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Adrenal splanchnic innervation contributes to the diurnal rhythm of plasma corticosterone in rats by modulating adrenal sensitivity to ACTH.

Activity of the hypothalamic-pituitary-adrenal axis is characterized by a diurnal rhythm with an AM nadir and PM peak. Splanchnic nerve transection disrupts the diurnal rhythm in plasma corticosterone; however, there is a controversy as to whether the nerve-mediated effect is 1) via inhibition in the AM vs. excitation in the PM, or 2) involves changes in adrenal sensitivity to ACTH. The present studies were designed to address these issues. Adult male rats were anesthetized and underwent bilateral transection of the thoracic splanchnic nerve or sham transection. One week after surgery, rats were killed in the AM or PM with collection of nonstress plasma for measurement of corticosterone and ACTH. Plasma corticosterone was increased in the PM relative to the AM; however, plasma corticosterone in the PM was attenuated by splanchnic nerve transection, without affecting plasma ACTH. This decrease in PM plasma corticosterone after nerve-transection was 1) associated with decreased adrenal responsivity to ACTH, 2) associated with decreased adrenal cAMP content, 3) prevented by adrenal demedullation, and 4) not affected by removal of adrenal capsaicin-sensitive afferent fibers. Repeated serial blood sampling from individual rats confirmed the excitatory effect of splanchnic innervation in the PM. These results support the hypothesis that the adrenal splanchnic innervation modulates the diurnal rhythm in plasma corticosterone by increasing adrenal responsivity to ACTH and augmenting steroidogenesis in the PM and suggest that alterations in adrenal corticosterone secretion obscured by pulsatile secretion are more clearly revealed with repeated serial blood sampling.

Adrenal Glands↗

Asymmetries and symmetries in the number of thoracic dorsal root ganglion cells.

The right/left ratio for the number of neurons in individual pairs as well as series of pairs of normal rat and guinea pig thoracic dorsal root ganglia have been investigated. After perfusion of the animals with aldehyde fixatives, the 13 pairs of thoracic ganglia were embedded in resin, serially sectioned, and stained with azure methylene blue. Counts of neuronal nucleoli (with correction for possible split nucleoli) were used as an indicator of the number of neurons in each ganglion. In individual pairs the right/left difference varied between 0 and 47% in the rat and 0 and 26% in the guinea pig. There appeared to be no particular level with a preference for large right/left differences. However, when the total number of neurons from the 13 ganglia on one side were compared with the corresponding figure from the other side, the right/left differences were reduced to less than 3% in the rat and less than 2% in the guinea pig. These results show that the organization of the thoracic spinal nerve unit is markedly asymmetrical at the segmental level, but strictly symmetrical in terms of the total number of dorsal root ganglion cells. The marked asymmetry in individual ganglion pairs necessitates caution when evaluating the effect of unilateral experimental manipulations on the number of neurons in thoracic spinal ganglia.

Animals↗

The effects of prolonged repetitive stimulation in hemicholinium on the frog neuromuscular junction.

1. Cutaneous pectoris nerve-muscle preparations from the frog were stimulated for prolonged periods in solutions with curare alone, curare and hemicholinium no. 3 (HC-3), or curare and glucose plus choline. End-plate potentials (e.p.p.s) and miniature end-plate potentials (m.e.p.p.s) were recorded intracellularly. Black widow spider venom (BWSV) was applied to determine the degree of depletion of the transmitter stores. 2. The ultrastructure of the neuromuscular junctions was studied in the electron microscope. Some of the preparations were fixed immediately at the end of the period of stimulation and others were fixed about an hour after BWSV had been applied. In some experiments horseradish peroxidase (HRP) was present during the period of stimulation and the fixed tissue was treated to reveal the distribution of the tracer. 3. The amplitude of the e.p.p. fell rapidly to almost zero during 2 hr of stimulation at 2/sec in 100 muM HC-3 and little recovery occurred during a subsequent hour of rest. About 2-7 times 10-5 quanta were secreted. The e.p.p.s usually persisted throughout the period of stimulation in the other solutions and 2-2-6 times as much transmitter was secreted. 4. When BWSV was applied immediately at the end of the period of stimulation in HC-3, almost no m.e.p.p.s were discharged and only small m.e.p.p.s were discharged when the venom was applied after an hour of rest. 5. When BWSV was applied to unstimulated terminals that had been bathed in HC-3, or to terminals that had been stimulated and rested for an hour in glucose plus choline, m.e.p.p.s of nearly normal amplitude were discharged. 6. Terminals stimulated for 2 hr at 2/sec in 100 muM HC-3 contained a normal complement of synaptic vesicles and a large proportion of vesicles were labelled with HRP when the tracer was present during the period of stimulation. 7. BWSV induced the almost complete depletion of vesicles from terminals that had been stimulated in HC-3. 8. Depletion of vesicles also occurred when terminals were stimulated for 20 min at 10/sec after they had been previously stimulated for 2 hr at 2/sec in HC-3. These terminals showed extensive infolding of the axolemma and they contained swollen mitochondria. 9. These results indicate that stimulation in HC-3 depletes terminals of their store of transmitter but not of their population of vesicles and that vesicles empty of transmitter can fuse with and reform from the axolemma of the nerve terminal.

