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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiac sympathetic afferents are known to reflexly activate the cardiovascular system, leading to increases in blood pressure, heart rate, and myocardial contractile function. During myocardial ischemia, these sensory nerves also transmit the sensation of pain (angina pectoris) and cause tachyarrhythmias. The authors' laboratory has been interested in defining the mechanisms of activation of this neural system during ischemia and reperfusion. During these periods, reactive oxygen species, particularly hydroxyl radicals, are produced from the breakdown of purine metabolites and lead to stimulation of sympathetic (and vagal) ventricular chemosensitive nerve endings. For example, stimulation with hydrogen peroxide leads to a small reflex increase in blood pressure from the predominant sympathetic afferent activation that is reduced by simultaneous activation of cardiac vagal afferents (known to exert predominantly depressor reflexes). Central integration of these two opposing reflexes likely occurs at several regions of the brain stem, including the nucleus tractus solitarii, where neural occlusion occurs during simultaneous cardiac sympathetic and vagal-afferent stimulation. Activation of platelets also appears to play a role during myocardial ischemia, leading to local release of serotonin (5HT), which, through a 5HT3 mechanism, stimulates sympathetic afferents. Finally, regional changes in pH from lactic acid (but not hypercapnia), stimulate ventricular afferents and may activate kallikrein to increase bradykinin (BK), which, in turn, breaks down arachidonic acid to form prostaglandins. Prostaglandins sensitize cardiac sympathetic afferents to BK. Thus, stimulation of cardiac sympathetic afferents during ischemia and reperfusion and the resulting reflex events form a multifactorial process resulting from activation of a number of chemical pathways in the myocardium.
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PMID:Cardiac sympathetic afferent activation provoked by myocardial ischemia and reperfusion. Mechanisms and reflexes. 1145 9

Neuropathic pain syndromes with sympathetically maintained pain are often associated with a deep somatic pain component. An adrenergic interaction between sympathetic vasoconstrictor neurons and cutaneous afferents has been demonstrated. To determine whether a sympathetic-afferent interaction exists in deep somatic tissues, we investigated the effect of sympathetic muscle vasoconstrictor activity on experimentally induced pain. In 12 healthy volunteers, capsaicin was infused into the anterior tibial muscle. Intensity and quality of muscle and referred pain were assessed. The analyses were performed during the presence of low sympathetic muscle vasoconstrictor activity induced by breathing 100% O(2) gas (normocapnia), and during high activity induced by inspiration of 95% O(2) and 5% CO(2) (hypercapnia). The degree of sympathetic muscle vasoconstrictor discharge was monitored indirectly by measuring systemic blood pressure and end-expiratory CO(2) and by performing duplex sonography of muscle resistance vessels. The intensity, quality, and spatial distribution of muscle and referred pain were not significantly different during resting and increased sympathetic muscle vasoconstrictor discharge, indicating that such activity does not influence pain after intramuscular infusion of capsaicin.
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PMID:Effect of sympathetic muscle vasoconstrictor activity on capsaicin-induced muscle pain. 1211 56

About 80,000 polio survivors are still living 40 years after the last polio epidemics in Germany. Of these 40-70% have developed the so called post-polio syndrome (PPS) decades after the infection. The main symptoms of PPS are decreasing strength in voluntary muscles, pain and fatigue which occur spontaneously but may also be induced by physical stress and general illness. We report the case of a 79-year-old male who developed hypercapnia due to ventilatory failure which necessitated reintubation several times after cholecystectomy. The medical history revealed that he had had poliomyelitis at the age of 8 years. There was only a slight residual handicap from this infection which included mild pareses of the left limbs but had remained stable for about 70 years. Electromyography revealed signs of chronic neurogenic changes in muscles of the left upper limb as well as in the pectoralis major. The diagnostic criteria of a post-polio syndrome were fulfilled and other neuromuscular diseases were excluded. The patient could be discharged from intensive care only after treatment by intermittent positive pressure ventilation via a facial mask. This case report shows that even patients who have a mild handicap after poliomyelitis can develop weaning problems. A PPS can exacerbate with inclusion of respiratory muscles in critically ill patients.
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PMID:[40 years after the last polio epidemic. Postpolio syndrome as a cause of "weaning failure"]. 1212 9

