Forebrain and lower brainstem participation in facilitatory and inhibitory regulation of the display of lordosis in female rats

Neural transection of the dorsal extrahypothalamic descending afferents by means of an L-shaped Halász knife at the anterior commissure (anterior roof deafferentation. ARD) markedly potentiated the display of lordosis and soliciting behaviors. Bilateral lesions of the ventromedial hypothalamus (VMH) attenuated lordotic activity in the ARD sham females but not in the ARD females. In contrast, the lesions in the pontine central gray concurrently with ARD effectively inhibited the display of lordosis but not soliciting behaviors. These results suggest that the VMH may not be a primary focus of the dorsal extrahypothalamic inhibitory influence on lordosis. The influence of this inhibitory system seems to be dominant in regulating the expression of lordosis behavior, compared to that of the hypothalamic lordosis facilitating system. Furthermore, the dorsal extrahypothalamic inhibitors influence which could be removed by ARD must be modified by the neural mechanism in the lower brain stem in which the pontine central gray may be actively involved.     

A simple intra-operative maneuver to decrease a duodenal ulcer hemorrhage temporarily: description and anatomical bases

Intraoperative hemostatic suture to treat a bleeding duodenal ulcer is sometimes difficult when there is massive hemorrhage. The aims of this paper are: (1) to describe a practical and easy intraoperative procedure which quickly decreases a massively bleeding duodenal ulcer, allowing the surgeon to identify the bleeding site clearly and obtain definitive hemostasis by suturing the involved vessels with a low risk of common bile duct lesion; and (2) to study in cadavers the anatomical basis of this surgical procedure already successfully performed on patients. Fourteen patients with massive duodenal ulcer bleeding, after unsuccessful endoscopic hemostasis, were operated on and included in this study. After surgical anterior gastroduodenotomy, the surgeon introduced a finger in a downward and forward direction in the bursa omentalis vestibule through the omental foramen. This simple and quick procedure decreased hemorrhage by compressing the gastroduodenal artery against the first part of the posterior surface of the duodenum. Twenty-four fresh blocks of normal tissue were removed from cadavers and were injected with silicone rubber through the common hepatic artery. The distance between the gastroduodenal artery and the omental foramen was measured. With this maneuver the surgeon can clearly see the exact bleeding site and perform an adequate suture with a minor risk of common bile duct lesion.     

Perivascular Drainage of Amyloid-β Peptides from the Brain and Its Failure in Cerebral Amyloid Angiopathy and Alzheimer's Disease

Alzheimer's disease is the commonest dementia. One major characteristic of its pathology is accumulation of amyloid-β (Aβ) as insoluble deposits in brain parenchyma and in blood vessel walls [cerebral amyloid angiopathy (CAA)]. The distribution of Aβ deposits in the basement membranes of cerebral capillaries and arteries corresponds to the perivascular drainage pathways by which interstitial fluid (ISF) and solutes are eliminated from the brain—effectively the lymphatic drainage of the brain. Theoretical models suggest that vessel pulsations supply the motive force for perivascular drainage of ISF and solutes. As arteries stiffen with age, the amplitude of pulsations is reduced and insoluble Aβ is deposited in ISF drainage pathways as CAA, thus, further impeding the drainage of soluble Aβ. Failure of perivascular drainage of Aβ and deposition of Aβ in the walls of arteries has two major consequences: (i) intracerebral hemorrhage associated with rupture of Aβ-laden arteries in CAA; and (ii) Alzheimer's disease in which failure of elimination of ISF, Aβ and other soluble metabolites from the brain alters homeostasis and the neuronal environment resulting in cognitive decline and dementia. Therapeutic strategies that improve elimination of Aβ and other soluble metabolites from the brain may prevent cognitive decline in Alzheimer's disease.     

Synaptic mechanisms acting on lumbar motoneurons during postural augmentation induced by serotonin injection into the rostral pontine reticular formation in decerebrate cats

Intrapontine microinjections of serotonin in acutely decerebrated cats resulted in the bilateral augmentation of the postural muscle tone of the hindlimbs. Optimal injection sites were located in the dorsomedial part of the rostral pontine reticular formation corresponding to the nucleus reticularis ponds oralis (NRPo). In this study, attempts were made to elucidate the cellular basis for the serotoninergically induced augmentation of postural muscle tone by recording the electromyographic (EMG) activity of hindlimb extensor muscles, the monosynaptic reflex responses evoked by electrical stimulation of group Ia muscle afferent fibres and the membrane potentials of hindlimb alpha-motoneurons (MNs). Serotonin injections resulted not only in the augmentation of the EMG activity of gastrocnemius soleus muscles, but also in the restoration of EMG suppression, which was induced by previous injection of carbachol into the NRPo. Extensor and flexor monosynaptic reflex responses were facilitated by serotonin injections into the NRPo. Such reflex facilitation was not induced by serotonin injections into the mesencephalic or the medullary reticular formation. Intrapontine serotonin injections resulted in membrane depolarization of extensor and flexor MNs with decreases in input resistance and rheobase. Spontaneous depolarizing synaptic potentials (EPSPs) increased in both frequency and amplitude. Peak voltage of Ia monosynaptic EPSPs also increased. Serotonin injections which followed carbachol injections resulted in membrane depolarization of MNs along with an increase in the frequency of spontaneous EPSPs and a decrease in carbachol-induced inhibitory postsynaptic potentials. Following pontine carbachol injections, antidromic and orthodromic responses in MNs were suppressed. Discharges of MNs evoked by intracellular current injections were also suppressed, but were restored following serotonin injections. These results indicate that postsynaptic excitation, presynaptic facilitation and disinhibition (withdrawal of postsynaptic inhibition) simultaneously act on the hindlimb MNs during serotonin-induced postural augmentation and restoration.     