Animals↗

Non-nicotinic, non-adrenergic excitatory motor fibres in the preganglionic sympathetic supply to the feline colon. An axon reflex arrangement associated to thin sensory neurons, involving substance P?

Experiments were performed on chloralosed cats with ligated adrenals. The peripheral ends of the preganglionic sympathetic nerves to the colon were stimulated and colonic motility was monitored by a volumetric method. Electric nerve stimulation with various intensities elicited inhibitory motor responses and occasionally contractions. Hexamethonium and/or guanethidine blocked all inhibitory actions and revealed pure excitatory responses at high stimulation intensities. These colonic contractions were inhibited by atropine. However, atropine-resistant contractions were sometimes observed, predominantly in the colorectal region. Thoracic sympathetic nerves affected the motility in the proximal colon only, while lumbar sympathetic nerves acted on both proximal and distal parts. Strength-duration relationships and sensitivity to local heating suggest that the excitatory responses are due to an antidromic activation of thin, possibly afferent nerve fibres. Small doses of substance P injected close i.a. induced colonic contractions unchanged by hexamethonium and/or guanethidine but sensitive to atropine. The neurally-induced colonic contractions are suggested to be due to an antidromic activation of thin sensory neurons which in the periphery release substance P, in turn activating cholinergic motor neurons, thus constituting an axon reflex arrangement. The possibility of a similar axon reflex mechanism, associated to thin afferents, activating adrenergic inhibitory neurons at the prevertebral ganglionic level is discussed.

Animals↗

Evaluating and treating common upper extremity nerve compression and tendonitis syndromes ... without becoming cumulatively traumatized.

Cumulative trauma disorder, repetitive motion injury, and overuse syndrome are all umbrella descriptions of many specific injuries that require careful evaluation, diagnosis, and treatment to restore function, decrease pain, and minimize time spent in a patient role. This article describes anatomic sites of common nerve compressions and tendonitis in the upper extremity (UE). Evaluation techniques are described with emphasis on clinical, environmental, and psychological mitigating factors essential in identifying microtrauma of nerves and tendons to achieve the correct differential diagnosis. Conservative treatment recommendations, including splinting, ergonomics, corticosteroid injection, and hand surgery, are outlined to assist the practitioner in discerning the most appropriate course of action. Surgical intervention and postoperative care and follow-up for median, ulnar, radial, and thoracic outlet nerve compression syndromes are briefly described.

Arm↗

Pulmonary vasomotor nerve responses in isolated perfused lungs of Macaca mulatta and Papio species.

1. Lung lobes of Macaca mulatta and Papio species were isolated from the body and perfused by a pump delivering a constant volume inflow. The left atrial pressure was kept constant and therefore any recorded change in pulmonary arterial pressure reflected a change in pulmonary vascular resistance. 2. In five Macaca mulatta preparations stimulation of the upper thoracic sympathetic chain, the stellate ganglion, the middle cervical ganglion and the thoracic vagosympathetic nerve caused a small increase in calculated pulmonary vascular resistance usually followed by a larger decrease. Evidence is produced which suggests that the depressor response is mediated by adrenergic beta-receptors. In three preparations no change in pulmonary vascular resistance occurred. 3. In four Papio preparations stimulation of similar nerves invariably caused an increase in calculated pulmonary vascular resistance. In one animal no change in vascular resistance occurred. 4. A regression analysis of the results showed an inverse relationship between the magnitude of the pulmonary vascular response to nerve stimulation and the degree of excitement of the animals during capture, restraint and anaesthesia (P less than 0.01).