This issue of the Bulletin deals with the principles of anesthesia for outpatient female sterilization with emphasis on techniques for laparoscopy and minilaparotomy. General anesthesia techniques provide analgesia, amnesia, and muscle relaxation and are particularly useful for managing the anxious patient. Disadvantages include increased expense, need for specialized equipment, and highly trained personnel, and delayed recovery. Complications, though relatively rare, can be life-threatening and include aspiration of stomach contents, hypoxia, hypercarbia, hypotension, hypertension, cardiac arrhythmias, cardiorespiratory arrest, and death. There is no single preferred technique of general anesthesia, athough most anesthetists employ methods that allow rapid recovery of faculties, enabling the patient to be discharged soon after surgery. To accomplish this end, light anesthesia with sodium thiopental induction and nitrous oxide maintenance is often used. Short duration muscle relaxation with an agent such as succinylcholine supplements this technique. Other techniques include light anesthesia with inhalational anesthetic agents and the use of intravenous ketamine. Local anesthesia augmented by systemic and/or inhalational analgesia is supplanting general anesthesia techniques for laparoscopy in many locales. This approach is also particularly well-suited for minilaparotomy in developing countries, where it has achieved its greatest popularity. The local technique carries with it reduced morbidity and mortality but may not entirely relieve discomfort. The primary danger of local anesthesia is respiratory depression due to excessive narcosis and sedation. The operator must be alert to the action of the drugs and should always use the minimal effective dose. Although toxicity due to overdosage with local anesthetic drugs is occasionally experienced, allergic reactions to the amide-linkage drugs such as lidocaine or bupivacaine are exceedingly rare. For outpatient laparoscopy or minilaparotomy, local anesthesia with proper preoperative counselling and premedication should provide adequate relief of pain and is the method of choice, unless the patient cannot be examined awake or is totally uncooperative. The decision to utilize either general or local anesthesia should be made by the patient after thorough counselling by the surgical team. In many cases, the circumstances of the surgical environment will dictate the choice, but patient comfort and safety should always be the goal.
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PMID:Anesthesia for outpatient female sterilization. 1231 53

Allyl-2,5-dimethyl-1-piperazines have been of interest as analgesic agents for the management of moderate-to-severe pain. In this study, we compared the antinociceptive properties and respiratory depressant activity of one such agent, (+)-3-((alpha-R)-alpha-((2S,5R)-4-allyl-2,5-dimethyl-1-piperazinyl)-3-hydroxybenzyl)-N-(3-fluorophenyl)-N-methylbenzamide (DPI-3290), with those of established narcotic analgesics, morphine and fentanyl. Intravenous administration of DPI-3290 in conscious laboratory rats increased antinociception in a dose-dependent manner with a corresponding ED(50) value of 0.05 +/- 0.0072 mg/kg. Simultaneous measurement of arterial blood gas in animals treated with DPI-3290 demonstrated dose-dependent increases in pCO2 with an ED(50) value of 0.91 +/- 0.22 mg/kg. In comparison, morphine and fentanyl increased antinociception in rats with ED(50) values of 2.01 +/- 0.0005 and 0.0034 +/- 0.00024 mg/kg, respectively, and the ED(50) value for morphine-induced changes in pCO2 was 4.23 +/- 0.72 mg/kg, whereas the ED(50) value for fentanyl-induced changes in pCO2 was 0.0127 +/- 0.0035 mg/kg. A separate series of experiments were designed to examine the effects of DPI-3290 on mu-opioid receptor induced antinociception and hypercapnia. Intravenous bolus doses of DPI-3290 that ranged from 0.2 to 1.0 mg/kg had no effect on antinociception mediated by alfentanil (2 microg/kg/min i.v.) but reduced hypercapnia by approximately 50%. Results from these studies demonstrate the equivalent antinociceptive efficacy of DPI-3290, morphine, and fentanyl but dramatic differences in the hypercapnia that antinociceptive doses of these drugs produce. When measured simultaneously, DPI-3290 had an 18.2-fold difference in the ratio comparing the ED(50) value for antinociception with the ED(50) value for changes in pCO2; this ratio was 2.1 for morphine and 3.7 for fentanyl. Furthermore, DPI-3290 reduced the alfentanil-mediated hypercapnia without any effect on antinociception. Together, the balanced opioid agonist activity of DPI-3290 may provide a means of powerful analgesia while mitigating the mu-opioid receptor-mediated hypercapnia.
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PMID:DPI-3290 [(+)-3-((alpha-R)-alpha-((2S,5R)-4-Allyl-2,5-dimethyl-1-piperazinyl)-3-hydroxybenzyl)-N-(3-fluorophenyl)-N-methylbenzamide]. II. A mixed opioid agonist with potent antinociceptive activity and limited effects on respiratory function. 1453 67

Primary pulmonary hypertension (PPH) is an uncommon disease. We describe two cases of pulmonary hypertension crisis in patients with PPH during general anesthesia. Any factor that worsens primary pulmonary hypertension (strain, hypoxia, pain, hypercapnia, intubation, or hyperinflation) should be avoided.
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PMID:[Two cases of pulmonary hypertension crisis in patients with primary pulmonary hypertension]. 1496

Headache occasionally occurs during or after scuba diving. Although its significance often is benign, headache may signal a serious neurological disorder in some circumstances. In addition to the usual causes of headache, the diagnostic evaluation should consider otic and paranasal sinus barotrauma, arterial gas embolism, decompression sickness, carbon dioxide retention, carbon monoxide toxicity, hyperbaric-triggered migraine, cervical and temporomandibular joint strain, supraorbital neuralgia, carotid artery dissection, and exertional and cold stimulus headache syndromes. Focal neurologic symptoms, even in the migraineur, should not be ignored, but rather treated with 100% oxygen acutely and referred without delay to a facility with a hyperbaric chamber.
Curr Pain Headache Rep 2004 Aug
PMID:Headache and facial pain in scuba divers. 1522 93

