Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experimental acute hypercarbia in dogs produced significant blood loss from the upper gastrointestinal tract, as well as from the small and large intestines. At necropsy, gross and microscopic examinations demonstrated necrotizing lesions resembled the postmortem ulcerations found in some patients with severe hypercarbia. Superior mesenteric arteriograms performed in four animals shortly after onset of hypercarbia showed abnormalities consistent with vasoconstriction. Vagal inhibition by atropine and correction of respiratior acidosis by TRIS buffer failed either to reduce the blood loss or to alter the pathologic lesions. Multiple studies of blood coagulation in the hypercarbic animals revealed no consistent changes when compared with eucarbic animals. In four animals treated with phenoxybenzamine during hypercarbia, blood loss and hemorrhagic gastrointestinal lesions were diminished, suggesting possible pathogenetic role of alpha-adrenergic stimulation. Although the mechanism is not proved, vasoconstriction secondary to adrenergic stimulation may play an important bleeding occurring with hypercarbia.
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PMID:Acute gastrointestinal bleeding during experimental hypercarbia. 30 Jun 67

The pulmonary vasopressor response to acidemia was studied in intact dogs in a hemodynamically separated lobe which was pump perfused with systemic arterial or venous blood at a fixed rate. The magnitudes of the lobar vasopressor responses to perfusion with blood rendered acidic by infusions of hydrochloric lactic, and acetic acids, and by hypercapnia (membrane oxygenator) were significantly different. Although the PH of the perfusing blood in each group fell to similar extents (pH 7.1-7.0), the lobar pressor response was greatest with hydrochloric acid (HCl), smaller with lactic and acetic acids, and absent with hypercapnia. A lobar vasopressor response also occurred during lobar perfusion with blood which had been extracorporeally acidified with HCl or acetic acid, but then returned to control pH by infusions of sodium bicarbonate and Tris before reaching the lung. A lobar vasopressor response also resulted from pump perfusion of the lobar artery with femoral venous blood during perfusion of the isolated ipsilateral femoral artery with similarly treated aortic blood. However, no lobar vasopressor response resulted from pump perfusion of the lobar artery with blood removed transseptally from a right pulmonary vein during acidification (HCl) of the right pulmonary artery (to pH 7.0).The data indicate that, in this experimental preparation involving closed-chest dogs spontaneously breathing air or 35% oxygen, the lobar vasopressor response to infusions of acidifying agents is not directly related to the pH of blood actually perfusing the lobar vessels. Additionally, the vasopressor response is prevented by prior perfusion of the acidified blood through a pulmonary vascular bed but not by prior perfusion through the femoral vascular bed. Although these experiments do not establish the mediation of the lobar vasopressor response, activation of vasoactive agents in blood at or near the acidification site is suggested. In these experiments, the acidemia was produced under conditions which are not like the usual ones of developing metabolic acidosis or alveolar hypercapnia, in that strong acids were directly infused into blood which perfused only one lung lobe. The mediation of the present pressor responses and of those found in the more usual forms of experimental and clinical acidosis may therefore be dissimilar.
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PMID:The pulmonary vasopressor response to decreases in blood pH in intact dogs. 555 5

Mechanical hyperventilation of acidemic patients with acute lung injury (ALI) requires the use of high volumes and pressures that may worsen lung injury. However, permissive hypercapnia in the presence of shock, metabolic acidosis, and multi-organ system dysfunction may compromise normal cellular function. Tris-hydroxymethyl aminomethane (THAM) may be an effective method to control acidosis in this circumstance. Protonated THAM is excreted by the kidneys, so that carbon dioxide production is not raised. In an uncontrolled study, we administered THAM to 10 patients with acidosis (mean pH = 7.14) and ALI (mean lung injury score = 3.28) in whom adequate control of arterial pH could not be maintained during either eucapnic ventilation or permissive hypercapnia ventilation. THAM was given at a mean dose of 0.55 mmol/kg/h. Administration of THAM was associated with significant improvements in arterial pH and base deficit, and a decrease in arterial carbon dioxide tension that could not be fully accounted for by ventilation. Although further studies are needed to confirm these observations, THAM appears to be an effective alternative to sodium bicarbonate for treating acidosis during ALI.
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PMID:The treatment of acidosis in acute lung injury with tris-hydroxymethyl aminomethane (THAM). 1076 4

Inhibition of ventilatory drive may improve the sensation of dyspnea, because heightened ventilatory demand contributes to dyspnea. Tris-hydroxymethyl aminomethane (THAM) is an alkalizing agent that does not increase CO(2) production and exerts a depressant effect on respiration. The purpose of this study was to clarify the effect of THAM on dyspnea associated with increases in respiratory drive. We investigated the effects of THAM on dyspneic sensation produced by a combination of hypercapnia (mean PaCO(2)=52 mm Hg) and elastic loading (30 cm H(2)O/L) in 14 healthy subjects. The subjects were asked to rate their dyspneic sensation using a visual analogue scale (VAS) during the loaded breathing while monitoring ventilation using a pneumotachograph. THAM was infused at a rate of 0.4 mL/kg/minute for 10 minutes, and the effects of THAM on dyspnea and ventilation were evaluated by comparing the steady-state values of ventilatory variables and VAS score obtained before and after THAM administration. Administration of THAM corrected respiratory acidosis and was associated with significant improvements in VAS score and significant decreases in minute ventilation, respiratory frequency, and ventilatory drive. THAM administration greatly alleviates dyspneic sensation associated with the increase in respiratory drive and could be an effective therapy for treating severe dyspnea in patients with hypercapnia.
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PMID:THAM improves an experimentally induced severe dyspnea. 1880 42