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

In a search for CO2 chemoreceptor neurons in the brain stem, we used immunocytochemistry to monitor the expression of neuronal c-fos, a marker of increased activity, after 1 h of exposure to CO2 in five groups of Sprague-Dawley rats (294 +/- 20 g): five air breathing controls, three breathing 10% CO2, three breathing 13% CO2, three breathing 15% CO2, and three breathing 15% CO2 and treated with morphine (10 mg/kg sc). After exposure the rats were anesthetized with pentobarbital sodium and perfused intracardially with 4% paraformaldehyde. The brain stem was removed and cryoprotected, and then 50-microns frozen sections were cut and immunostained for the fos protein. Brain stem fos-immunoreactive neurons were plotted and counted in the superficial 0.5 mm of the ventral medullary surface. Thirteen to 15% CO2 evoked fos-like immunoreactivity (FLI) in 321 +/- 146 neurons/rat. Significant CO2-induced labeling was confined within the superficial 150 microns: 67% of identified cells were less than 50 microns below the surface, greater than 90% between 1.0 and 3.0 mm from the midline, and approximately 60% in the rostral half of the medulla. Thirteen to 15% CO2 also evoked FLI in the area of the nucleus tractus solitarius but not in other medullary regions. Morphine (10 mg/kg sc) did not suppress high CO2-evoked FLI in either the ventral medullary surface or the nucleus tractus solitarius, although it eliminated excitement and hyperventilation. We suggest that respiratory CO2 chemoreceptor neurons can be identified in rats by their expression of c-fos after 1 h of hypercapnia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Medullary CO2 chemoreceptor neuron identification by c-fos immunocytochemistry. 150 6

Thirty elderly patients undergoing major hip surgery under spinal analgesia were randomly allocated in a double-blind manner into three groups. The aim was to evaluate the influence of intrathecal morphine and postoperative naloxone infusion on the regulation of ventilation. The Bupivacaine Group received spinal analgesia with 20 mg bupivacaine intrathecally. The Morphine Group received spinal analgesia with 20 mg bupivacaine + 0.3 mg morphine intrathecally. The Naloxone Group received spinal analgesia with 20 mg bupivacaine + 0.3 mg morphine intrathecally + postoperative naloxone infusion intravenously (1 microgram/kg/h over 12 h, 0.25 micrograms/kg/h over the next 12 h). Evaluation of resting ventilation and the ventilatory responses to hypercarbia and hypoxaemia was made on three occasions: before surgery, and 8, and 24 h after the intrathecal injection. Intrathecal morphine had no significant effect on ventilatory regulation in elderly patients undergoing major hip surgery performed under bupivacaine spinal analgesia. Postoperative administration of opioids or sedatives after intrathecal morphine as well as postoperative blood loss associated with a fall in blood pressure appeared to increase the risk of developing respiratory depression. Naloxone infusion seemed to reduce the risk of developing respiratory depression. Furthermore, one third of the elderly had a poor response to hypoxaemia before surgery.
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PMID:Influence of intrathecal morphine and naloxone intervention on postoperative ventilatory regulation in elderly patients. 163 66

Morphine sulfate effects (30 mg, intramuscularly) on cerebral glucose utilization and subjective self-reports were examined in 12 polydrug abusers by positron emission tomography and [fluorine 18]fluorodeoxyglucose in a double-blind placebo-controlled crossover study. During testing, subjects sat with eyes covered, listening to white noise and "beep" prompts. Morphine significantly reduced glucose utilization by 10% in whole brain and by about 5% to 15% in telencephalic areas and the cerebellar cortex, assuming no contribution of hypercapnia. When the contribution of PaCO2 (45 minutes after morphine was administered) was partialled out, significant morphine-induced reductions persisted in whole brain and six cortical areas. Irrespective of morphine, left-greater-than-right asymmetry occurred in the temporal cortex, and an interaction between hemisphere and drug was noted in the postcentral gyrus. In most cases, effects on glucose utilization were not significantly related to measures of euphoria.
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PMID:Morphine-induced metabolic changes in human brain. Studies with positron emission tomography and [fluorine 18]fluorodeoxyglucose. 240 75

