peer reviewed | Owing to technical and ethical limitations, a substantial part of the knowledge about the pathophysiologic mechanism of the human diaphragm has been obtained from studies in which phrenic nerve activation was usually carried out by direct surgical exposure of the nerves in the neck of deeply anesthetized, mechanically ventilated animals. Novel information has been gleaned from such studies, but the restrictive conditions under which it was collected preclude reliable extrapolation. We, therefore, addressed the question of whether accurate electrophysiologic evaluation of the phrenic nerve-diaphragm pathway can be performed in intact, nonanesthetized calves. Transjugular phrenic activation was well tolerated, safe, specific, and able to achieve constant symmetric and supramaximal phrenic stimulations during prolonged periods. Eighteen noninvasive cutaneous and esophageal reception circuits were tested for their ability to record the diaphragmatic evoked potential. In addition, they were compared for specificity and reproducibility of the recorded potentials during prolonged periods of tidal or stimulated respiration. The best diaphragmatic potential was recorded from surface electrodes attached to the skin of the ninth and tenth intercostal spaces, using a xyphoidian reference. We describe a method that allows easy, longterm, and reliable electrophysiologic evaluation of the phrenic nerve-diaphragm pathway in intact, conscious calves. It is hoped that such a model will produce relevant novel information regarding pathophysiology of the diaphragm.

Owing to technical and ethical limitations, a substantial part of the knowledge about the pathophysiologic mechanism of the human diaphragm has been obtained from studies in which phrenic nerve activation was usually carried out by direct surgical exposure of the nerves in the neck of deeply anesthetized, mechanically ventilated animals. Novel information has been gleaned from such studies, but the restrictive conditions under which it was collected preclude reliable extrapolation. We, therefore, addressed the question of whether accurate electrophysiologic evaluation of the phrenic nerve-diaphragm pathway can be performed in intact, nonanesthetized calves. Transjugular phrenic activation was well tolerated, safe, specific, and able to achieve constant symmetric and supramaximal phrenic stimulations during prolonged periods. Eighteen noninvasive cutaneous and esophageal reception circuits were tested for their ability to record the diaphragmatic evoked potential. In addition, they were compared for specificity and reproducibility of the recorded potentials during prolonged periods of tidal or stimulated respiration. The best diaphragmatic potential was recorded from surface electrodes attached to the skin of the ninth and tenth intercostal spaces, using a xyphoidian reference. We describe a method that allows easy, long-term, and reliable electrophysiologic evaluation of the phrenic nerve-diaphragm pathway in intact, conscious calves. It is hoped that such a model will produce relevant novel information regarding pathophysiology of the diaphragm.

The area of skin supplied by the afferent fibers in one cutaneous nerve is called the cutaneous area (CA) for that nerve. The CA of peripheral branches of lumbar and sacral spinal nerves responsive to the stimulation of hair follicle mechanoreceptors were mapped in 27 dogs. The amount of overlap among the CA was similar to that found for other CA of the body. The CA of peripheral branches of the sciatic nerve were restricted to the lateral, cranial, and caudal aspects of the pelvic limb distal to the stifle. The CA of the saphenous nerve was located on the medial side of the limb, except for a small area located on the lateral side of the crus. The distal part of the CA of the saphenous nerve was completely overlapped in the hind paw by branches of the superficial peroneal nerve laterally and the medial plantar branch of the tibial nerve medially. The CA for the deep peroneal nerve was located on the dorsal surface of the webbing between digits 2 and 3 and the adjacent skin of these digits. The CA of the plantar branches of the tibial nerve were small in comparison with the diameter of the nerve, suggesting that these branches contained nerve fibers supplying other, deeper structures in the hindpaw and that damage to these nerves would interfere with cutaneous sensation in only a small region on the plantar surface of the hindpaw. Knowledge of the CA of the various branches of the sciatic nerve allows more accurate localization of injury to the sciatic nerve or its branches by using areas of anesthesia.

The motor-evoked potential can be reliably recorded in anesthetized dogs by use of percutaneous placement of active recording electrodes near the dorsal lamina of the vertebral column. Two types of responses were observed in this study; short (< 5.5 ms at T9-10)- and long (> 5.8 ms at T9-10)-latency waves. Short-latency waves are larger in amplitude and appear with higher stimulus intensities than do long-latency waves. Short-latency waves are conducted at > 80 m/s and may not reflect pyramidal tract activation. The safety of using higher intensity stimuli to generate short-latency waves has not been determined.

Somatosensory evoked potentials (SEP) were recorded at the scalp and at various levels along the lumbar and caudal thoracic parts of the spine in response to tibial nerve stimulations. The SEP were observed in 24 diseased dogs, 2 with a vertebral fracture, 1 with a spinal cord tumor, 1 with a vertebral tumor, and 20 with disk herniation. Cord compression location was confirmed by myelography, laminectomy, or both. The clinical state had significant (P < 0.0001) influence on SEP characteristics. The scalp-recorded SEP latency changed only in association with the most severe lesions; spine-recorded SEP conduction velocity was lower in association with mild lesions; scalp-recorded SEP amplitude changed with lesions of intermediary severity. Because these 3 electrophysiologic variables were influenced differently by cord damage, it was possible to discriminate the various clinical grades by use of these techniques. However, dogs with signs of pain only could not be differentiated from clinically normal dogs. The evoked injury potential was observed in all but 4 diseased dogs, and its maximal amplitude corresponded, in all cases, with cord damage location. Increased duration (P < 0.05) of the spine-recorded SEP was associated with longstanding problems, but not necessarily with clinically detectable malfunction. Use of SEP and evoked injury potential for identifying lateralized cord damage may be of value.

