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

The intrinsic processes involved in the initiation and arrest of seizures are not completely understood. Cortical and cerebellar inhibitory mechanisms, accumulation of metabolic products, and glial uptake of extracellular potassium (K+o), anions, and released neurotransmitters are all important processes that limit focal firing and terminate a seizure once it has been initiated. Of these, the intrinsic cortical inhibitory mechanisms--i.e., recurrent and surround inhibition--appear to be the most important. Active cation and anion transport processes are two metabolic events that have yet to be elucidated but clearly could be involved in terminating a seizure discharge. For example, without an active mechanism to transport chloride, opening of the chloride channel by the inhibitory transmitter GABA would not result in increased chloride permeability. The transient hypoxia and hypercapnia and lactic acidosis that follows a severe tonic-clonic seizure produces a mixed systemic metabolic and respiratory acidosis. In experimental animals, the hypercapnia that results is sufficient to block seizure discharges. Increasing the CO2 concentration significantly reduces the extension to flexion (E/F) ratio of mice given maximal electroshock seizures (MES) and increases the time required for 50% of the animals to recover sufficiently from a first MES to be able to have another MES. The decreased E/F ratio and the increased recovery time (RT50) are both indicative of a decrease in seizure activity. Since the extent to which CO2 is allowed to accumulate in the brain is regulated by the glial specific enzyme carbonic anhydrase (CA), it follows that the glial cell has an integral role in the mechanisms involved in arresting seizure activity. In contrast, hypoxia increased the E/F ratio and decreased the RT50, evidence that seizure activity was enhanced. Another metabolic factor affecting duration of seizure activity, susceptibility to seizures, and recovery from seizures is glucose. Recovery from seizures depends in part on an adequate supply of this energy source. An inverse correlation (R = 0.95) between RT50 and blood sugar was found when the blood sugar was altered experimentally by treatments that altered the endocrine status (pancreatectomy, treatment with alloxan, cortisol, insulin, glucagon, and dextrose). Since glial cells contain (as glycogen) the small amount of glucose present in the brain, they probably hasten the ability of the brain to recover normal function following a seizure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of glial cation and anion transport mechanisms in etiology and arrest of seizures. 370 23

The purpose of this investigation was to examine the effects of norepinephrine cardiomyopathy (NE-CM) on left ventricular (LV) performance in diabetic rabbits. Diabetes mellitus was produced in 11 rabbits by giving them alloxan monohydrate, 120 mg/kg. Cardiomyopathy was produced in five animals by a 90-min infusion of norepinephrine (2 micrograms/min/kg). Left ventricular contractility and pump function (VF) were examined 2 days later. The effects of hypercapnia and inotropic responsiveness to NE were also determined. VF was assessed by means of left ventricular function curves obtained with constant mean aortic pressure and heart rate and quantified by determining stroke volume (SV) at a left ventricular pressure of 10 cm H2O (SV10). Mean SV10 was 1.22 +/- 0.08 ml in control diabetics but averaged only 0.95 +/- 0.08 ml in diabetics with NE-CM (P less than 0.05). NE-CM markedly reduced LV dP/dt max responses to NE infusion but the increments in SV10 did not differ. Hypercapnia caused significantly greater ventricular depression in NE-CM than in control diabetic rabbits (P less than 0.001). The depressive effect of hypercapnia can be countered in part by the administration of NE in both groups, but differential depression in VF to hypercapnia was persistent between the two groups.
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PMID:Ventricular performance in diabetic rabbits with norepinephrine cardiomyopathy. 394 45