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

In the proximal tubules, fractional reabsorption remains essentially unchanged during variations in glomerular filtration rate (GFR). Glomerulotubular balance (GTB), defined as the linear relationship between proximal tubular reabsorption and GFR, is quantitatively the most important regulator of tubular reabsorption, which may be stopped by inhibiting Na, K-ATPase activity completely. However, ouabain in doses inhibiting 80% of the Na, K-ATPases, exerts no effect on proximal reabsorption of water, NaCl and NaHCO3. At constant plasma pH, the same relationship between filtered and reabsorbed bicarbonate is obtained whether bicarbonate reabsorption is altered by varying GFR or plasma concentration of bicarbonate. In contrast, a selective rise in plasma NaCl concentration at constant plasma pH (hypernatremia) reduces NaHCO3 reabsorption and fails to stimulate NaCl reabsorption. Other characteristics of proximal tubular reabsorption are that nonreabsorbable solutes, such as mannitol, inhibit water and NaCl reabsorption with little or no change in NaHCO3 reabsorption and renal oxygen consumption. Mannitol reduces the slope of the GTB curve for NaCl but not for NaHCO3. Hypertonic NaHCO3 exerts an osmotic effect on proximal water and NaCl reabsorption comparable to that of mannitol, whereas hypertonic NaCl is without osmotic effect. By reducing plasma pH (hypercapnia at high plasma bicarbonate concentration), the slope of the GTB curves for NaCl and NaHCO3 can be greatly increased. By raising plasma pH either by hypocapnia or bicarbonate loading, proximal reabsorption of NaHCO3 and NaCl is greatly depressed and remains almost unaltered during variations of GFR (abolished GTB). Similarly, carbonic anhydrase inhibitors, such as acetazolamide, reduce the reabsorption of NaCl and NaHCO3 in the same proportion as a rise in plasma pH, and abolish GTB. Examinations of proximal tubular oxygen consumption indicate that the energy requirement for NaHCO3 reabsorption is as expected for transcellular transport by Na, K-ATPases, whereas proximal NaCl reabsorption requires no additional energy. These data indicate that transcellular energy-requiring NaHCO3 reabsorption provides the main osmotic force across the tight junction for paracellular reabsorption of proximal tubular fluid containing NaCl and other solutes of low reflection coefficient. The main factors influencing GTB are the filtered load of bicarbonate, plasma pH and nonreabsorbable solutes in the proximal tubular fluid.
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PMID:Essentials of glomerulotubular balance. 267 97

Trauma victims are directly transferred to a level I trauma center bypassing local hospitals. First, airways and cervical stability are secured. Intracranial hematoma should be promptly evacuated. Endotracheal intubation and mechanical ventilation are initiated for children with a Glasgow Coma Score of 10 or less, anisocoria, apnea, and/or hypercarbia. Isotonic crystalloid is used for intravenous fluid maintenance. The goal of intracranial pressure (ICP) management is to maintain the ICP at less than 15 mmHg and to maintain minimum cerebral perfusion pressure at 45-55 mmHg. External ventricular drainage provides direct control of the ICP by allowing intermittent drainage of the CSF (5-10 ml/hour). Mannitol is effective but hyperventilation is not recommended.
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PMID:[Management of acute-stage head trauma in childhood]. 1072 87

The objective of the treatment of intracranial hypertension is to decrease intracranial pressure (ICP) while maintaining cerebral blood flow (CBF). Despite numerous treatments, none of them associates total efficiency and security. Systemic secondary cerebral injuries, which are responsible for cerebral ischemia, lead us to administer non specific treatments in order to optimize CBF and cerebral oxygenation. Thus, the goals are: 1) to maintain cerebral perfusion pressure> or =70 mmHg; 2) to control metabolic status by preventing hyperglycaemia, anaemia and hyperthermia; 3) to maintain normoxia and normocapnia (hypercapnia increases ICP and hypocapnia decreases CBF). Beside the neurosurgical evacuation of extra- and intraparenchymatous haematomas, osmotherapy and cerebrospinal fluid (CSF) evacuation are the two specific treatments of intracranial hypertension. Osmotherapy consists in an administration of a hypertonic solution which induces a decrease in cerebral water and finally in ICP. Mannitol (20%), which is the reference, associates osmotic and rheologic effects, and decreases CSF production too. Recent data conduct us to administer larger doses, between 0.7 and 1 g/kg in 15 minutes. Hypertonic saline solution associates osmotic effects and plasma volume loading. Thus, this solution is particularly appropriate in severe head injury with arterial hypotension. CBF evacuation decreases rapidly ICP without any major side-effect. Until now, there is no proof of a superior efficiency of a treatment for intracranial hypertension compared to another. Considering their mechanism of action, all of them are efficient but potentially dangerous too. Indeed, the choice between treatments depends on data which are issued from the multimodal monitoring. General non specific treatments are always necessary. Specific treatments are indicated if ICP is above 20-25 mmHg. Maintaining cerebral perfusion pressure represents the first therapeutic goal. If intracranial hypertension persists, evacuation of CBF or osmotherapy may be advocated. In case of refractory intracranial hypertension, it may be useful to deepen neurosedation. Controlled hypocapnia and barbiturates remain a third line therapy providing to monitor and maintain an appropriate CBF and cerebral oxygenation. Controlled hypothermia and decompressive craniectomy must be individually discussed.
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PMID:[Hierarchical strategy for treating elevated intracranial pressure in severe traumatic brain injury]. 1785 Oct 25