预负荷／共同负荷联合血管收缩药对腰麻剖宫产术血流动力学变化

目的探讨预负荷／共同负荷联合小剂量血管收缩药盐酸麻黄碱注射液（上海信谊金朱药业有限公司）、盐酸去氧肾上腺索注射液（上海禾丰制药有限公司）对腰麻剖官产术中血流动力学的变化及预防低血压的有效性及安全性。方法选择剖官产术90例,随机分为3组,每组30例．ASAI～Ⅱ级。预负荷晶体液乳酸林格氏注射液（石家庄西药有限公司）6～8ml／kg联合共同负荷输入羟乙基淀粉130／0．4氯化钠溶液（万汶,北京费森尤斯卡比医药有限公司）10ml／kg。术中监测记录SBP、DBP、HR、ECG、SpO2。结果预负荷／共同负荷联合血管收缩药预防剖宫产术腰麻后低血压。P组和E组的低血压发生率明显低于C组（P〈0．05）;P组术中HR低于E组和C组。预防恶心、呕吐给于盐酸昂丹司琼注射液（齐鲁制药有限公司）,不良反应少,无明显呼吸抑制、无术后头痛现象。结论预负荷／共同负荷联合小剂量血管收缩药,有效降低腰麻后低血压的发生率,去氧肾上腺素比麻黄碱能更好维持产妇血流动力学的稳定。对新生儿无不良影响,安全。     

Effects of spinal anesthesia on response to main pulmonary arterial distension

Nonocclusive main pulmonary arterial distension produces peripheral pulmonary hypertension. The mechanism of this response is unknown. The effects of total spinal anesthesia on the response were studied in halothane-anesthetized dogs. Before total spinal anesthesia, main pulmonary arterial balloon inflation increased pulmonary arterial pressure and resistance without affecting systemic hemodynamic variables. Both right and left pulmonary arterial pressures were monitored to exclude unilateral obstruction with main pulmonary arterial balloon inflation. Total spinal anesthesia decreased cardiac output and systemic arterial pressures. After total spinal anesthesia, main pulmonary arterial distension still increased pulmonary arterial pressure and resistance. Right atrial pacing, discontinuation of halothane anesthesia, and norepinephrine infusion during total spinal anesthesia partially reversed the hemodynamic changes caused by total spinal anesthesia. The percent increase in pulmonary vascular resistance due to main pulmonary arterial distension was similar before total spinal anesthesia and during all experimental conditions during total spinal anesthesia. The pulmonary hypertensive response is therefore not dependent on central synaptic connections.     

腰- 硬联合麻醉用于老年人手术的应用体会

目的:探讨和总结腰-硬联合麻醉在老年人手术中的应用。方法:对128例老年下腹部和下肢手术患者,在腰-硬联合麻醉和硬膜外麻醉下进行手术,对其低血压发生率、镇痛效果和肌松效果情况进行研究析。结果:CSEA组低血压发生率4.67%,镇痛效果优为89.1%,肌松效果优为90.6%;CEA组低血压发生率17.18%,镇痛效果组优为67.2%,肌松效果优为60.9%。结论:老年人下腹部和下肢手术应用CSEA效果满意,安全性好。     

Hemodynamic monitoring and care of the patient of high risk for anesthesia.

Hemodynamic monitoring and care of the patient at high risk for anesthesia require a careful and systematic approach. During preoperative evaluation the patient at increased risk must be identified and correctable problems must be solved. The patient''s current medications must be reviewed because they may influence the choice of anesthetic approach and may alter the physiologic response to the stresses commonly associated with anesthesia. In addition to conventional clinical and electrocardiographic monitoring, perioperative hemodynamic monitoring may be desirable for patients at special risk, who are likely to have significant associated medical problems or to undergo complicated surgical procedures. No ideal induction agent exists, and hypotension secondary to peripheral vasodilation or myocardial depression, or both, is a potential problem. Patients with an inordinately high risk may benefit from mechanical circulatory assistance prior to induction of anesthesia. Attention to oxygenation, blood volume replacement and the prevention of hypertensive episodes are particularly important during anesthesia so that optimal cardiac performance is ensured and ischemia avoided. The stresses during emergence from anesthesia contribute to lability of the cardiovascular status and hypoxemia. The period of risk does not conclude with immediate recovery from anesthesia but extends through the postoperative phase. Careful monitoring and attention to the control of pain, prevention of hypotension and hypertension, adequate oxygenation, early mobilization and resumption of the administration of cardiac medications are important factors in a successful outcome.     

