Background-Therapeutic angiogenesis is thought to be beneficial for serious ischemic diseases. This investigation was designed to establish a simple and practical procedure applicable to therapeutic angiogenesis. Methods and Results-When cultured skeletal muscle cells were electrically stimulated at a voltage that did not cause their contraction, vascular endothelial growth factor (VEGF) mRNA was augmented at an optimal-frequency stimulation. This increase of VEGF mRNA was derived primarily from transcriptional activation. Electrical stimulation increased the secretion of VEGF protein into the medium. This conditioned medium then augmented the growth of endothelial cells. The effect of electrical stimulation was further confirmed in a rat model of hindlimb ischemia. The tibialis anterior muscle in the ischemic limb was electrically stimulated. The frequency of stimulation was 50 Hz and strength was 0.1 V, which was far below the threshold for muscle contraction. After a 5-day stimulation, there was a significant increase in blood flow within the muscle. Immunohistochemical analysis revealed that VEGF protein was synthesized and capillary density was significantly increased in the stimulated muscle. Rats tolerated this procedure very well, and there was no muscle contraction, muscle injury, or restriction in movement. Conclusions-We propose this procedure as a simple and practical method of therapeutic angiogenesis. (Circulation.1999;99:2682-2687.)
A multichannel functional electrical stimulation (FES) system for the restoration of quadriplegic upper extremity function is described. The system is composed of a personal computer NEC PC-8801mkII, peripheral electronic circuits, CRT display and respiratory sensors for volitional control by the patient, and percutaneous electrodes. A C4 quadriplegic patient could drink canned tea by herself by using this FES system. Distinct features of the system are as follows: 1) Versatile volitional control was realized by controlling the memory allocation of the stored stimulation data by voluntary respiratory signals. 2) Sophisticated fine control of the fingers, wrists, and elbow was realized by creating the multichannel stimulation data from recorded myoelectric activities of normal subjects during movements of the upper limb.
In order to study how immune-inflammatory responses are involved in the pathogenesis of cerebral vasospasm after subarachnoid haemorrhage (SAH), the kinetics of expression of the intercellular adhesion molecule 1 (ICAM-1), a ligand for the leucocyte adhesion receptor, were studied on the cerebral arteries following SAH in rats. The SAH was induced by intracisternal injection of arterial blood. The rats were sacrificed at specified times: immediately after induction of SAH to seven days after SAH. Cryostat sections of the basilar artery (BA) were prepared and incubated with anti-rat ICAM-1 antibody. Morphometric analysis of the BA revealed a significant narrowing of the luminal diameter on Day 2 following SAH. While in the non-treated normal animals, no nor only weak expression of ICAM-1 was observed on the endothelial layer of the BA, there was greater expression of ICAM-1 on the endothelial layer of the BA in SAH rats, and the expression was observed also in the medial layer of the artery from Day 2 to Day 5 following SAH. The present results indicate that SAH really causes responses in the cellular immunity not only in the endothelial layer, but also in the medial layer of the artery as a target of immune damage, which is presumed to be one of the important steps in the development of cerebral vasospasm.
Complete transection of the midthoracic spinal cord was performed on adult female dogs. Development of reflexes and locomotive movements in the hindlimbs after spinal transection was investigated over several months. In the earlier stages after the surgery, dogs showed flaccid paralysis of the hindlimbs. Within several weeks, muscle tone of the hindlimbs was gradually increased accompanied by development of flexion reflex with after-discharge in addition to monosynaptic reflexes. Alternating stepping movement also began to develop. Afterward, extensor thrust and crossed extension reflex were observed. Standing behavior of the hindlimbs was found after enough development of the extensor thrust and correct placement of the pads of the toes. Steady development of stepping and standing caused forward locomotion using fore-and hindlimbs. This walking behavior of the hindlimbs was never inhibited by additional spinal cord transection. These findings indicate that the isolated spinal cord caudal to the transected site is responsible for the locomotive behavior of the hindlimbs in adult spinal dogs. Spinal automatism and development of responses induced by afferent inflow from outside the cord may help to explain such functional recovery of the paralyzed hindlimbs.
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