Cardiovascular Effects of Acrylic Bone Cement in Rabbits and Cats

The cardiovascular responses to forcing acrylic bone cement, Plasticine, or soft paraffin wax into the medullary cavity of the femur have been studied in rabbits and cats. An acute fall in blood pressure, occurring within a few seconds of insertion, was demonstrated with each substance. In a few of the animals the blood pressure response had a second more protracted component and it is suggested that more than one mechanism is involved. The cardiovascular effects that have been observed in man when acrylic cement is used in prosthetic hip surgery also may be due to more than one mechanism.     

Cardiovascular Effects of Methylmethacrylate Cement

Experiments were carried out on dogs in an attempt to identify the mechanisms underlying the systemic hypotension associated with the application of acrylic cement substances to raw bone surfaces, as in reconstructive hip surgery. Intravenous injection of the liquid component of such cements (monomeric methylmethacrylate) into six dogs produced a significant fall in blood pressure together with an increase in heart rate and cardiac output. This seemed to be due to peripheral vasodilatation caused directly by the monomer and not through the release of histamine. Absorption of free monomer from the mixed cement into the systemic circulation at operation is likely to have the same effect. Precautionary measures can be taken and groups of patients who are especially at risk can be identified, thus reducing the hazards of total hip replacement.     

Catheterization of the Carotid Artery and Jugular Vein to Perform Hemodynamic Measures,Infusions and Blood Sampling in a Conscious Rat Model

The success of a small animal model to study critical illness is, in part, dependent on the ability of the model to simulate the human condition. Intra-tracheal inoculation of a known amount of bacteria has been successfully used to reproduce the pathogenesis of pneumonia which then develops into sepsis. Monitoring hemodynamic parameters and providing standard clinical treatment including infusion of antibiotics, fluids and drugs to maintain blood pressure is critical to simulate routine supportive care in this model but to do so requires both arterial and venous vascular access. The video details the surgical technique for implanting carotid artery and common jugular vein catheters in an anesthetized rat. Following a 72 hr recovery period, the animals will be re-anesthetized and connected to a tether and swivel setup attached to the rodent housing which connects the implanted catheters to the hemodynamic monitoring system. This setup allows free movement of the rat during the study while continuously monitoring pressures, infusing fluids and drugs (antibiotics, vasopressors) and performing blood sampling.     

Some factors affecting tissue Po2 in the carotid body.

In the carotid body (CB) of the anesthetized cat tissue Po2 (Pto2) measured with a micro O2 electrode averaged about 65 mmHg at normal arterial pressure (mean = 96 mmHg). Pto2 correlated significantly with the hematocrit of the arterial blood but not with % saturation. When arterial pressure was reduced (mean = 58 mmHg) by bleeding Pto2 fell significantly. Phentolamine injection (1 mg/kg iv) at the reduced pressure caused Pto2 to rise significantly. At normal arterial pressure blowing moistened O2 over the CB did not affect Pto2 if the electrode tip was about 90 mum into the CB. At a reduced pressure (and blood flow) the sensitive depth increased to about 301 mum, and to about 600 mum when flow was stopped. We concluded that a) the increased chemoceptor discharge usually seen with hemorrhage is due to reduced Pto2; b) the reduction in Pto2 is probably due to reduced blood flow which is, in turn, caused partly, at least, by sympathetic nervous system activity; c) O2 content, rather than Po2, may determine chemoreceptor discharge rate; and d) there are no barriers in the CB which are impermeable to O2.     

Effect of nicergoline and dihydroergotamine, injected into the cerebral ventricles, on arterial pressure in the cat

Nicergoline, injected into the cerebral ventricles of anaesthetized cats induced a moderate, but longlasting and dose-dependent fall of the blood pressure. Dihydroergotamine, in moderate doses, had no effect on the arterial blood pressure. Toxic doses of nicergoline and dihydroergotamine provoked a pronounced fall of the arterial blood pressure and inhibition of the respiration. Bradycardia only appeared after toxic doses of dihydroergotamine. It is concluded that the hypotensive effect of nicergoline is at least in part central in origin.     

