Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. Activation of the sympathetic input to the urinary bladder by electrical stimulation of afferent fibres in the pelvic nerve evoked three responses: (1) an initial transient rise in intravesical pressure, (2) an inhibition of neurally evoked bladder contractions and (3) an inhibition of transmission in vesical parasympathetic ganglia. Similar responses were elicited by stimulation of the hypogastric nerve. 2. The reflex responses were observed in acute spinal preparations (T10-T12) and in cats with intact spinal cords, but were abolished by bilateral transection of the hypogastric nerves. 3. The inhibition of bladder contractions was antagonized by the administration of propranolol (200-400 mug, I.A.), a beta-adrenergic blocking agent. The inhibition of ganglionic transmission was antagonized by dihydroergotamine (30-75 mug, I.A.), an alpha-adrenergic blocking agent. The initial rise in intravesical pressure was not antagonized by either agent. 4. Electrical stimulation of other afferents (carotid sinus nerve and sciatic nerve) did not consistently elicit responses in the urinary bladder. However, stimulation of these afferents as well as pelvic nerve afferents evoked reflex firing in nerve filaments on the surface of the urinary bladder. The firing was abolished by transection of the ipsilateral hypogastric nerve. 5. It is concluded that stimulation of vesical afferents activates a spinal sympathetic reflex which results in closing of the internal urethral sphincter and a depression of bladder activity. The latter occurs by a direct depression of detrusor smooth muscle as well as a block of the neural input to the bladder. This vesico-sympathetic reflex represents a negative feed-back mechanism which may have an important role in the maintenance of urinary continence.
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PMID:Reflex activation of sympathetic pathways to vesical smooth muscle and parasympathetic ganglia by electrical stimulation of vesical afferents. 95 14

This study examined the effects of a computerized functional electrical stimulation exercise program on plasma beta-endorphin-like immunoreactivity (BEP-ir), cortisol levels and depression parameters in spinal cord-injured individuals. Nine subjects from 1.2 to 33.5 yr postinjury with both motor and sensory complete lesions between C5 and T12 participated. It was determined that patients who sustained spinal cord-injuries less than 5 yr before this study had lower than normal baseline levels of BEP-ir and flattened circadian rhythms. Patients who sustained their injury greater than 5 yr before this study had higher baseline levels of BEP-ir with some return to normal circadian rhythmicity. Baseline cortisol levels, regardless of time since injury, appeared to be dysregulated. Regular exercise with computerized functional electrical stimulation caused significantly (P less than 0.05) sustained increases in BEP-ir in all patients and improved the regulation of cortisol. Furthermore, the more strenuous the exercise training, greater increases in BEP-ir levels were seen. Last, depression scores improved, which suggests a possible association between subjective mood and BEP-ir levels.
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PMID:Neuroendocrine changes during functional electrical stimulation. 162 80

A 72-year-old female patient was scheduled for abdominal surgery with epidural block in combination with general anesthesia. An 18 G epidural catheter was inserted through an 18 G Tuohy needle between T12 and L1 using the midline approach and the 'loss of resistance' technique. A test dose of 13 ml bupivacaine 0.25% showed no effect and a bolus of 12 ml bupivacaine 0.25% was added 8 min later. Bilateral analgesia between S5 and C4 developed over the following 17 min but was not accompanied by any cardiovascular or respiratory depression. The patient became sleepy and was finally intubated after the administration of thiopentone 175 mg and pancuronium 6 mg. There were no objections to surgery, so the hemicolectomy was continued as planned. Intraoperatively the systolic blood pressure dropped twice, to a minimum of 105 mm Hg, coinciding with eventration of the intestine, but this was reversed immediately on administration of a vasoconstrictor. Extubation of the patient was possible 90 min later on the termination of surgery, when the level of anesthesia had reached T2. A spinal X-ray with radiopaque dye showed a typical intrathecal distribution. Most remarkable in this case is the stability of the cardiovascular function which in our opinion is related to the 0.25% solution. Serious complications of an inadvertent dural puncture can be avoided or alleviated with this concentration if the epidural block is to be combined with general anesthesia.
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PMID:[Subarachnoid placement of a peridural catheter with high spinal anesthesia. The advantage of 0.25 % bupivacaine]. 186 77