Bionic epidural stimulation restores arterial pressure regulation during orthostasis.

A bionic baroreflex system (BBS) is a computer-assisted intelligent feedback system to control arterial pressure (AP) for the treatment of baroreflex failure. To apply this system clinically, an appropriate efferent neural (sympathetic vasomotor) interface has to be explored. We examined whether the spinal cord is a candidate site for such interface. In six anesthetized and baroreflex-deafferentiated cats, a multielectrode catheter was inserted into the epidural space to deliver epidural spinal cord stimulation (ESCS). Stepwise changes in ESCS rate revealed a linear correlation between ESCS rate and AP for ESCS rates of 2 pulses/s and above (r2, 0.876-0.979; slope, 14.3 +/- 5.8 mmHg.pulses(-1).s; pressure axis intercept, 35.7 +/- 25.9 mmHg). Random changes in ESCS rate with a white noise sequence revealed dynamic transfer function of peripheral effectors. The transfer function resembled a second-order, low-pass filter with a lag time (gain, 16.7 +/- 8.3 mmHg.pulses(-1).s; natural frequency, 0.022 +/- 0.007 Hz; damping coefficient, 2.40 +/- 1.07; lag time, 1.06 +/- 0.41 s). On the basis of the transfer function, we designed an artificial vasomotor center to attenuate hypotension. We evaluated the performance of the BBS against hypotension induced by 60 degrees head-up tilt. In the cats with baroreflex failure, head-up tilt dropped AP by 37 +/- 5 mmHg in 5 s and 59 +/- 11 mmHg in 30 s. BBS with optimized feedback parameters attenuated hypotension to 21 +/- 2 mmHg in 5 s (P < 0.05) and 8 +/- 4 mmHg in 30 s (P < 0.05). These results indicate that ESCS-mediated BBS prevents orthostatic hypotension. Because epidural stimulation is a clinically feasible procedure, this BBS can be applied clinically to combat hypotension associated with various pathophysiologies.     

The osmopressor response to water drinking

Water drinking elicits profound pressor responses in patients with impaired baroreflex function and in sinoaortic-denervated mice. Healthy subjects show more subtle changes in heart rate and blood pressure with water drinking. The water-induced pressor response appears to be mediated through sympathetic nervous system activation at the spinal level. Indeed, water drinking raises resting energy expenditure in normal weight and obese subjects. The stimulus setting off the response is hypoosmolarity rather than water temperature or gastrointestinal stretch. Studies in mice suggest that this osmopressor response may involve transient receptor potential vanniloid 4 (Trpv4) receptors. However, the (nerve) cell population serving as peripheral osmosensors and the exact transduction mechanisms are still unknown. The osmopressor response can be exploited in the treatment of orthostatic and postprandial hypotension in patients with severe autonomic failure. Furthermore, the osmopressor response acutely improves orthostatic tolerance in healthy subjects and in patients with neurally mediated syncope. The phenomenon should be recognized as an important confounder in cardiovascular and metabolic studies.     