基于卷积神经网络-长短期记忆神经网络模型利用光学体积描记术重建动脉血压波信号

目的 直接动脉血压（arterial blood pressure,ABP）连续监测是侵入式的,传统袖带式的间接血压测量法无法实现连续监测。既往利用光学体积描记术（photoplethysmography,PPG）实现了连续无创血压监测,但其为收缩压和舒张压的离散值,而非ABP波的连续值,本研究期望基于卷积神经网络-长短期记忆神经网络（CNN-LSTM）利用PPG信号波重建ABP波信号,实现连续无创血压监测。方法 构建CNN-LSTM混合神经网络模型,利用重症监护医学信息集（medical information mart for intensive care,MIMIC）中的PPG与ABP波同步记录信号数据,将PPG信号波经预处理降噪、归一化、滑窗分割后输入该模型,重建与之同步对应的ABP波信号。结果 使用窗口长度312的CNN-LSTM神经网络时,重建ABP值与实际ABP值间误差最小,平均绝对误差（mean absolute error,MAE）和均方根误差（root mean square error,RMSE）分别为2.79 mmHg和4.24 mmHg,余弦相似度最大,重建ABP值与实际ABP值一致性和相关性情况良好,符合美国医疗器械促进协会（Association for the Advancement of Medical Instrumentation,AAMI）标准。结论 CNN-LSTM混合神经网络可利用PPG信号波重建ABP波信号,实现连续无创血压监测。     

Estimation of blood pressure-related parameters by electrical impedance measurement.

In 13 healthy volunteers a computerized experimental set-up was used to measure the electrical impedance of the upper arm at changing cuff pressure, together with the finger arterial blood pressure in the contralateral arm. On the basis of a model for the admittance response, the arterial blood volume per centimeter length (1.4 +/- 0.3 ml/cm), the venous blood volume as a percentage of the total blood compartment (49.2 +/- 12.6%), and the total arterial compliance as a function of mean arterial transmural pressure were estimated. The effective physiological arterial compliance amounted to 2.0 +/- 1.3 microliters.mmHg-1.cm-1 and the maximum compliance to 33.4 +/- 12.0 microliters.mmHg-1.cm-1. Additionally, the extravascular fluid volume expelled by the occluding cuff (0.3 +/- 0.3 ml/cm) was estimated. These quantities are closely related to patient-dependent sources of an unreliable blood pressure measurement and vary with changes in cardiovascular function, such as those found in hypertension. Traditionally, a combination of several methods is needed to estimate them. Such methods, however, usually neglect the contribution of extravascular factors.     

A simplified method for metabolic studies in conscious swine

Reliable short-term blood access in conscious swine was provided by implanting multiple silastic catheters. Catheters were inserted into the aorta, hepatic vein, portal vein, and inferior vena cava through a midline laparotomy incision. Multiple catheters also were placed into the external jugular vein through a separate cervical incision. Catheter patency rates for blood withdrawal on the sixth post-operative day were: arterial 100%, hepatic 91%, portal 86%, inferior vena cava 71%. No animal had major wound or catheter infection on the seventh post-operative day. The methods described allow metabolic studies, including measurements of splanchnic blood flow, to be carried out either acutely or for up to at least 7 days post-operatively.     

Microvascular pressure and functional capillary density in extreme hemodilution with low- and high-viscosity dextran and a low-viscosity Hb-based O2 carrier

Blood losses are usually corrected initially by the restitution of volume with plasma expanders and subsequently by the restoration of oxygen-carrying capacity using either a blood transfusion or possibly, in the near future, oxygen-carrying plasma expanders. The present study was carried out to test the hypothesis that high-plasma viscosity hemodilution maintains perfused functional capillary density (FCD) by preserving capillary pressure. Microvascular pressure responses to extreme hemodilution with low- (LV) and high-viscosity (HV) plasma expanders and an exchange transfusion with a polymerized bovine cell-free Hb (PBH) solution were analyzed in the awake hamster window chamber model (n = 26). Systemic hematocrit was reduced from 50% to 11%. PBH produced a greater mean arterial blood pressure than the nonoxygen carriers. FCD was higher after a HV plasma expander (70 +/- 15%) vs. PBH (47 +/- 12%). Microvascular pressure spanning the capillary network was higher after a HV plasma expander (16-19 mmHg) compared with PBH (12-16 mmHg) and a LV plasma expander (11-14 mmHg) but lower than control (22-26 mmHg). FCD was found to be directly proportional to capillary pressure. The use of a HV plasma expander in extreme hemodilution maintained the number of perfused capillaries and tissue perfusion by comparison with a LV plasma expander due to increased mean arterial blood pressure and capillary pressure. The use of PBH increased mean arterial pressure but reduced capillary pressure due to vasoconstriction and did not maintain FCD.     