1. Activation of vesical afferent fibres in the Agammadelta range by electrical stimulation of the pelvic nerve or by bladder distension elicited reflex firing in hypogastric nerves and in preganglionic nerves to the inferior mesenteric ganglion.2. The multisynaptic reflex was present in cats with an intact spinal cord and in acute and chronic spinal animals (transections at T10-T12). The reflex pathway was partially crossed in the sacral cord, and in the periphery at the level of the inferior mesenteric ganglia. In contrast, an inhibitory response to raised intravesical pressure was mediated by a supraspinal inhibitory mechanism which was activated in parallel with the micturition reflex.3. Since enhancement as well as depression of sympathetic firing accompanied reflex micturition, it is concluded that at least two distinct populations of lumbar preganglionic neurones are responsive to vesical afferent activity: one population being excited, the other depressed, during micturition. The latter population may be involved in an inhibitory feed-back mechanism on to the bladder.
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PMID:Reflex firing in the lumbar sympathetic outflow to activation of vesical afferent fibres. 450 51

Twenty five healthy pregnant women received an epidural injection (at levels varying from T11-T12 to L3-L4) of morphine (2 or 3 mg in 10 ml of saline solution 9 p. thousand) in order to achieve pain relief for delivery. The degree of dilation never exceeded 5 cm at time of injection. Pain level decreased in 22 cases (88 p. cent) but only 16 women (64 p. cent) were fully satisfied. Hypoalgesia begun after 25 minutes and disappeared after 19 hours. No respiratory or haemodynamic changes were noted. On the other hand, the duration of the first stage of labour decreased. The best results are seen when injection is achieved at highest levels, facing spinal cord segments supplying the cervix and the perineum. No newborn showed any sign of respiratory or neurologic depression.
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PMID:[Epidural morphine for obstetrical pain relief (author's transl)]. 724 51

The possibility that opioid peptides participate in alteration of spinal cord conduction following trauma to the cord was investigated in a rat model using a pharmacological approach. Spinal cord injury was produced in urethane anesthetized animals by a longitudinal incision into the right dorsal horn of T10-11 segments (2 mm deep and 5 mm long). Spinal cord evoked potentials (SCEP) were recorded epidurally from the T9 (rostral) and T12 (caudal) segments after stimulation of the ipsilateral tibial and sural nerves at the ankle. SCEP from both rostral and caudal segments consisted of a small positive peak followed by a high negative peak. Infliction of trauma in untreated rats resulted in an immediate depression of the rostral maximal negative peak (MNP) amplitude. This depression was long-lasting. Later, a significant increase in the latency of the rostral MNP amplitude occurred. Naloxone was administered in a high dosage (10 mg/kg, i.p.) to block mu-, delta- and kappa-opioid receptors 30 min before injury. This drug treatment inhibited the immediate post-injury decrease of the rostral MNP amplitude without any significant effect on latency changes. Measurement of water content in the traumatized spinal cord segment showed a significant reduction in the drug treated animals 5 h after trauma (71.46 +/- 0.54) as compared with untreated controls (74.65 +/- 0.76). However, 1 mg or 5 mg/kg dosages of the drug were not effective in reducing the SCEP changes or edema after injury. These results strongly suggest that blockade of kappa-opioid receptors with high doses of naloxone is important in reduction of trauma induced alteration of SCEP and edema formation in spinal cord injury.
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PMID:Opioid receptors influence spinal cord electrical activity and edema formation following spinal cord injury: experimental observations using naloxone in the rat. 770 96