Animals↗

Increased cardiac sympathetic nerve activity following acute myocardial infarction in a sheep model.

The time course of cardiac sympathetic nerve activity (CSNA) following acute myocardial infarction (MI) is unknown. We therefore undertook serial direct recordings of CSNA, arterial blood pressure (MAP) and heart rate (HR) in 11 conscious sheep before and after MI, and compared them with 10 controls. Conscious CSNA recordings were taken daily from electrodes glued into the thoracic cardiac nerves. Infarction was induced under pethidine and diazepam analgesia by applying tension to a coronary suture. MI size was assessed by left ventricular planimetry (%) at postmortem, peak troponin T and brain natriuretic peptide levels (BNP). Baroreflex slopes were assessed daily using phenylephrine-nitroprusside ramps. The mean infarcted area was 14.4 +/- 2.9%, troponin T 1.88 +/- 0.39 microg l(-1) and BNP 8.4 +/- 1.3 pmol l(-1). There were no differences in haemodynamic parameters or CSNA between groups at baseline. MAP and HR remained constant following MI. CSNA burst frequency increased from baseline levels of 55.8 +/- 7.1 bursts min(-1) to levels of 77.5 +/- 8.7 bursts min(-1) at 2 h post-MI, and remained elevated for 2 days (P < 0.001). CSNA burst area also increased and was sustained for 7 days following MI (P= 0.016). Baroreflex slopes for pulse interval and CSNA did not change. CSNA increases within 1 h of the onset of MI and is sustained for at least 7 days. The duration of this response may be longer because the recording fields decrease with time. This result is consistent with a sustained cardiac excitatory sympathetic reflex.

Action Potentials↗

Continual recordings of cardiac sympathetic nerve activity in conscious sheep.

Cardiac sympathetic nerve activity (CSNA) is of major importance in the etiology of heart disease but is impossible to measure directly in humans. Ovine and human cardiovascular systems are similar; therefore, we have developed a method for the daily recording of CSNA in conscious sheep. After thoracotomy, electrodes were glued into the left thoracic cardiac nerve and CSNA, blood pressure (BP), and heart rate were recorded daily. Satisfactory recordings > or =7 days of CSNA were obtained in 11 of 28 sheep (40%), mean recording time 10.6 days, range 7-47. During the first week, CSNA decreased gradually from 78 +/- 8 at baseline to 60 +/- 7 bursts/min on day 5 (P = 0.02) or from 76 +/- 9 to 57 +/- 7 bursts/100 beats on day 7 (P = 0.04). Similarly, BP decreased from 103 +/- 4 to 94 +/- 4 mmHg (P = 0.03). Low-frequency heart rate variability decreased from 0.12 +/- 0.02 to 0.06 +/- 0.02 ms(2) on day 6 (P = 0.004) but was not correlated to CSNA. In conclusion, CSNA that can be continually recorded in conscious sheep decreases during the first week postsurgery and, thereafter, stabilizes. This model should provide valuable insights in future investigations of cardiac disease.

Animals↗

Anatomical variant of the lateral pectoral nerve innervating the anterior portion of the deltoid muscle: a case report.

BACKGROUND: The deltoid muscle is innervated by the axillary nerve. There is no collateral nerve supply described for this muscle. Palsy of the axillary nerve is common in shoulder trauma due to its close relationship to the surgical neck of humerus. METHODS: A dissection of the pectoral and axillary regions of two female cadavers was performed bilaterally for a detailed analysis of the innervation of the deltoid muscle. RESULTS: A branch of the lateral pectoral nerve provided supplemental innervation to the anterior portion of the deltoid muscle bilaterally in both cadavers. CONCLUSION: A branch of the lateral pectoral nerve could provide collateral nerve supply to the deltoid muscle. The frequency of this anatomical variation requires further exploration.