Finite element modelling of polymethylmethacrylate flow through cancellous bone

A mathematical model based on the Finite Element Method is developed to simulate the non-linear flow of acrylic bone cement through cancellous bone. The cancellous bone bed is modelled as a bed of parallel capillaries filled with equal spaced toroidal trabeculae. By manipulating the relative size of the torus and the capillary, the flow within bone of varying porosity is simulated. An apparent permeability based on the volume weighted average viscosity and Darcy's law is developed to describe the flow of the acrylic through the cancellous bone bed. The model predicts a cancellous bone permeability of 5.6 x 10(-9)-8.3 x 10(-9) m2 for linear flow. The non-linear behavior of the acrylic cement results in an increase of apparent permeability when compared to the permeability computed for linear flow. Estimates of penetration are achieved by running the model in a quasi-steady state fashion with pressure applied over a fixed time increment. Close agreement is shown between model predictions of penetration depth and experimental results available in the literature.     

Aminopeptidase A, which generates one of the main effector peptides of the brain renin-angiotensin system, angiotensin III, has a key role in central control of arterial blood pressure

Overactivity of the brain renin-angiotensin system (RAS) has been implicated in the development and maintenance of hypertension in several experimental animal models. We have recently reported that, in the murine brain RAS, angiotensin II (AngII) is converted by aminopeptidase A (APA) into angiotensin III (AngIII),which is itself degraded by aminopeptidase N (APN), both peptides being equipotent to increase vasopressin release and arterial blood pressure when injected by the intracerebroventricular (i.c.v.) route. Because AngII is converted in vivo into AngIII, the exact nature of the active peptide is not precisely known. To delineate their respective roles in the central control of cardiovascular functions, specific and selective APA and APN inhibitors are needed to block the metabolic pathways of AngII and AngIII respectively. In the absence of such compounds for APA, we first explored the organization of the APA active site by site-directed mutagenesis. This led us to propose a molecular mechanism of action for APA similar to that proposed for the bacterial enzyme thermolysin deduced from X-ray diffraction studies. Secondly, we developed a specific and selective APA inhibitor, compound EC33 [(S)-3-amino-4-mercaptobutylsulphonic acid], as well as a potent and selective APN inhibitor, PC18 (2-amino-4-methylsulphonylbutane thiol). With these new tools we examined the respective roles of AngII and AngIII in the central control of arterial blood pressure. A central blockade of APA with the APA inhibitor EC33 suppressed the pressor effect of exogenous AngII, suggesting that brain AngII must be converted into AngIII to increase arterial blood pressure. Furthermore, EC33, injected alone i.c.v. but not intravenously, caused a dose-dependent decrease in arterial blood pressure by blocking the formation of brain AngIII but not systemic AngIII. This is corroborated by the fact that the selective APN inhibitor PC18 administered alone via the i.c.v. route increased arterial blood pressure. This pressor response was blocked by prior treatment with the angiotensin type 1 receptor antagonist losartan, showing that blocking the action of APN on AngIII metabolism leads to an increase in endogenous AngIII levels, resulting in arterial blood pressure increase through an interaction with angiotensin type 1 receptors. These results demonstrate that AngIII is a major effector peptide of the brain RAS, exerting a tonic stimulatory control over arterial blood pressure. Thus APA, the enzyme responsible for the formation of brain AngIII, represents a potential central therapeutic target that justifies the development of APA inhibitors, crossing the blood-brain barrier, as central anti-hypertensive agents.     