Adaptive changes of locomotion after central and peripheral lesions

This paper reviews findings on the adaptive changes of locomotion in cats after spinal cord or peripheral nerve lesions. From the results obtained after lesions of the ventral/ventrolateral pathways or the dorsal/dorsolateral pathways, we conclude that with extensive but partial spinal lesions, cats can regain voluntary quadrupedal locomotion on a treadmill. Although tract-specific deficits remain after such lesions, intact descending tracts can compensate for the lesioned tracts and access the spinal network to generate voluntary locomotion. Such neuroplasticity of locomotor control mechanisms is also demonstrated after peripheral nerve lesions in cats with intact or lesioned spinal cords. Some models have shown that recovery from such peripheral nerve lesions probably involves changes at the supra spinal and spinal levels. In the case of somesthesic denervation of the hindpaws, we demonstrated that cats with a complete spinal section need some cutaneous inputs to walk with a plantigrade locomotion, and that even in this spinal state, cats can adapt their locomotion to partial cutaneous denervation. Altogether, these results suggest that there is significant plasticity in spinal and supraspinal locomotor controls to justify the beneficial effects of early proactive and sustained locomotor training after central (Rossignol and Barbeau 1995; Barbeau et al. 1998) or peripheral lesions.     

Effects of sodium nitroprusside-induced hypotension on the cerebral and hindlimb blood flow in dogs

Sodium nitroprusside (SNP) has been commonly used as a vasodilator agent for deliberate hypotension with general anesthesia. The purpose of this study was to observe whether cerebral blood flow (CBF) was significantly reduced when SNP infusion was accomplished to decrease peripheral blood flows with systemic hypotension. We conducted the experiments in 15 pentobarbital-anesthetized dogs. CBF was measured in 7 dogs using a venous outflow method. Hindlimb blood flow (HBF) serving as a representative of the peripheral circulations was obtained by flow measurement in the femoral artery in 8 dogs. The systemic arteral pressure (SAP) was decreased stepwise (approximately 5 mmHg for each step) by adjusting the SNP infusion rate. During the systemic hypotension, the CBF remained fairly constant despite a marked decline in the mean SAP to 40 mmHg. The calculated cerebral vascular resistance was progressively decreased with the systemic hypotension. On the contrary, a reduction in the HBF was observed accompanying the fall in SAP. When the mean SAP was decreased to 50 mmHg, the HBF was only 46.3 +/- 7.6% of the control value. The calculated hindlimb vascular resistance was slightly elevated during the whole course of SNP-induced hypotension. The results reveal the disparity between the brain and hindlimb in the resistance and flow responses to SNP-induced hypotension. The constancy of CBF subserves adequate brain perfusion when deliberate hypotension is conducted for surgery in the peripheral organs.     

Role of vagal and spinal sensory pathways on eupneic diaphragmatic activity

The interactions between vagal and spinal afferents in the control of eupneic diaphragmatic activity were studied in two groups of cats anesthetized either with pentobarbital sodium (SPB) or with ethyl carbamate-alpha-chloralose (ECC), which enhanced spinal reflexes. Under both conditions of anesthesia two experimental protocols were performed: 1) bilateral cervical vagotomy followed by spinal section at C8 level or 2) spinal section followed by vagotomy. Changes in integrated diaphragmatic activity (Edi) were studied during eupneic ventilation and tracheal occlusion at end expiration. Vagotomy always significantly increased the amplitude of Edi during eupnea (SPB + 30%; ECC + 15%) and prolonged its duration (Tdi) (SPB + 110%; ECC + 75%) but did not modify the overall shape of the Edi vs. time relationship. Spinal section induced reverse changes in the amplitude of Edi, whether vagal afferents were present or suppressed and modified the shape of the Edi wave, but did not significantly modify Tdi. These results indicate that both vagal and spinal afferents may participate in the control of eupneic inspiration but exert different and interdependent influences on the recruitment and firing time of phrenic motoneurons. In addition, Tdi measured during tracheal occlusion (Todi) was markedly prolonged under ECC anesthesia. In this situation spinal section reduced Todi, which became close to the values obtained in intact or spinal cats under SPB anesthesia. Thus the response to tracheal occlusion at end expiration cannot be interpreted as resulting from the sole suppression of volume related vagal information.     