The influence of naloxone (an opioid receptor antagonist) on spinal cord conduction and edema formation as a result of trauma to the cord was investigated in a rat model. The spinal cord injury (SCI) was inflicted in urethane anesthetized animals by a longitudinal incision into the right dorsal horn of the T10-11 segments, about 2 mm deep and 5 mm long. Spinal cord evoked potentials (SCEP) were recorded epidurally from the T9 (rostral) and T12 (caudal) segments after stimulation of the ipsilateral tibial and sural nerves at the ankle. The edema was measured by determining water content of the cord at s h after injury. In rats not given naloxone SCI resulted in an immediate long-lasting depression of the rostral maximal negative peak (MNP) amplitude (about 60%) and a significant increase in the latency of the rostral maximal positive peak (MPP). Pretreatment with naloxone inhibited the immediate post-injury decrease of the rostral MNP and some of the increase of MPP latency. The water content in the traumatized spinal cord was reduced by 3% in naloxone treated animals compared with untreated injured controls. Our results indicate that endogenous opioid peptides participate in changes of spinal cord conduction after trauma and influence edema formation probably via multiple opioid receptors.
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PMID:Naloxone reduces alterations in evoked potentials and edema in trauma to the rat spinal cord. 797 34

Thoracic epidural analgesia combined with chronic beta-adrenergic blocker medication may cause cardiac depression. We investigated the cardiovascular and myocardial metabolic effects of a T1-T12 epidural block in 18 patients (age < 65 yr, ejection fraction > 0.5), receiving chronic beta-adrenergic blocker medication and scheduled for aortocoronary bypass surgery. After randomization into a light or deeper general anesthetic group, the cardiovascular and myocardial metabolic effects of a subsequent general anesthesia induction were investigated. Thoracic epidural analgesia induced a moderate decrease in mean arterial pressure, coronary perfusion pressure, free fatty acids, and myocardial consumption of free fatty acids. General anesthesia with thiopental (2-4 mg/kg) and a low fentanyl dose (5 micrograms/kg) increased heart rate, coronary perfusion pressure, and coronary vascular resistance, whereas mean pulmonary arterial pressure and pulmonary capillary wedge pressure decreased. After thiopental (2-4 mg/kg) and a high fentanyl dose (30 micrograms/kg), mean arterial pressure and left ventricular stroke work index decreased. We conclude that a T1-T12 epidural block in well sedated, beta-adrenergic blocked patients does not induce clinically significant cardiovascular effects. Induction of general anesthesia was well tolerated, but the light general anesthetic could not prevent an increase in heart rate and coronary vascular resistance, whereas the deeper anesthetic induced slight myocardial depression. No effect on the atrioventricular conduction, as measured by the PQ-time, was noted.
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PMID:The influence of thoracic epidural analgesia alone and in combination with general anesthesia on cardiovascular function and myocardial metabolism in patients receiving beta-adrenergic blockers. 810 48