Polymer composites for use in orthopedic surgery

Ever since Movin in (1950) and McKee in (1951) introduced the use of acrylic cement for fixation of hip prosthesis components a number of investigators have proposed various hip prosthesis designs using this cement fixation concept (Neale, 1967). This study was undertaken to support the hypothesis that certain dental materials could provide a more satisfactory bone-prosthesis bond than that presently possible with acrylic bone cement.^‡ Two restorative resins were found to have superior strength and resistance to thermal degradation when compared to acrylic bone cement. Tests of acrylic cement combined with apatite fillers suggest that restorative resin-anorganic bone composites would exhibit improved strength and toxicity properties and would also promote improved bonding due to resorption of the surface anorganic bone particles with subsequent bone infiltration and anchorage. Relatively high degradation of acrylic bone cement in accelerated aging tests suggests caution in using this material for implantation.     

Comparison of two methods of altering blood pressures for assessing neonatal cerebral blood flow autoregulation

The cerebral blood flow of newborn lambs at reduced and elevated arterial blood pressures, induced by intravenous infusion of sodium nitroprusside and phenylephrine hydrochloride as well as blood withdrawal and reinfusion, were compared. Both blood withdrawal and sodium nitroprusside infusion reduced mean arterial pressure from 83 to 60 mmHg (1 mmHg = 133 Pa). Reinfusion of blood increased arterial pressure to 94 mmHg. Phenylephrine hydrochloride infusion increased arterial pressure to 102 mmHg. The cerebral blood flows at corresponding arterial pressures were similar (coefficient of correlation = 0.88, P less than 0.01). Cerebral blood flow before and after infusion of phenylephrine hydrochloride and sodium nitroprusside into the brain via the carotid artery did not change. The results indicate that blood-borne phenylephrine hydrochloride and sodium nitroprusside, in concentrations that would alter arterial blood pressure significantly from its resting level, do not change cerebral blood flow directly.     

Effect on vasopressin release of microinjection of cholinergic agonists into the rat supraoptic nucleus.

It is likely that central cholinergic pathways to the paraventricular and supraoptic nuclei participate in the control of vasopressin release. We have shown previously that this is due, in part, to activation of muscarinic, but not nicotinic, receptors in the paraventricular nucleus. There is, however, reason to believe that this cholinergic effect in the supraoptic nucleus may be the result of activation of nicotinic receptors. To test this possibility, we have studied in conscious unrestrained rats the effect of microinjection of muscarinic and nicotinic agonists into the supraoptic nucleus on vasopressin release, mean arterial blood pressure, and heart rate. Under ether anesthesia, a stainless steel guide cannula was placed in the supraoptic nucleus 5-7 days before the experiment, and femoral, arterial, and venous catheters were implanted 1 day before the experiment. Microinjection of nicotine into the supraoptic nucleus at doses of 1 and 10 micrograms resulted in transient increases in the plasma vasopressin concentration that were 7-fold and 11-fold greater, respectively, than control values at 3 min. There were also small transient increases in mean arterial blood pressure, but heart rate was unchanged. The microinjection of 2 and 20 ng of oxotremorine, a muscarinic agonist, into the supraoptic nucleus had no effect on the plasma vasopressin concentration, mean arterial blood pressure, or heart rate. These doses of oxotremorine were previously shown to have potent stimulatory effects on vasopressin release when microinjected into the paraventricular nucleus. These findings suggest that the central cholinergic stimulation of vasopressin release is due, in part, to activation of muscarinic receptors in the paraventricular nucleus and nicotinic receptors in the supraoptic nucleus.     

Increases in platelet and red cell counts,blood viscosity,and arterial pressure during mild surface cooling: factors in mortality from coronary and cerebral thrombosis in winter.

Six hours of mild surface cooling in moving air at 24 degrees C with little fall in core temperature (0.4 degree C) increased the packed cell volume by 7% and increased the platelet count and usually the mean platelet volume to produce a 15% increase in the fraction of plasma volume occupied by platelets. Little of these increases occurred in the first hour. Whole blood viscosity increased by 21%; plasma viscosity usually increased, and arterial pressure rose on average from 126/69 to 138/87 mm Hg. Plasma cholesterol concentration increased, in both high and low density lipoprotein fractions, but values of total lipoprotein and lipoprotein fractions were unchanged. The increases in platelets, red cells, and viscosity associated with normal thermoregulatory adjustments to mild surface cooling provide a probable explanation for rapid increases in coronary and cerebral thrombosis in cold weather. The raised arterial pressure and possibly cholesterol concentration may contribute to slower components of the increased thrombosis.     