中枢苯环立啶受体介导的心血管效应

有关中枢苯环立啶（PCP）受体的心血管效应,尚未见报道,本文采用大鼠侧脑室注射（icv)、脊髓蛛网膜下腔注射（ith)和皮下注射（sc)PCP受体的激动剂或拮抗剂,观察其对血压、心率和呼吸的影响,以了解脑和脊髓PCP受体的心血管效应,结果表明,icv250nmolPCP产生强烈的降压和快速持久的心率减慢作用。ithPCP立即产生强烈的降压和心率减慢作用。并呈量效关系。ithPCP受体篁 异性拮抗剂右吗喃15nmol,可拮抗PCP（150nmol)所产生的降奔驰主和心率减慢作用,ithPCP受体特异性拮抗剂右吗喃15nmol,可拮抗PCP（150nmol)所产生的降压和心率减慢作用,ithPCP受体激动剂TCP250nmol,立即产生强烈的降压和心率减慢作用。scPCP10ng/kg则产生升压作用,对心率没有影响,上述结果表明,中枢PCP受体具有心血管抑制效应。     

Cardiovascular effects of atrial natriuretic extract in the whole animal

Atrial tissue extract (AE) and ventricular tissue extract cause identical decreases in total peripheral resistance when they are injected i.v. into anesthetized rats. However, only AE causes significant hypotension because of cardiac inhibition. This involves both bradycardia and failure of stroke volume to increase appropriately. The observations cannot be explained by direct action of AE on myocytes, but are more likely to be the result of interactions with cardiovascular reflex mechanisms. Excitation of chemosensitive cardiac receptors with vagal afferents appears to be an important afferent mechanism. The efferent limb for the negative chronotropic response resides partly in the vagus nerves and partly in cardiac sympathetic nerves. The negative inotropic response of AE was not altered by vagotomy, spinal section, atropine, or propranolol. These results suggest that atrial peptides may cause the release of a negatively inotropic substance from a site that is not yet identified.     

脊髓苯环立啶受体的心血管效应与去甲肾上腺素能系统

本文应用受体阻断、高效液相,6-OHDA 化学损毁神经末梢和放射自显影等多学科技术方法,探讨脊髓苯环立啶受体的心血管效应与去甲肾上腺素能神经系统的关系。结果表明,哌唑嗪、育亨宾均可对抗 ith PCP 的降压和减慢心率作用,ith PCP 产生降压和减慢心率作用时,脊髓脑脊液内 MHPG 的含量升高;用6-OHDA 损毁脊髓 NA 能神经末梢后,ith PCP的降压和减慢心率作用大为减弱,脊髓 PCP 受体密度亦同时大为降低。可以认为,脊髓内有 PCP 受体分布于 NA 能神经末梢上,促进 NA 释放或抑制 NA 重摄取,可能是脊髓 PCP 受体产生心血管抑制效应的重要机理。     

预负荷/共同负荷联合血管收缩药在剖宫产术中对母婴血气的影响

目的探讨预负荷/共同负荷联合血管收缩药在剖宫产术中对产妇和新生儿血气的影响。方法将择期剖宫产产妇（ASA I～Ⅱ）,在排除酸中毒（pH〈7.35或BE〈-6）或碱中毒（pH〉7.45或BE〉6）后,随机分为麻黄素组（E组）和去氧肾上腺素组（P组）,每组30例。两组预负荷晶体液乳酸钠林格氏液6～8ml/kg,穿刺到硬膜外间隙时,分别静脉给予麻黄素5mg、去氧肾上腺素100μg。腰麻注药后,两组均输入羟乙基淀粉130/0.4氯化钠溶液10ml/kg（共同负荷）,并分别静脉泵注麻黄素和去氧肾上腺素。观察记录两组产妇的BP、HR、ECG、SpO2,至胎儿娩出即刻查母体和脐动脉血血气,记录新生儿出生后第1min及第5min时的Apgar评分。结果 P组脐动脉血pH、BE值均高于E组（P〈0.05）。结论预负荷/共同负荷联合血管收缩药能有效减少腰麻后低血压的发生,维持产妇血流动力学稳定。去氧肾上腺素比麻黄素能更好地减少新生儿酸中毒的发生。     