Spinal cord stimulation (SCS) has routinely been used since the beginning of the 1970s. The initial indications for stimulation were the so-called deafferentation or neurogenic pain. Further work has confirmed that neurostimulation is useful in severe peripheral vascular disease in relieving pain and increasing capillary blood flow and oxygen tension. The effects are similar to those of sympathectomy. In 1964 Apthorp et al. discovered that sympathectomy relieved angina in about 75% of patients. The use of SCS to treat angina follows logically from its use in peripheral vascular disease. METHODS. The pain-relieving effect of SCS was investigated in two patients, 54 and 69 years old, who were hospitalised for 8 and 28 days. Both patients had severe angina pectoris (duration 2 and 15 years, New York Heart Association class III and II), related to three-vessel disease, and one of them had previously undergone his third bypass operation. The other patient was not considered suitable for surgery. The antianginal treatment (long-acting nitrates, beta-blockers, calcium antagonists) was regarded as optimal and was not changed during the observation period (Table 1). SURGICAL TECHNIQUE AND STIMULATION EQUIPMENT. We used the commercially available Medtronic SCS system. The operation was performed under local anaesthesia to allow the patient to answer questions during the intraoperative stimulation. The epidural space was punctured at the level of T7-T8 in one case and T11-T12 in the other. The electrode tip was positioned in the midline or a few millimetres to the left at the T1-T2 level (Figs. 1, 2), so that the patient felt a prickling sensation in the precordial area and into the arms. The distal end of the electrode was sutured to the fascia and connected via a tunnelled extension lead to the external pulse generator. The pulse width was 200 microseconds, frequency 80 Hz. An appropriate amplitude (usually 8-10 V) was used for comfortable paraesthesia. The study consisted of two parts: a run-in period (1 week) to standardise the stimulation when mobilisation was performed. A treatment period (18 months) to determine the patient's working capacity after continuous stimulation (Table 2). After a successful run-in period a Medtronic receiver was implanted, connected to the electrode and stimulated by external pulse generator. Different variables were used to assess the effect: pulse rate, blood pressure, the product of pulse rate and systolic blood pressure, estimated anginal pain, and ST changes in the electrocardiogram (ECG) before, during and after mobilisation. RESULTS. The stimulation was carried out for 30 min 10-12 times a day during the run-in period and five to six times a day during the treatment period. Altogether there was slight lowering of heart rate and systolic blood pressure. Consequently the product of heart rate and systolic blood pressure was diminished. In one case (NYHA II) the distinct disorder of repolarisation reverted to the normal condition as shown on ECG. In the other case (NYHA III) the ECG remained unchanged because of a severe aneurysm of the cardiac wall. Both patients experienced nearly complete pain relief after a few days for 6 and 12 months respectively. However, an increasing effort tolerance could be demonstrated in both patients by reducing the extent of the heart failure (NYHA II/III to NYHA I/II) (Table 2). DISCUSSION. Our two hospitalised patients had clinically intractable angina pectoris and severe manifestations of heart disease corresponding to at least NYHA functional class II-III. Both were unsuitable for operation and showed no improvement on individually titrated maximal oral antianginal drug treatment. During SCS treatment significant improvement was obvious: chest pain, ST-segment depression, and the extent of heart failure could be reduced. Both patients reached a better NYHA functional class, exhibited increased working capacity and reported reductions in anginal attacks and pain. Th
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PMID:[Epidural spinal cord stimulation in therapy-resistant angina pectoris]. 836 77

The potential efficacy of indomethacin (a potent inhibitor of endogenous prostaglandin synthesis) on spinal cord-evoked potentials and edema formation occurring after a focal trauma to the spinal cord was examined in a rat model. The spinal cord evoked potentials were recorded in urethane-anesthetized male rats using monopolar electrodes placed epidurally over the T9 (rostral) and T12 (caudal) segments after stimulation of the ipsilateral right tibial and sural nerves. Reference electrodes were placed in the corresponding paravertebral muscles. The spinal cord evoked potential consisted of a small positive peak followed by a broad and high negative peak. Amplitudes and latencies of the maximal positive peak and the maximal negative peak were measured. The latencies and amplitudes 30 min before injury were used as references (100%). A complete loss was denoted as 0%. All the potentials were quite stable during 30 min of recording before injury. Infliction of trauma to the T10-T11 segments of the spinal cord with a sterile scalpel blade (about 5 mm longitudinal and 2 mm deep incision into the right dorsal horn extending to Rexed's laminae VII) in untreated animals resulted in an immediate depression of the rostral maximal negative peak amplitude (60-100%) which persisted during 5 h of recording. The latencies of the rostral as well as caudal maximal negative and positive peaks increased successively from 2 h post-trauma. In this group of animals, 5 h after injury the spinal cord water content in the traumatized segments was increased by more than 6% as compared with a group of uninjured animals. Pretreatment with indomethacin (10 mg/kg body weight i.p. 30 min before injury) markedly attenuated the immediate decrease in the maximal negative peak amplitude after injury, but did not influence the successive latency increase. However, the increase in the water content of the traumatized cord after 5 h was less pronounced compared with untreated injured rats. Our results show a beneficial effect of indomethacin on trauma-induced spinal cord evoked potential changes and edema formation. Prostaglandins may thus influence early bioelectrical changes occurring in traumatized spinal cord not reported earlier. The findings support the view that early recording of spinal cord evoked potential may be useful to predict the outcome in some forms of spinal cord injuries.
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PMID:Indomethacin, an inhibitor of prostaglandin synthesis attenuates alteration in spinal cord evoked potentials and edema formation after trauma to the spinal cord: an experimental study in the rat. 845 Sep 74


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