Aged↗

Anatomical study on 2 cases of the congenital partial defect of pectoralis major and minor muscles.

2 cases of the defect of pectoralis major muscle observed in male cadavers allocated for routine dissection were investigated anatomically, especially on the nerve supply for the defected muscles. In both cases, one on the left and the other on the right side, pectoralis major muscle was defected, the clavicular portion and a small part of sternocostal portion only persisting. Meanwhile, the ipsilateral pectoralis minor muscle was defected in the first case to be a string-like muscle band and was missing in the second case substituted by a membrane which seemed not to be the degenerated same muscle. Both the lateral and medial pectoral nerves supplied the pectoral muscles in the first case. One of rami of the medial pectoral nerve was distributed unusually to the most lateral part of the persisted sternocostal portion. Only the lateral pectoral nerve existed in the second case. In both cases nerves derived from 2 caudal segments, C8 and Th1, were lacking or poor. However, it was suggested that the defect of the muscles was not due to the nonparticipation of these nerves but due to the failure of caudal growth of the pectoral premuscle mass in a five-week embryo (Lewis 1901).

Aged↗

Effects of vagal deafferentation on oesophageal motility and transit in the sheep.

Effects of vagal deafferentation on oesophageal motility and transit were studied in conscious sheep by recording the electromyographic activity of different parts of oesophagus during swallowing of saliva, or balloons inflated with 20 ml of air. Surgical isolation and subsequent sectioning of the nodose ganglion, leaving the bundles of motor fibres intact, can be performed in sheep. Division of both ganglia led to immediate death of sheep. However, vagal deafferentation of the thoracic oesophagus could be achieved by sectioning the thoracic vagus nerve in association with sectioning the contralateral nodose ganglion. The sectioning of one vagus nerve did not affect primary oesophageal peristalsis during swallowing of saliva or of a bolus. Balloons inflated in the pharyngeal cavity and left free to move caudally, failed to pass into the stomach within the normal time of 2-2.3 s in only 4-16% of the tests. In these cases, they were always stopped in the thoracic oesophagus. Following total deafferentation of the thoracic oesophagus, balloons were prevented from being propelled into the stomach in each test. They were stopped for several minutes at the beginning of the deafferented part of the oesophagus. Electromyographic activity recorded from the deafferented part was reduced during swallowing of balloons or saliva. Deafferentation was confirmed by the failure of the presumed deafferented segment of oesophagus to respond to distension. These experiments provide direct evidence that the vagus carries information from the oesophagus which influences the central pattern generator during swallowing of a bolus or saliva. In sheep, this feed-back is essential for the effective swallowing of a bolus although not for saliva.

Animals↗

Spinal inhibitory effects of cardiopulmonary afferent inputs in monkeys: neuronal processing in high cervical segments.