Plasma thromboxane B2 levels and thromboxane B2 production by platelets are increased in patients during spinal and epidural anesthesia

Concentrations of thromboxane (Tx) B2 in plasma and its production by platelets were measured in 20 spinal and 10 epidural anesthesia patients scheduled for small operations in the lower extremities. The main metabolite of prostacyclin, 6-keto-PGF1 alpha and prostaglandin (PG) E2 in plasma were also determined. Plasma TxB2 and TxB2 production by platelets increased during both spinal and epidural anesthesia. Plasma TxB2 levels also remained elevated 1 h after anesthesia. The plasma concentrations of 6-keto-PGF1 alpha and PGE2 did not change during spinal or epidural anesthesia. In in vitro studies, only low concentrations of lidocaine (0.5-1.0 micrograms/ml) and bupivacaine (0.5-3.0 micrograms/ml) increased platelet TxB2 production. In platelet rich plasma, neither lidocaine nor bupivacaine in concentrations of 0.5-3.0 micrograms/ml caused constant changes in ADP-induced platelet aggregation, but they inhibited it in toxic concentrations (12 micrograms/ml). The results suggest that the increased TxB2 plasma levels and platelet TxB2 production during regional anesthesia are not caused by local anesthetics itself but by other factors, e.g. tissue trauma. In clinically found concentrations, local anesthetics do not cause any constant changes in platelet aggregation.     

Distribution of lumbar spinal evoked potentials and their correlation with stimulation-induced paresthesiae

In 7 awake patients with neuropathic lower extremity pain, spinal somatosensory evoked potentials (SEP) were elicited from the non-painful leg by electrical stimulation of the peroneal nerve and mechanical stimulation of the hallux ball. Recording was made epidurally in the thoraco-lumbar region by means of an electrode temporarily inserted for trial of pain-suppressing stimulation.In response to peroneal nerve stimulation, two major SEP complexes were found. The first complex consisted, as has been described earlier, of an initial positivity (P12), a spike-like negativity (N14), a slow negativity (N16) and a slow positivity (P23). The second complex consisted of a slow biphasic wave, conceivably mediated by a supraspinal loop. Both complexes had a similar longitudinal distribution with amplitude maxima at the T12 vertebral body.The SEP evoked by mechanical hallux ball stimulation had a relatively small amplitude, and there was no significant second complex. The relationship between stimulus intensity and SEP amplitude was negatively accelerating.The longitudinal distribution of spinal SEP was compated with the somatotopic distribution of paresthesiae induced by stimulation through the epidural electrode. It was found that stimulation applied at the level of maximal SEP generally induced paresthesiae in the corresponding peripheral region. Therefore, spinal SEP may be used as a guide for optimal positioning of a spinal electrode for therapeutic stimulation when implanted under general anesthesia.An attempt was made to record the antidromic potential in the peroneal nerve elicited from the dorsal columns by epidural stimulation. The antidromic response was, however, very sensitive to minimal changes of stimulus strength and body position of the patient, and was also contaminated by simultaneously evoked muscular reflex potentials.Thus, peripheral responses evoked by epidural stimulation appeared too unreliable to be useful for the permanent implantation of a spinal electrode for therapeutic stimulation.     

Plasticity of connections underlying locomotor recovery after central and/or peripheral lesions in the adult mammals

This review discusses some aspects of plasticity of connections after spinal injury in adult animal models as a basis for functional recovery of locomotion. After reviewing some pitfalls that must be avoided when claiming functional recovery and the importance of a conceptual framework for the control of locomotion, locomotor recovery after spinal lesions, mainly in cats, is summarized. It is concluded that recovery is partly due to plastic changes within the existing spinal locomotor networks. Locomotor training appears to change the excitability of simple reflex pathways as well as more complex circuitry. The spinal cord possesses an intrinsic capacity to adapt to lesions of central tracts or peripheral nerves but, as a rule, adaptation to lesions entails changes at both spinal and supraspinal levels. A brief summary of the spinal capacity of the rat, mouse and human to express spinal locomotor patterns is given, indicating that the concepts derived mainly from work in the cat extend to other adult mammals. It is hoped that some of the issues presented will help to evaluate how plasticity of existing connections may combine with and potentiate treatments designed to promote regeneration to optimize remaining motor functions.     