Spinal-evoked potentials were recorded from 2 litters of clinically normal mixed-breed dogs between 35 and 300 days of age. Summated responses to tibial nerve stimulation were recorded from percutaneous needle electrodes placed at L7-S1, L4-5, T13-L1, C7-T1, and the cisterna cerebellomedullaris. The ulnar nerve was stimulated with recordings at C7-T1 and the cisterna cerebellomedullaris. Amplitudes did not change significantly with age, but were significantly (P < 0.05) different between various recording sites. On day 35, segmental and overall (L7-cisterna cerebellomedullaris) conduction velocities were less than half of the adult values. Spinal cord conduction velocities increased with age, reaching adult values at approximately 9 months of age. It was determined that quadratic equations best predicted the conduction velocities during maturation.

Five 5 to 6 month old horses were surgically prepared with silver electrodes sutured to the serosa of gastric antrum, duodenum and proximal portions of the jejunum. Normal migrating motility complex (MMC) periodicity was determined during daytime hours in horses that were fed and horses from which food was withheld for 24 hours. Periodicity was defined as time span from the end of one period of regular spike activity (RSA) to the end of the next RSA in the MMC. The periodicity was 120.5 +/- 9.5 (SEM) minutes in horses from which food was withheld, and was 125.7 +/- 20.3 minutes in horses fed hay free choice. Coincident with each duodenal RSA, antral spike activity ceased. Xylazine (0.25 and 0.5 mg/kg), given IV during the period of intermittent spike activity of the MMC to either fed or unfed horses induced, within 2 minutes, a RSA complex in the duodenum that migrated to the proximal portion of the jejunum. This was followed by a period of no spike activity of normal duration, which proceeded on to a period of intermittent spike activity of varying duration to complete the MMC cycle. Pretreatment IV administration of an alpha 2-adrenergic antagonist, tolazoline (1 mg/kg) also provoked a RSA complex, but blocked the xylazine effect. The results indicated that xylazine resets the duodenal MMC in the horse, but does not seriously disrupt proximal gastrointestinal tract motility, and that control of MMC periodicity in this region probably involves more than alpha 2-adrenergic receptors.

Objective—To investigate the in vitro differentiation of canine bone marrow stromal cells (BMSCs) into functional, mature neurons. Sample—Bone marrow from 6 adult dogs. Procedures—BMSCs were isolated from bone marrow and chemically induced to develop into neurons. The morphology of the BMSCs during neuronal induction was monitored, and immunocytochemical analyses for neuron markers were performed after the induction. Real-time PCR methods were used to evaluate the mRNA expression levels of markers for neural stem or progenitor cells, neurons, and ion channels, and western blotting was used to assess the expression of neuronal proteins before and after neuronal induction. The electrophysiological properties of the neuron-like cells induced from canine BMSCs were evaluated with fluorescent dye to monitor Ca2+ influx. Results—Canine BMSCs developed a neuron-like morphology after neuronal induction. Immunocytochemical analysis revealed that these neuron-like cells were positive for neuron markers. After induction, the cells’ mRNA expression levels of almost all neuron and ion channel markers increased, and the protein expression levels of nestin and neurofilament-L increased significantly. However, the neuron-like cells derived from canine BMSCs did not have the Ca2+ influx characteristic of spiking neurons. Conclusions and Clinical Relevance—Although canine BMSCs had neuron-like morphological and biochemical properties after induction, they did not develop the electrophysiological characteristics of neurons. Thus, these results have suggested that canine BMSCs could have the capacity to differentiate into a neuronal lineage, but the differentiation protocol used may have been insufficient to induce development into functional neurons.

The effect of xylazine, cisapride, and naloxone on myoelectric activity of the ileum, cecum, and proximal loop of the ascending colon (PLAC) was determined in 4 healthy Jersey cows implanted with 8 pairs of bipolar electrodes. A 4 X 4 Latin square design was used. The treatments included xylazine (0.04 mg/kg of body weight), cisapride (0.08 mg/kg), naloxone (0.05 mg/kg), and 0.9% sodium chloride solution (20 ml). All treatments were administered IV during early phase I of the migrating myoelectric complex in the ileum. Myoelectric activity was recorded for 4 hours after treatment, and data were analyzed for each hour separately. Xylazine significantly (P < 0.05) increased the duration of phase I of the first migrating myoelectric complex in the ileum to 220.72 +/- 26.89 minutes, compared with 30.91 +/- 10.11 minutes after administration of 0.9% sodium chloride solution. The number of cecocolic spikes per minute per electrode and the duration of cecocolic spike activity (percentage of recording time) were significantly (P < 0.05) decreased for the first 3 hours, and the number of propagated spike sequences in the cecum and PLAC was significantly (P < 0.05) decreased for the first 2 hours after administration of xylazine. Significant difference was not found between control and either,cisapride or naloxone treatment of healthy cows. However, during hour 1 after treatment with cisapride, number of spikes per minute, duration of spike activity, and number of propagated spike sequences were highest, compared with the other treatments. It was concluded that naloxone at the dosage used in this study was not suitable for medical treatment of cecal dilatation in cattle, when hypomotility of the cecum and PLAC must be reversed. Xylazine should not be used for relief of signs of pain in cases of cecal dilatation, because it significantly reduced myoelectric activity of the cecum and PLAC for at least 2 hours after treatment. Furthermore, results of this study indicated a trend (P > 0.05) toward increase of cecocolic myoelectric activity after administration of cisapride. It is the authors' opinion that the potential benefit of cisapride for medical treatment of cecal dilatation in cattle needs further evaluation.