Noxious stimulation of spinal afferents inhibits primate spinothalamic tract (STT) neurons in segments distant from the region of afferent entry. Inhibitory effects of cardiopulmonary sympathetic afferent (CPSA) stimulation remain after C(1) transection but disappear with spinal transection between C(3) and C(7). We hypothesized that spinal inhibitory effects produced by CPSA stimulation are processed by neurons in C(1)-C(3) segments. One purpose of this study in anesthetized monkeys was to determine whether chemical activation of high cervical neurons reduced sacral STT cell responses to colorectal distension (CRD) and urinary bladder distension (UBD). First, effects and interactions of pelvic and cardiopulmonary visceral afferent inputs were determined in 10 monkeys on extracellular activity of sacral STT neurons recorded in deep dorsal horn. CRD and UBD increased activity in 95 and 91% of sacral STT neurons, respectively. CPSA and cardiopulmonary vagal stimulation decreased activity in 84 and 56% of STT neurons, respectively. CPSA stimulation decreased CRD-evoked activity in six of eight sacral STT neurons and decreased UBD-evoked activity in five of eight STT neurons tested. Excitatory amino acid application at C2 segment decreased CRD-evoked responses in 7 of 10 sacral STT neurons and decreased UBD-evoked responses in 9 of 12 STT neurons. The second purpose of this study was to examine responses of C(1)-C(3) descending propriospinal neurons to stimulation of cardiopulmonary afferent fibers. If C(1)-C(3) neurons process CPSA input to suppress STT transmission, then CPSA stimulation should excite C(1)-C(3) neurons with descending projections. Effects of thoracic vagus nerve stimulation also were examined. Vagal stimulation inhibits STT neurons in segments below C(3) but excites C(1)-C(3) STT neurons; we theorized that vagal inhibition of sensory transmission might relay in high cervical segments and, therefore, excite C(1)-C(3) descending propriospinal neurons. Extracellular discharge rate was recorded for C(1)-C(3) neurons antidromically activated from thoracic or lumbar spinal cord in 24 monkeys. CPSA stimulation increased activity of 16 of 45 neurons and inhibited one cell. Thoracic vagus stimulation increased activity of 20 of 43 neurons and inhibited one cell; stimulation of abdominal vagus fibers did not affect activity of six of six cells that were excited by thoracic vagal input. Mechanical stimulation of somatic fields excited 30 of 41 neurons tested. All neurons activated by visceral input received convergent somatic input from noxious pinch of somatic receptive fields that generally included the neck and upper body; 11 C(1)-C(3) propriospinal neurons did not respond to any afferent input examined. Results of these studies were consistent with the idea that modulation of spinal nociceptive transmission might involve neuronal connections in high cervical segments.

Animals↗

Medial and lateral pectoral nerves: course and branches.

During modified radical mastectomy or cosmetic surgery, denervation of the lower part of the pectoralis major frequently occurs and may reduce muscle spasm, with consequent better reconstruction of the breast. The aim of this study was to determine the relationship between the pectoral nerves and the pectoral muscles. Eight unembalmed female cadavers were dissected and vascular and radiologic studies performed. The lateral pectoral nerves showed a constant course, parallel to the thoraco-acromial vessels. They coursed for 55 +/- 7 mm inferomedially on the deep surface of pectoralis major, under its fascia. The medial pectoral nerves showed two main patterns of branching, which correlated with the extent of the costal attachments of the pectoralis minor muscles. In pattern A (56%), associated with costal attachments narrower than 6.0 cm, the nerve pierced the deep aspect of the pectoralis minor as a single trunk, ramified in the muscle, and gave some branches that appeared on the superficial aspect to enter the pectoralis major. In pattern B (44%), associated with costal attachments wider than 6.6 cm, the nerve divided before entering pectoralis minor and its branches passed through the muscle or round its lower border to reach pectoralis major. The most medial branch of the medial pectoral nerve directed to the pectoralis major muscle emerged from pectoralis minor at the third intercostal space in the midclavicular line, a mean of 10.3 cm lateral to the margin of the sternum. Knowledge of the relationship between the extent of the costal attachment of pectoralis minor and the two patterns of branching of the medial pectoral nerve may be useful when performing elective denervation of the major pectoralis muscle.

Aged↗

The anatomy of the pectoral nerves and its significance to the general and plastic surgeon.

It has previously been shown that in 62% of patients the medial pectoral nerve courses through the pectoralis minor muscle to innervate the lower half or two thirds of the pectoralis major muscle. In the other 38% of patients, the medial pectoral nerve exits around the lateral aspect of the pectoralis minor muscle. The lateral pectoral nerve courses on the undersurface of the pectoralis major muscle, innervating the proximal one third or more of the muscle. Consequently, when the pectoralis minor muscle is removed in a modified radical mastectomy, or dissection between the two muscles is performed, there is partial deinnervation of the pectoralis major muscle with partial atrophy and a decrease in size. Further, if the lateral pectoral nerve also is injured or removed, it can result in total deinnervation of the pectoralis major muscle with more severe atrophy and fibrosis of the muscle. In cosmetic augmentations, when the breast implant is placed behind the pectoralis major muscle, that muscle is partially deinnervated. In this clinical situation, this is believed to be advantageous because it allows the breast to project better. This paper details the anatomy of the pectoral nerves and discusses the clinical implications of surgery in this region as it relates to the size and function of the pectoral muscles.

Breast↗