The role of sympathetic nervous system in the development of neurogenic pulmonary edema in spinal cord-injured rats

The pronounced activation of sympathetic nervous system is a necessary prerequisite for the development of neurogenic pulmonary edema (NPE) in rats with balloon compression of spinal cord. In this study we examined whether this is a consequence of rapid activation of spinal pathways leading to sympathetic venoconstriction, blood pressure rise, and reflex bradycardia. We found that NPE development can be prevented by epidural upper thoracic anesthesia or by transection of the upper spinal cord. This indicates an important role of spinal pathways activation. NPE development can also be prevented by moderate blood loss, supporting the role of blood redistribution to pulmonary circulation. In rats developing NPE the catecholamine surge following spinal cord compression involved not only a dramatic increase of circulating norepinephrine but also of epinephrine levels. The pretreatment of rats with α-1 adrenoceptor blocker prazosin, α-2 adrenoceptor blocker yohimbine, or calcium channel blocker nifedipine prevented NPE development, whereas the effect of β-adrenoceptor blockade with propranolol was less convincing. In conclusion, considerable activation of thoracic spinal pathways, followed by marked catecholamine secretion, play a major role in the development of NPE in spinal cord-injured rats. Enhanced α-adrenergic nifedipine-sensitive vasoconstriction is responsible for observed blood pressure changes, subsequent baroreflex bradycardia, and blood volume redistribution, which represent major pathogenetic mechanisms of NPE development.     

Changes in the blood vessels of the spinal cord and spinal ganglia following chronic stimulation of the lumbar regions of the sympathetic trunks and gangliosympathectomy

Morphological studies in 40 rabbits demonstrated that chronic irritation of the lumbar sympathetic trunks resulted in more pronounced architectonic changes, in vessel walls and in neurons of the lumbar sympathetic ganglia in 15 days than did the bilateral lumbar gangliosympathectomy at the same time. In both series of experiments more prominent changes were noticed in the spinal ganglia than in the spinal cord, that could be explained by different degree of lesions in the nerves supplying them and by organic specification of their angioarchitectonics. The data obtained made it possible to include novocain block (anesthesia) into complex therapy to manage spinal apoplexy in clinic.     

SPINAL ANESTHESIA—A Survey of Neurologic Complications

The incidence of severe neurologic complications from spinal anesthesia in San Diego County in a series of 32,882 cases in a five-year period was 0.012 per cent. Morbidity of 1 in 10,000 cases compares favorably with morbidity associated with general anesthesia.Meticulous technique and abandonment of continuous spinal anesthesia can further reduce the incidence of complications.More emphasis should be placed on the elimination of preexisting neurologic disease as a contraindication to spinal anesthesia.     

"Phenomenon" of vestibular compensation]

The role of spinal afferentation from the lower part of the body in establishing compensation of the consequences of the vestibular function abaissement was studied in experiments on guinea pigs. The ligation of the spinal cord at the level of thoracic segements performed under local anesthesia neither produced appreciable effect on the compensatory development at simultaneous or subsequent destruction of the labyrinth nor destroyed it in the preliminarily labyrinthectomized animals. The ligation of the spinal cord in the labyrinthectomized animals under ether or chloroform anesthesia was accompanied by a strong disorder of the compensation. The above substances also provoked analogous decompensation in the unilaterally labyrinthectomized animals with an intact spinal cord. The results obtained indicate that the reported disorder of the vestibular compensation induced by ligation of the spinal cord under ether anesthesia is consequent on an immediate effect of inhalation anesthetics on the compensatory mechanisms rather than is resultant of abolishing spinal afferentation from the lower part of the body.