Hull Laboratory of Physiology, the University of Chicago.
J Exp Med. 1906 Mar 26;8(2):289-321. doi: 10.1084/jem.8.2.289.
The cerebral circulation was interrupted for periods of three to eighty-one minutes by ligation of the innominate and left subclavian arteries proximal to the origin of the vertebral, in ninety-three cats. Eleven dogs were used in the earlier experiments. The eye reflexes disappear very quickly and a period of high blood pressure follows the occlusion immediately; vagus inhibition causes cardiac slowing and a fall in blood pressure, followed by a second rise after the vagus center succumbs to anaemia. Respiration stops temporarily (twenty to sixty seconds) after the beginning of occlusion, and then follows a series of strong gasps of the Cheyne-Stokes type, after which it stops until some time after the restoration of the cerebral circulation. The respiratory and vagus centers lose their power of functioning at approximately the same time. Asphyxial slowing of the heart may occur without the agency of the vagus center. The blood pressure slowly falls to a level which is maintained throughout the remainder of the period of occlusion. The anterior part of the cord and the encephalon lose all function; no reflexes are obtainable. The reflexes of the posterior part of the cord persist; the intravenous injection of strychnine does not affect the anterior part of the cord during the period of occlusion; but does affect the posterior portion of the cord. There is no secretion of tears or saliva, and the intra-ocular pressure is reduced. The blood pressure falls still more after release of the cerebra arteries, but soon begins to rise. The respiration returns suddenly, two to sixty minutes after restoration of the cerebral circulation, the first gasp being a strong one. The rate gradually increases until rapid enough for natural respiration. The eye reflexes and intra-ocular tension return more gradually, ten minutes to three hours after restoration of the cerebral circulation. The anterior part of the cord recovers its functions gradually. The first reflexes occur only on the same side as the stimulus, crossing of reflexes, to involve the other side, not occurring till later. As a rule, all reflexes return, and a short period of quiet follows. The anterior part of the cord again becomes irritable to strychnine, but succumbs to its action before the normal part. Spasms, of tonic, clonic, or mixed type, then appear, terminating in (a) death, (b) partial or (c) complete recovery. In partial recovery, disturbances of locomotion, such as walking in a circle, paralysis, dementia, loss of sight, hearing, and general intelligence, characterize the post-convulsive period. After complete recovery, there is a return to normal deportment. No gross lesions of the nervous system, other than a congested appearance of the previously anaemic area, were observed. Transection of the spinal cord stops the spasms below the level of section. Hemisection of the cord stops the spasms on the same side, below the level of section. Death, without any return of the reflexes after release of the cerebral arteries, has followed an occlusion of seven and one-half minutes. Respiration has returned after an occlusion of one hour. Five animals have recovered completely after an occlusion of seven minutes or more. Only one animal has recovered completely after an occlusion of fifteen minutes. No animal has recovered completely after an occlusion of twenty minutes. In Herzen's (26) resuscitation of an animal after several hours of cerebral anaemia, there must have been some anastomotic channels to the brain. Mayer's (27) limit of ten to fifteen minutes of cerebral anaemia, beyond which resuscitation is not practicable, is close to the correct one. It appears to us that, in cases of resuscitation two hours after cessation of the heart-beat, (Prus., loc.cit.) the auricles must have kept up a slow but, in some degree, an efficient movement of the blood through the brain. The truth of this suggestion might be tested by introducing some easily recognized, non-diffusible substance into a vein after the heart-beat ceases to affect a manometer, and later searching for it in the brain and other parts of the body. But, whatever the reason, cerebral anaemia in these cases must have been less complete than in our experiments. The histological alterations of the cord and brain are now being studied. The results will be published later.
通过结扎无名动脉和左锁骨下动脉,阻断 93 只猫的大脑循环 3 至 81 分钟。11 只狗用于早期实验。眼反射很快消失,立即出现高血压;迷走神经抑制导致心率减慢和血压下降,随后在迷走神经中枢因贫血而衰竭后再次升高。阻断开始后,呼吸暂时停止(20 至 60 秒),然后出现一系列类似 Cheyne-Stokes 类型的强烈喘息,之后呼吸停止,直到大脑循环恢复一段时间后。呼吸和迷走神经中枢大约同时失去功能。没有迷走神经中枢的作用,心脏可能会出现窒息性减慢。血压缓慢下降到阻断期间维持的水平。脊髓前角和脑失去所有功能;无法获得反射。脊髓后角的反射仍然存在;在阻断期间,静脉注射士的宁不会影响脊髓前角;但会影响脊髓后角。没有眼泪或唾液分泌,眼内压降低。大脑动脉释放后血压进一步下降,但很快开始上升。呼吸在大脑循环恢复后突然恢复,2 至 60 分钟后恢复,第一声喘息是强烈的。心率逐渐增加,直到足以进行自然呼吸。眼反射和眼内压恢复得更缓慢,在大脑循环恢复后 10 分钟至 3 小时。脊髓前角逐渐恢复其功能。最初的反射仅在刺激的同侧发生,交叉反射涉及对侧,直到稍后才会发生。通常,所有反射都会恢复,并在一段时间内保持安静。脊髓前角再次对士的宁敏感,但在正常部分之前屈服于其作用。然后出现强直、阵挛或混合性痉挛,最终导致(a)死亡,(b)部分或(c)完全恢复。在部分恢复中,运动障碍,如转圈行走、瘫痪、痴呆、视力、听力和一般智力丧失,是惊厥后时期的特征。完全恢复后,行为恢复正常。除先前贫血区域的充血外观外,未观察到神经系统的任何明显病变。脊髓横断可阻止截瘫以下部位的痉挛。脊髓半横断可阻止截瘫以下部位的同侧痉挛。在大脑动脉释放后,没有任何反射恢复的情况下,七分钟半的阻塞会导致死亡。在阻断一个小时后,呼吸已经恢复。五只动物在阻断 7 分钟或更长时间后完全恢复。只有一只动物在阻断 15 分钟后完全恢复。在阻断 20 分钟后,没有动物完全恢复。在 Herzén(26)在大脑贫血数小时后对动物进行复苏的情况下,必须有一些吻合通道通向大脑。Mayer(27)的大脑贫血 10 至 15 分钟的极限,超过这个极限复苏就不可行,这与正确的极限非常接近。在我们看来,在心脏停止跳动两小时后进行复苏的情况下(Prus.,同前),心房必须通过大脑保持缓慢但在某种程度上有效的血液流动。通过在心脏停止跳动后将一种易于识别的、非扩散物质注入静脉,然后在大脑和身体其他部位寻找它,也许可以验证这一假设。但是,无论原因是什么,这些情况下的大脑贫血肯定比我们的实验中要轻。现在正在研究脊髓和大脑的组织学改变。结果稍后将公布。