Overall results in 304 consecutive patients with acute spontaneous subarachnoid hemorrhage

The results obtained in 304 consecutive patients with spontaneous subarachnoid hemorrhage are described, the majority of whom (86%) were admitted while in acute condition. Only 46% of the patients in this series were in good condition at admission. The initial management was standardized for all patients, but the protocol of "delayed surgery" was applied to patients with subarachnoid hemorrhage from aneurysmal rupture. Two hundred and twenty-two patients (73%) had intracranial aneurysms. Of these, 20 (9%) were moribund and died shortly after admission; nine (4%) underwent emergency surgery due to the coexistence of a life-threatening cerebral hematoma; seven (3%) were operated upon within 3 days of admission; 78 (35%) died after rebleeding or after steady deterioration of the patient's condition due to vasospasm while awaiting surgery. Of the remaining 108 patients ready for delayed surgery, 12 (11%) (operation refused, elderly patients in poor general condition, spontaneous thrombosis of the aneurysm) were treated conservatively, and 96 (89%), who were in various clinical conditions, were actually operated on. Of these 96 patients, 79 (82%) exhibited excellent or good results, 5 (5%) were disabled, and 12 (12%) died. In the authors' experience, the overall management of intracranial aneurysms in unselected patients according to the protocol of delayed surgery results in significant loss of patients awaiting surgery, and good surgical results in the survivors.     

尼莫地平联合亚低温疗法治疗SAH后脑血管痉挛的疗效观察

目的探讨尼莫地平联合亚低温疗法治疗蛛网膜下腔出血(SAH)后脑血管痉挛的疗效。方法 93例SAH后脑血管痉挛患者随机分为两组。在常规治疗基础上,对照组采用亚低温疗法治疗,观察组采用尼莫地平联合亚低温疗法治疗。比较两组的治疗效果。结果观察组的总有效率为95.74%,高于对照组的80.43%(P <0.05)。治疗后,观察组的IL-6、 TNF-α、 hs-CRP水平均低于对照组,动脉平均血流速度高于对照组(P <0.05)。结论尼莫地平联合亚低温疗法治疗SAH后脑血管痉挛的效果显著,可有效抑制机体炎性反应,提升动脉平均血流速度。     

急性非静脉曲张性上消化道出血治疗的护理

目的研究分析急性非静脉曲张性上消化道出血治疗的护理效果。方法选择我院于2019年3月—2020年12月内收治的360例急性非静脉曲张性上消化道出血患者,将所有患者按照随机数表方法,分为对照组(180例,进行基础性护理干预)和观察组(180例,进行细节性护理干预)。对两组患者在护理完成后的效果进行收集和分析。结果对照组患者在采取常规护理方法干预后,其消化道功能恢复时间与住院时间分别为(6.84±1.24)d、(9.26±2.18)d;观察组患者在采取个性化护理方式干预后,消化道功能恢复时间与住院时间分别为(4.48±0.87)d、(6.05±1.24)d。两组相比较,观察组住院时间较短、消化道功能恢复较快,差异具有统计学意义(P<0.05)。结论在胃镜下治疗急性非静脉曲张性上消化道出血患者给予细节性护理干预能够提高手术效果,减少住院时间,加快病情恢复。     

脑出血急性期血肿扩大的临床分析

目的：探讨脑出血急性期血肿扩大的发生率、原因、临床表现、预后及采取的相应措施。方法：回顾性分析1994-2000年间诊治的867例脑出血病人的临床和CT资料。结果：脑出血急性期血肿扩大的发生率为20.1%,其主要与血压增高的程度、凝血功能、出血部位、血肿形态及早期过度脱水有关,血肿扩大增加了病人的死亡率。结论：血肿扩大的发生影响病人预后,应尽早确诊,采取积极防治措施,改善病人预后。     

糖尿病脑梗死合并上消化道出血的危险因素分析

目的　探讨糖尿病性脑梗死 (DCI)并发上消化道出血的可能危险因素。方法　对DCI合并上消化道出血患者进行临床分析及病例对照研究。结果　上消化道出血发生率为 18 75 % (9/ 48) ,经 t及 χ2 检验发现 :年龄 ,有TIA或CI史 ,血糖、血尿素氮或肌酐升高 ,CI面积 >2cm或多发性CI、ECG异常等因素与对照组比较有显著性差异 (P <0 0 5 )。逐步回归显示上消化道出血与年龄、高血压、随机血糖、糖化血红蛋白、CI病灶面积>2cm或多发性CI呈正相关。结论　认为老年、高血压、高血糖、大面积及多发性CI可能是DCI合并上消化道出血的危险因素。     

巯甲丙脯酸用于流行性出血热治疗临床观察

目的观察巯甲丙脯酸用于流行性出血热治疗的临床效果。方法病人随机分为A、B、C3组,A组在进入少尿期口服巯甲丙脯酸25mg,日3次;B组在少尿期并发高血压时开始服用,剂量方法同A组。C组在少尿期并发高血压时口服复方降压片1～2片,每日3次。其他治疗相同。结果A组无1例发生高血压;B组用药后4～6小时血压开始下降,72小时后血压稳定且正常。C组血压偏高。A、B组肾功能恢复快,并发症少,病程短。结论巯甲丙脯酸用于治疗流行性出血热可减少或防止急性肾功能衰竭,减少并发症。