐｒａｇｕｅ－Ｄａｗｌｅｙ大鼠,用乌拉坦腹腔麻醉,在侧脑室注射神经降压素（ＮＴ）（１０,２０μｇ）可引起血压升高或降低,心率减慢,预先ｉｃｖ ａ１受体阻断剂哌唑嗪,可阻断ＮＴ的中枢升压反应,预先ｉｃｖ Ｍ受体阻断剂硫酸阿托品,可阻断ＮＴ的中枢降压反应,预先ｉｃｖ Ｈ１受体阻断剂扑尔敏或Ｈ２受体阻断剂甲氰咪胍,对ＮＴ的中枢心血管效应均无明显影响。实验结果表明：脑中ＮＴ升高可使血压升高或降低;在     

Reduced preprandial dipping accounts for rapid elevation of blood pressure and renal sympathetic nerve activity in rabbits fed a high-fat diet

Consumption of a high-fat diet (HFD) by rabbits results in increased blood pressure (BP), heart rate (HR), and renal sympathetic nerve activity (RSNA) within 1 wk. Here, we determined how early this activation occurred and whether it was related to changes in cardiovascular and neural 24-h rhythms. Rabbits were meal-fed a HFD for 3?wks, then a normal-fat diet (NFD) for 1 wk. BP, HR, and RSNA were measured daily in the home cage via implanted telemeters. Baseline BP, HR, and RSNA over 24?h were 71?±?1?mm Hg, 205?±?4 beats/min and 7?±?1 normalized units (nu). The 24-h pattern was entrained to the feeding cycle and values increased from preprandial minimum to postprandial maximum by 4?±?1?mm Hg, 51?±?6 beats/min, and 1.6?±?.6 nu each day. Feeding of a HFD markedly diminished the preprandial dip after 2?d (79–125% of control; p?<?0.05) and this reduction lasted for 3?wks of HFD. Twenty-four-hour BP, HR, and RSNA concurrently increased by 2%, 18%, and 22%, respectively. Loss of preprandial dipping accounted for all of the BP increase and 50% of the RSNA increase over 3?wks and the 24-h rhythm became entrained to the light-dark cycle. Resumption of a NFD did not alter the BP preprandial dip. Thus, elevated BP induced by a HFD and mediated by increased sympathetic nerve activity results from a reduction in preprandial dipping, from the first day. Increased calories, glucose, insulin, and leptin may account for early changes, whereas long-term loss of dipping may be related to increased sensitivity of sympathetic pathways. (Author correspondence: geoff.head@baker.edu.au)     

Differential acquisition of specific components of a classically conditioned arterial blood pressure response in rat

Presenting a 15-s pulsed tone, the conditional stimulus (CS(+)), followed by 0.5-s tail shock, to a well-trained rat causes a sudden, but transient, pressor response (C(1)). Blood pressure (BP) then drops before increasing again (C(2)). A steady tone of the same frequency never followed by a shock (a discriminative stimulus, or CS(-)) evokes a C(1) but not a C(2) response. Experiment 1 tested the hypothesis that this BP response pattern does not depend on the nature of the tone (i.e., pulsed vs. steady) used for CS(+) and CS(-). The tones were reversed from the traditional paradigm, above, in nine rats. The C(1) BP increase for a steady-tone CS(+) (+4.8 +/- 1.9 mmHg, mean change +/- SE) and a pulsed CS(-) (+2.9 +/- 1.3 mmHg) did not differ. Conversely, C(2) showed a clear discrimination (CS(+): +5.1 +/- 1.2 mmHg, CS(-): +0 .7 +/- 0.8 mmHg; P < 0.05). Experiment 2 tested the hypothesis that the C(1) and C(2) BP responses first appear at different times during training. On training day 1, five 15-s pulsed tones (CS(+)) were presented to each of 18 rats; the last tone was followed by a tail shock. Likewise, five steady CS(-) tones never followed by shock were given. Training continued for 2 more days, with each CS(+) followed by shock. At the end of day 2, CS(+) evoked a C(1) BP response (+3.9 +/- 0.9 mmHg) but no C(2) (+0.6 +/- 0.4 mmHg, not significant vs. pretone). By the end of day 3, CS(+) evoked a significant (vs. baseline) C(1) (+7.3 +/- 1.4 mmHg) and C(2) (+3.3 +/- 0.8 mmHg). Conversely, although CS(-) evoked a C(1) response (3.5 +/- 1.3 mmHg), there was no C(2) (+0.7 +/- 0.5 mmHg; not significant). We conclude that 1) C(1) and C(2) are acquired at different rates, 2) early in training C(1) is an orienting response evoked by both tones, and 3) C(2) is only acquired as an animal learns to associate the CS(+) tone with shock. This suggests that C(1) and C(2) are controlled by different processes in the brain.     