The effects of subcutaneous doses of morphine and verapamil on respiratory and cardiovascular parameters have been assessed in conscious rats. Verapamil (10 mg kg-1) was injected simultaneously with morphine (16 mg kg-1) or at 10, 30, or 60 min before morphine administration. Morphine induced respiratory depression, as indicated by marked hypercapnia, hypoxia and acidosis, and caused marked tachycardia. Although morphine produced only a minor and inconsistent (but statistically significant, P less than 0.01) reduction of mean arterial blood pressure, morphine potentiated verapamil-induced hypotension. Verapamil suppressed morphine-induced hypercapnia only when injected simultaneously with morphine. Verapamil alone did not affect arterial blood gases or pH, but decreased heart rate and mean arterial blood pressure. Verapamil attenuated and delayed the maximum positive chronotropic effects of morphine at all times tested. Antagonism by verapamil of respiratory depression and tachycardia produced by morphine was unrelated to morphine levels in plasma. Thus, the explanation of verapamil-morphine interactions on respiration and cardiovascular function is not pharmacokinetic.
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PMID:Time course of verapamil interaction with morphine effects on physiological parameters in rats. 257 6

Morphine and clonidine both elevated plasma levels of lidocaine to the same extent in mice while slowing lidocaine metabolism to deethylated products. The effects of clonidine on lidocaine disposition were reversed by yohimbine. Mice given morphine, 20 mg/kg sc, or clonidine, 0.2 mg/kg sc, had similar, 30-50%, elevation of plasma lidocaine levels at 15 min after lidocaine, 15 mg/kg iv, when compared to saline-treated animals. Despite similarity of effect on plasma lidocaine, mice treated with morphine were much more susceptible to lethal effects of lidocaine than were mice given clonidine. At iv doses of 22 mg/kg or higher, lidocaine caused death in nearly all morphine-treated mice, while even 32 mg/kg lidocaine caused only 11% mortality after saline or clonidine. Clonidine, 0.5 mg/kg sc, and morphine, 20 mg/kg sc, both raised plasma lidocaine levels in rats, but only morphine depressed respiration, causing hypoxia, hypercapnia, and acidosis and increasing lidocaine lethality. These data suggest that potentiation of lidocaine toxicity by morphine is due primarily to changes in blood gases rather than to elevation in lidocaine levels.
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PMID:Interaction of clonidine and morphine with lidocaine in mice and rats. 281 81

The individual and combined effects of subcutaneous morphine and diltiazem, a calcium channel inhibitor, on arterial blood gases and pH were assessed in conscious Fischer-344 rats. Morphine (4 mg kg-1) produced hypercapnia, hypoxia and slight acidosis, as compared with control values. Diltiazem (10 mg kg-1) alone did not affect these parameters; however, it significantly delayed the onset of the aforementioned effects of morphine.
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PMID:Effects of diltiazem on morphine-induced respiratory decline. 287 84

Effects of s.c. doses of morphine and verapamil, alone and in combination, on arterial blood gases and pH, mean blood pressure and heart rate were assessed in partially restrained, awake Fischer-344 rats. As expected, morphine (4-16 mg/kg) produced a dose-dependent respiratory depression, as indicated by hypoxia, hypercapnia and acidosis. Verapamil, a calcium channel antagonist, alone (10 mg/kg) did not affect these parameters; however, it significantly attenuated and delayed the aforementioned effects of morphine. Morphine caused a slight increase in mean blood pressure, which was not dose dependent, whereas verapamil reduced blood pressure dramatically even in the presence of morphine. All groups showed some tachycardia, but rats treated with morphine alone showed the most pronounced increase in heart rate, which was antagonized by verapamil. The authors conclude that the interaction of verapamil with morphine's respiratory depressant effects differs from the previously reported potentiation of morphine's antinociceptive and hypothermic actions.
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PMID:Interactions between verapamil and morphine on physiological parameters in rats. 372 97