Vasoactive properties of dihomo-gamma-linolenic acid and series one prostaglandins in a freshwater teleost, Channa maculata

1. Prostaglandins A1, B1, E1 and F1 alpha (2-120 micrograms/kg), arachidonic acid and dihomo-gamma-linolenic acid (0.1-2 mg/kg) were injected intravenously into Channa maculata and changes in arterial blood pressure were recorded. 2. Injection of PGF1 alpha had no significant effect on arterial blood pressure. Injection of PGA1 and PGE1 was followed by dose-dependent hypotension whereas injection of PGB1 elicited significant dose-dependent increase in arterial blood pressure. 3. Both dihomo-gamma-linolenic acid and arachidonic acid were also depressor agents but dihomo-gamma-linolenic acid was more potent. 4. A single bolus intravenous injection of indomethacin (5 mg/kg) or 4 daily intraperitoneal injections (4 x 10 mg/kg) significantly lowered arterial blood pressure. One hour after pre-treatment of indomethacin, the vascular effects of both prostaglandin precursors were abolished. 5. It appears that the vascular effects of prostaglandins in Channa maculata are qualitatively different from those reported for mammals.     

去甲痛上腺素在大鼠缰核引起的心血管效应及其机制

Cardiovascular effect of norepinephrine (NE) in the habenular nucleus (Hb) and the underlying mechanism were investigated in urethane-anesthetized rats. NE microinjection into Hb produced a dose-dependent increase in mean arterial blood pressure and heart rate, an effect that could be attenuated by the pretreatment in Hb with alpha-receptor blocker phentolamine, but not by the pretreatment with beta-receptor blocker propranolol or physiological saline. Microinjection of kainic acid into Hb gave rise to a marked increase in mean arterial blood pressure and heart rate, but microinjection of lidocaine did not elicit significant cardiovascular effect. The above results suggest that NE in Hb plays an important role in cardiovascular control as a result of Hb excitation through activation of alpha-receptor.     

慢性动脉血压调节与原发性高血压病——Ⅰ.慢性动脉血压调节

机体在不同条件下维持动脉血压恒定的机理是不相同的。目前认为,长时程或慢性血压调节的关键器官是肾脏,这种调节与机体的水盐平衡有密切的关系。动脉血压的升高可以导致肾脏排尿量（或排钠量）的升高,即动脉血压与肾脏的排尿量（或排钠量）呈明显的正相关关系,称之为“压力-利尿作用”。当血容量升高时,通过肾脏的压力-利尿作用,可以排出过多的容量,维持动脉血压的恒定。只有在肾脏功能受到损伤的条件下,高血容量才可能引起高血压。     

NO在胆道加压引起的反射活动中的作用

向胆道加压至 4kPa ,可同时引起血压降低和Oddi括约肌 (SO)肌电活动减弱或消失 ,这总称为胆道加压反射 ,其中前者称为胆道 血压反射 ,后者称为胆道 SO反射。本实验应用 3 2只家兔观察一氧化氮 (NO)对胆道加压反射活动的影响。在静脉滴注去甲肾上腺素 4 μg/(kg·min)引起血压升高和SO肌电振幅增大的基础上 ,再行胆道加压至 4kPa ,仍同时引起血压降低和Oddi括约肌 (SO)肌电活动减弱 ;而在静脉注射NO合酶抑制剂NG 硝基 L 精氨酸 (L NNA) 10mg/kg引起血压升高和SO肌电振幅增大的基础上 ,再行胆道加压至 4kPa,全部动物胆道 血压反射受到完全抑制 ,即未出现血压降低反应 ;少数 ( 3 /8)动物胆道 SO反射受到完全抑制 ,多数 ( 5 /8)动物该反射受到明显抑制 (P <0 0 1)。向SO局部灌注L NNA ,只引起SO肌电振幅增大而不影响血压 ,在此基础上行胆道加压 ,对胆道 SO反射的影响与全身用药相似 ,对胆道 血压反射却无影响。这提示 ,这两种反射活动是相对独立的 ,是经不同传出途径和效应器实现的 ;且这两种反射都主要是通过NO介导的