急性低氧对家兔血压心率微血管反应性及自由基的影响

目的 :探讨不同急性低氧下的血压、心率、微血管反应性和自由基的影响。方法 :实验采用家兔人工吸入含氧量为 12 .5 %和 8.5 %氮氧混合气体 (模拟 4 0 0 0m和 6 5 0 0m高原急性低氧 )。急性低氧时间分别为 5、10、15、2 0min ,观察血压、心率、微血管反应性和自由基影响。结果 :①急性低氧 5min时收缩压略有升高 ,以后变为降低 ;舒张压在急性低氧 2 0min后明显降低 (P <0 .0 5 ) ;②心率随急性低氧时间的延长变慢 ,尤其含氧量 8.5 %急性低氧组明显 (P <0 .0 5 )。③眼结膜微血管管径随急性低氧时间延长呈现扩张 (P <0 .0 5 ) ,血细胞流速减慢 (P <0 .0 5 ,P <0 .0 1)。④急性低氧 2 0min后SOD活力明显降低 (P <0 .0 5 ) ,MDA含量升高 (P <0 .0 5 )。结论 :急性低氧可使血压降低 ,心率减慢 ,微血管管径变大和血细胞流速减慢 ,同时体内自由基产生增加。     

Ontogeny of a new enteric peptide, neuropeptide W (NPW), in the developing rat stomach

Neuropeptide W (NPW), a novel endogenous peptide for G protein-coupled receptors GPR7 and GPR8, is expressed in the gastric antral mucosa of rat, mouse, and human stomachs. Here, we studied the ontogeny of NPW in the developing rat stomach. Real-time RT-PCR showed that NPW gene expression was initially detectable in embryonic day 14 (E14) stomach and gradually increased during the progress of age until birth, postnatal day 1 (P1). NPW mRNA level in the stomach increased again from the weaning period (P21) until reaching adulthood. Immunohistochemistry using polyclonal antibodies raised against rat NPW revealed that NPW-positive cells were detected in the P1 antral stomach and gradually increased during the development of age. Furthermore, double immunohistochemistry demonstrated that NPW colocalized with gastrin in P1 rat stomach. These data will provide clues to physiological functions of NPW in the development of rat stomach.     

葛根素对冷激诱导的高血压小鼠的影响

目的：检测葛根素灌胃对冷激诱导的高血压小鼠的血压血脂及肾脏结构的影响。方法：小鼠分为正常对照组、冷激对照组、冷激葛根素饲喂组（2,5,10ms／kg bw3组）（n=12）。以寒冷刺激（4±2℃）建立小鼠高血压模型,每天定时灌胃葛根素治疗,对照组给予聚乙烯吡咯烷酮溶液。连续饲喂18d．检测各组小鼠血压、血脂含量,石蜡切片观察肾脏结构。结果：冷激对照组小鼠血压显著高于正常对照组（P〈0．01）,葛根素饲喂组血压显著低于冷激对照组（P〈0．05）。冷激对照组TG含量显著高于正常对照组（P〈0．01）,而冷激饲喂组TG含量明显降低（P〈0．05）;冷激饲喂组TC含量与冷激对照组相比有所降低但无统计学意义;2mg／kg BW葛根素组LDL-C显著低于冷激对照组（P〈0．01）,各组间HDL-C含量比较无统计学意义,但葛根素饲喂组HDL-C／LDL-C值显著高于冷激对照组。冷激对照组肾小管上皮细胞水肿,内腔极度缩小,肾小球明显胀大,肾小囊腔显著变窄,葛根素饲喂组肾小管水肿基本消失,内腔明显增大,肾小球、肾小囊结构趋于正常。结论：葛根素灌服具有降血压、降血脂、改善病变肾脏结构的作用。     