The effects of morphine, hypoxaemia or hypercapnia on gastric acid secretion, gastric mucus synthesis and the gastric mucosa were studied in conscious rats with pyloric occlusion. Hypoxaemia and hypercapnia were induced by morphine 32 mg/kg given i.p., or each condition was produced separately by adjusting the composition of respired air in the chamber where the animals were kept during the experimental period. Hypoxia significantly enhanced gastric mucus synthesis whereas hypercapnia significantly reduced gastric acid secretion. These effects were significantly alleviated by atropine pretreatment. Morphine-treated rats exhibited decreased gastric acid secretion, increased gastric mucus synthesis and a higher mean ulcer index but only the reduced gastric acid output was significantly prevented by atropine. It is suggested that the effect of morphine on gastric acid secretion may result from its respiratory depressant action and consequent acute stress production. However, the mechanisms by which morphine can increase mucus synthesis and produce ulceration remain obscure.
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PMID:Effects of morphine, hypoxaemia and hypercapnia on the rat stomach. 375 55

Morphine, 20 mg X kg-1, sc, halved the plasma clearance of sulfobromophthalein (BSP) while tripling hepatic tissue levels of this dye. Since narcotics depress respiration, effects of hypoxia, hypercapnia, and acidosis on BSP disposition were studied. Ambient gases breathed by rats were adjusted to achieve blood gas levels identical to those of morphine-induced respiratory depression. Saline-treated rats breathing room air had PAO2 of 87 +/- 3 mmHg (mean +/- SE) and PaCO2 of 40 +/- 2 mmHg. After intraarterial injection of BSP, 100 mg X kg-1, plasma clearance of this dye was 7.1 +/- 1.1 ml X min-1 and BSP levels in the liver at 40 min after injection were 163.3 +/- 19.8 micrograms X g-1. After morphine, 20 mg X kg-1, PaO2 decreased to 47 +/- 4 mmHg and PaCO2 increased to 89 +/- 5 mmHg. In these rats BSP clearance dropped to 3.5 +/- 0.4 ml X min-1, and 40-min liver dye levels were increased to 596.4 +/- 60.4 micrograms X g-1. Similar hypoxia and hypercapnia caused by breathing 9% O2 and 8% CO2 in the absence of morphine caused plasma BSP clearance to be decreased to 4.4 +/- 0.2 ml X min-1 and 40-min hepatic BSP to be increased to 292.5 +/- 31.8 micrograms X g-1. Hypercapnia and acidosis alone did not affect BSP disposition, while hypoxia without hypercapnia decreased its plasma clearance to 5.5 +/- 0.3 ml X min-1 and increased liver levels to 339.1 +/- 35.1 micrograms X g-1. Hypoxia was reversed completely in morphine-treated rats by placing them in 40% O2. In these animals, despite normal oxygen, plasma BSP clearance was decreased to 4.4 +/- 0.6 ml X min-1, and liver BSP was increased to 497.9 +/- 65.6 micrograms X g-1. Thus, respiratory depression with hypoxia may contribute to morphine-induced effects on BSP disposition, but altered blood gases cannot account fully for these narcotic effects.
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PMID:Effects of morphine and respiratory depression on sulfobromophthalein disposition in rats. 673 7

Morphine reduces ventilation (VE) in exercising man. The mechanism of this ventilatory depression remains unclear. Recent evidence suggests that morphine may reduce exercise VE by simultaneously reducing exercise metabolic rate. We measured exercise VE in six normal subjects after intravenous injection of either saline or 0.1 mg/kg morphine sulfate. During treadmill walks requiring 1/3 and 2/3 of the maximal oxygen uptake, morphine reduced VE (P < 0.05), while it left metabolic rate unchanged. Morphine treatment elevated end-tidal PCO2 at both work levels (P < 0.05). Lower VE and higher PETCO2 in exercise after morphine persisted after elevation of alveolar PO2 to 200 torr. Thus, morphine left unchanged the contribution of the hypoxic chemoreflex to normoxic exercise VE. In addition, morphine failed to alter the ventilatory responses to hypercapnia measured at each exercise level. These results suggest that analgesic dosages of morphine reduce the ventilatory response to exercise through a mechanism other than alterations in metabolic rate or chemical ventilatory responses.
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PMID:Morphine reduces ventilation without changing metabolic rate in exercise. 677 68


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