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

This study explores the influence of severe lactic acidosis in the ischemic rat brain on postischemic recovery of the tissue energy state and neurophysiological parameters. Severe incomplete brain ischemia (cerebral blood flow below 5% of normal) was induced by bilateral carotid artery clamping combined with hypovolemic hypotension. We varied the production of lactate in the tissue by manipulating the blood glucose concentrations. A 30-min period of incomplete ischemia induced in food-deprived animals caused lactate to accumulate to 15-16 mumol g-1 in cortical tissue. Upon recirculation these animals showed: (1) a considerable recovery of the cortical energy state as evaluated from the tissue concentrations of phosphocreatine, ATP, ADP, and AMP; and (2) return of spontaneous electrocortical activity as well as of somatosensory evoked response (SER). In contrast, administration of glucose to food-deprived animals prior to ischemia caused an increase in tissue lactate concentration to about 35 mumol g-1. These animals did not recover energy balance in the tissue and neurophysiological functions did not return. In other experiments the production of lactate during 30 min of complete compression ischemia was increased from about 12 mumol g-1 (normoglycemic animals) to 20-30 mumol g-1 by preischemic hyperglycemia and, in separate animals, combined hypercapnia. The recovery of the cortical energy state upon recirculation was significantly poorer in hyperglycemic animals. It is concluded that a high degree of tissue lactic acidosis during brain ischemia impairs postischemic recovery and that different degrees of tissue lactic acidosis may explain why severe incomplete ischemia, in certain experimental models, is more deleterious than complete brain ischemia.
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PMID:Brain lactic acidosis and ischemic cell damage: 1. Biochemistry and neurophysiology. 732 45

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.
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PMID:Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection. 744 74

Thick, 0.34 mm, 38% water hydrogel lenses were fitted, under a pressure patch, to one eye of 18 type I diabetic patients (aged 18-40 years) to assess the acute response to hypoxia and hypercapnia; the response was compared with that in 18 healthy, aged-matched non-diabetic subjects; the closed-eye lens wear was started mid-morning. Pre-lens wear assessments were made of acuity, intraocular pressure (IOP), central corneal thickness (CCT) and corneal appearance by biomicroscopy. The mean duration of the diabetes was 13 +/- 7 years and the average fasting blood glucose was 8.7 +/- 3.3 mMl-1. Baseline CCT values were marginally greater in diabetic patients (600 +/- 33 microns) compared with a group of non-diabetic control subjects (584 +/- 26 microns; P > 0.5). A 7.7 +/- 2.1% increase in CCT was measured after 3 h lens wear in the diabetic patients while an average 10.6 +/- 2.4% increase in CCT was measured in the control subjects (P < 0.05). The recovery of corneal thickness to baseline values in diabetic patients was slower (at 44.8 +/- 2.0% per hour) than the control subjects (53.9 +/- 2.1 per hour; P < 0.05) although recovery of corneal thickness occurred in both groups within 2.5-3h. IOP values (non-contact tonometry) were higher in the diabetic patients than in the controls (14.5 +/- 2.9 vs 12.4 +/- 1.7 mmHg; P < 0.01). Overall, those corneas with greater baseline CCT values tended to swell less than those with lower baseline CCT values (r = 0.582). Positive correlations were also found between corneal thickness and IOP and blood glucose. The diabetic patients thus tended to have slightly thicker corneas (but this could be related to blood glucose or IOP rather than true corneal disease) and also had corneas that tended to swell less with a contact lens stress test (but this could be constitutively due to the slight oedema already present). The different corneal response in diabetic patients may thus be the result of physical determinants such as initial oedema and IOP and not the result of a disease of the cornea itself.
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PMID:Corneal swelling and recovery following wear of thick hydrogel contact lenses in insulin-dependent diabetics. 766 21

It has been observed that traumatic brain injury (TBI) increases the susceptibility of the brain to subsequent hypoxia, and prolonged apnea occurs in ethanol (EtOH)-treated animals following brain injury. This investigation tests the hypothesis that EtOH suppresses ventilation and hypercapnic respiratory drive following TBI. Immature pigs were anesthetized with halothane and received a 2 to 3 atm fluid-percussion brain injury. Respiratory parameters, including tidal volume, frequency, ventilation (VE), and arterial blood gases were measured on 100% O2 and on 5% to 6% inspired CO2 in O2 prior to and at 10, 60, 120, and 180 minutes after TBI. Hypercapnic response sensitivity (S) was measured as the change in VE per mm Hg increase in PaCO2. Intracranial pressure, mean arterial blood pressure, heart rate, brain temperature, glucose, and EtOH levels were also monitored. Three groups were studied: the first group of six received EtOH (3.5 gm/kg, intragastrically) without brain injury; the second group of six received TBI without EtOH; the third group of eight received EtOH and TBI. Ethanol levels were 121 +/- 13 (standard error of the mean) mg/dl in the EtOH/TBI group (136 +/- 25 in the EtOH group) at the time of injury, and 175 +/- 12 mg/dl in the EtOH/TBI group (200 +/- 20 mg/dl in the EtOH group) at 120 minutes after injury. The EtOH/TBI animals had significantly lower VE and S, and higher PaCO2 following brain injury (p < 0.05, repeated-measures analysis of variance). No significant differences were identified between groups for pH, PaCO2, intracranial pressure, heart rate, brain temperature, or glucose levels. Ethanol intoxication leads to significant impairment of respiratory control following traumatic brain injury and may contribute to brain injury in intoxicated trauma victims.
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PMID:Effects of ethanol on respiratory function in traumatic brain injury. 771 8