Influence of nitric oxide-mediated vasodilation on the blood pressure measured with the tail-cuff method in the rat

Systolic blood pressure (SBP) is frequently measured in rats by the tail cuff method, which usually comprises pulse/flow disappearance and reappearance during cuff inflation (Inf) and deflation (Def), separated by an interval between cycles (IBC). Although Def values are habitually used to estimate SBP, in 58 Wistar rats we found (Def–Inf) to be −6 ± 1 mmHg, indicating that Def  < Inf in most cases. When the IBC was lengthened to 2 min, (Def–Inf) was increased to −17 ± 2 mmHg, indicating the probable accumulation of a vasodilating metabolite. This increase of (Def–Inf) was prevented by papaverine, indicating its relation to smooth muscle contractility. Adrenergic blockade did not prevent the increase of (Def–Inf), but pretreatment with L-NAME decreased it to −5 ± 2 mmHg (p < 0.05). Simultaneous measurement of SBP by tail-cuff method and carotid cannulation revealed that the Inf value was the most accurate estimation of intravascular SBP. We conclude that: (1) the Inf value should be taken as representative of SBP, since depending on the duration of suprasystolic compression the Def value can underestimate it, and (2) nitric oxide accumulation due to flow deprivation was the main cause of SBP underestimation by Def values. Mariana Fritz—Recipient of a Fellowship from the Agencia Nacional de Promoción Científica y Tecnológica (ANPCYT), República Argentina. Gustavo Rinaldi—Established Investigator of the Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET), República Argentina.     

肥厚型心肌病患者运动血压反应异常的两类表现及其相关因素分析*

目的: 运动血压反应不足及运动后恢复期血压降低是肥厚型心肌病（HCM）患者常见的异常表现,本研究的目的是分析HCM患者这两类异常血压反应表现的相关因素及其与心肺运动功能的关系。方法: 回顾性研究2018年4月至2020年1月期间在阜外医院功能检测中心行心肺运动试验（CPET）的HCM患者219例。111例行CPET的性别、年龄匹配的正常体检者作为正常对照组。比较正常对照组与HCM组的CPET运动血压反应。将HCM患者分为运动血压反应正常组及运动血压反应不足组,以及运动后血压正常组及运动后恢复期血压降低组,分别比较上述两类运动血压反应异常者的临床情况及CPET功能指标。结果: 与正常对照组相比,HCM患者运动血压反应不足（8.7%比1.8%,P=0.016）及运动后恢复期血压降低（6.8%比0.0%,P=0.003）的发生率显著升高。在HCM患者中,与运动血压反应正常者相比,运动血压反应不足的HCM患者更多合并冠心病（P=0.029）、肺动脉高压（P=0.002）及房颤/房扑（P=0.036）;与运动后血压正常者相比,运动后恢复期血压下降的HCM患者静息流出道压差（P=0.017）更高,合并流出道梗阻比例（P=0.015）、合并收缩期二尖瓣前移现象（P=0.022）及左室射血分数（P=0.043）更高。经过Logistic多元回归分析,运动血压反应不足的独立相关因素为冠心病（β=1.519,P=0.013）、肺动脉高压（β=2.292, P=0.000）。而运动后恢复期血压下降仅与左室流出道压差有独立的相关性（β=0.018, P=0.005）。运动血压反应不足的HCM患者峰值摄氧量（P=0.003）、峰值心率（P=0.014）及心率储备（P=0.003）更低,NT末端B型脑钠肽前体（P=0.019）及二氧化碳通气当量斜率（P=0.000）更高。运动后恢复期血压下降与各种心肺功能指标均无相关性。结论: HCM运动血压反应不足及运动后恢复期血压降低的发生率均较正常人群显著升高。HCM患者运动血压反应不足与合并冠心病和肺动脉高压有显著的独立相关性,而运动后血压下降仅与左室流出道压差独立相关。运动血压反应不足的HCM患者心肺运动功能降低,而运动后恢复期血压降低与心肺运动功能无显著相关性。