The purpose of this study was to examine the effect of low dose halothane on the acute ventilatory response to hypercapnia, and to assess whether arousal (due to audiovisual (AV) stimulation or pain) modulates the response to halothane. Single step increases in end-tidal Pco(2) using dynamic end-tidal forcing were performed from eucapnia (end-tidal Pco(2) held 1 mmHg (0.13 kPa) above ambient) to hypercapnia (end-tidal Pco(2) 6 mmHg (0.79 kPa) above ambient) in eight healthy volunteers, with end-tidal PO(2) held at 100 mmHg (13.2 kPa), in six protocols: 1) control conditions (darkened, quiet room, eyes closed) without halothane; 2) control conditions with 0.1 MAC halothane; 3) AV stimulation (bright room, loud television) without halothane; 4) AV stimulation with 0.1 MAC halothane; 5) pain (electrical stimulation of skin over tibia to produce visual analogue pain score 5-6/10) without halothane; 6) pain with 0.1 MAC halothane. Both AV stimulation (p = 0.014) and pain (p = 0.0003) significantly increased the baseline eucapnic minute ventilation modestly (by approximately 1.5-4 l.min(-1)). Halothane did not influence the baseline minute ventilation in any arousal state (p = 0.572), nor did it affect the hypercapnic ventilatory response in any arousal state (p = 0.208). Arousal (either AV stimulation or pain) did not affect the ventilatory response to CO(2), regardless of the presence or absence of halothane (p = 0.585). We conclude that halothane affects neither baseline minute ventilation nor the response to CO(2). Arousal can increase baseline ventilation but has no influence on the ventilatory response to CO(2).
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PMID:Interaction of arousal states and low dose halothane on the acute hypercapnic ventilatory response in humans. 1564 10

We previously demonstrated that lumbar intrathecal alpha(2) agonists attenuate hypercapnia-induced cerebral vasodilation. The combination of intrathecal clonidine and neostigmine is being investigated as pain therapy. The effects of their combination on cerebrovascular reactivity are unknown. We allocated rabbits anesthetized with pentobarbital to two groups: (a) clonidine (normal saline followed 30 min later by clonidine 2 microg/kg, both into the lumbar intrathecal space; n = 6), and (b) neostigmine-pretreatment (neostigmine 2 microg/kg followed 30 min later by clonidine 2 microg/kg, both into the lumbar intrathecal space; n = 6). We then evaluated the hypercapnia-induced changes in pial arteriolar diameter in these two groups using the closed cranial window preparation. The pial arteriolar dilator response to hypercapnia was significantly attenuated in the clonidine group (14% +/- 4%, 4% +/- 4%, 6% +/- 6%, and 5% +/- 7% for before and 30, 60, and 90 min, respectively). Neither normal saline nor neostigmine alone induced any change in the cerebral reactivity to hypercapnia. Pretreatment with neostigmine completely prevented the clonidine-induced attenuation of the hypercapnic cerebral vasodilation attenuated by intrathecal clonidine (16% +/- 7%, 15% +/- 6%, 12% +/- 6%, and 16% +/- 8%, respectively).
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PMID:Intrathecal neostigmine prevents intrathecal clonidine from attenuating hypercapnic cerebral vasodilation in rabbits. 1578 25

This paper reviews published studies (identified by a Medline-assisted search) on the effect of <or= 0.2 minimum alveolar concentration inhaled anaesthetic agents on the hypercapnic ventilatory response in healthy subjects. Each article was examined for the anaesthetic agent used, whether CO(2) was administered using a rebreathing or a steady state (step hypercapnia) technique, and subject arousal (by audiovisual stimulation or by pain). Analysis of variance was used to assess the influence of each of these factors on the standardised hypercapnic response (the hypercapnic ventilatory response in l.min(-1) x kPa(-1) in the presence of anaesthetic, expressed as a fraction of the response without anaesthetic). There were 21 separate studies embedded within 14 published articles. When considered together, the effect of anaesthetics on the hypercapnic ventilatory response was not significant (p = 0.089). Furthermore, when each agent was considered separately, no agent alone had a significant effect on the hypercapnic response. Neither subject arousal (p = 0.396) nor the method used to induce hypercapnia (p = 0.625) had any significant influence on the response. This suggests that the hypercapnic response is more resistant to the effects of anaesthetics than the hypoxic ventilatory response. These results indicate areas for future work. It would seem important to identify the cellular mechanisms which might underlie the difference in hypercapnic and hypoxic responses, and possible ways in which subject arousal might interact in the brain with the chemoreflexes.
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PMID:Effect of low dose inhaled anaesthetic agents on the ventilatory response to carbon dioxide in humans: a quantitative review. 1581 67


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