Functional eggshell qualities, thyroid hormones, and carbohydrate metabolism of chick embryos at the end of incubation were compared between a modern (Arbor Acres line) and a randombred control population (Athens-Canadian Randombred). Embryos from the Arbor Acres genetic line developed in larger eggs with more albumen and less yolk than Athens Canadian Randombred lines. Percentage shell and functional eggshell properties measured as eggshell conductance constants did not differ between genetic lines. On a relative basis, hearts were generally smaller and livers heavier in Arbor Acres than in Athens-Canadian Randombred birds. Heart and liver glycogen concentrations were greater in Athens-Canadian Randombred than in Arbor Acres embryos. However, blood glucose was greater in Randombred than in Arbor Acres embryos only at internal pipping, a time of hypoxia and hypercapnia. Blood plasma concentrations of thyroxine did not differ significantly between the modern and Randombred embryos at any stage examined. Modern broiler chick embryos possessed greater concentrations of triiodothyronine as well as greater triiodothyronine to thyroxine ratios than Randombred embryos at external pipping and hatching. It can be inferred from the data that chick embryos differ in their use of carbohydrate during late development between modern and Randombred genetic lines.
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PMID:Egg characteristics, carbohydrate metabolism, and thyroid hormones in late chick embryos from different genetic lines. 776 40

Serotonin-containing nerve fibres innervate cerebral blood vessels, but the source of this innervation and the physiological effects of perivascular serotonin release remain controversial. The purpose of the present study was to examine the effects of central serotonergic depletion upon the relationship between CBF and glucose utilization under both normo- and hypercapnic conditions. To induce the loss of serotonergic terminals, rats were injected twice daily for 4 consecutive days with 20 mg/kg of the specific serotonergic neurotoxin methylenedioxyamphetamine (MDA). Between 4 and 6 weeks later, local CBF and glucose utilization were measured using the fully quantitative [14C]iodoantipyrine and [14C]2-deoxyglucose autoradiographic techniques, respectively, and the efficacy of the lesioning protocol was assessed using [3H]paroxetine radioligand binding analysis. In all animals treated with MDA, there was a significant decrease in serotonin uptake sites throughout the brain, falling from 223 +/- 20 to 40 +/- 16 fmol/mg tissue in parietal cortex, for example, although the raphe nuclei themselves were unaffected (300 +/- 20 fmol/mg tissue in controls and 291 +/- 18 in MDA-treated rats). In normocapnic rats, the effects of MDA pretreatment upon blood flow and glucose use were slight and focally concentrated. However, when the animals were rendered hypercapnic, CBF was significantly higher in MDA-treated rats than in normal controls, for example, increasing from 356 +/- 22 ml 100 g-1 min-1 in frontal cortex of hypercapnic controls to 700 +/- 81 ml 100 g-1 min-1 in MDA-pretreated rats with similar levels of hypercapnia. In some brain areas of hypercapnic MDA-pretreated rats, blood flows were too high (> 800 ml 100 g-1 min-1) to be accurately quantified.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced cerebrovascular responsiveness to hypercapnia following depletion of central serotonergic terminals. 779 Apr 20

This investigation determined the effects of sustained hypercapnia on cerebral blood flow (CBF; radiolabeled microspheres), cerebral metabolic rates for O2 and glucose (CMRO2 and CMRglc), and brain water content in conscious sheep instrumented with aortic, left ventricular, vena cava, and brain sagittal sinus catheters. PaCO2 was elevated from 38 +/- 3 to 53 +/- 3 (mean +/- SD) mm Hg and PaO2 from 109 +/- 7 to 131 +/- 4 mm Hg for 96 h in an environmental chamber. Hypercapnia did not alter sheep behavior, food and water intake, arterial pressures, core temperature, or brain lactate release. Total and regional CBF and CBF/CMRO2 reached peak values at 1 h and then readjusted, to stabilize at lower, but still elevated levels at 24 h and thereafter. CMRO2 and CMRglc increased at 6 h and thereafter during hypercapnia. PaCO2, CBF, CMRO2, and CMRglc remained elevated at 3 h after restoration to room air, while CBF/CMRO2 returned to the control value. Frontal and occipital lobe wet-to-dry weight ratios increased modestly but significantly after hypercapnic exposure. It is concluded that sustained hypercapnia induces stable and nonadapting increases in both CBF and brain metabolism that persist for at least 3 h after restoration to room air in association with hypoventilization and modest elevations of brain water.
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PMID:Cerebral blood flow and metabolic responses to sustained hypercapnia in awake sheep. 779 28

Rats were tested in the forced swim test in 35 or 20 cm of water or in an open field to evaluate the effects of different intensities of stress on blood gases, electrolytes, and metabolic indices, compared to nontested controls. Animals tested in the open field did not differ from controls on any measure. Immersion in deep water resulted in a greater mixed metabolic and respiratory acidemia (low pH, low bicarbonate, high pCO2), higher glucose and higher lactate levels than immersion in shallow water which in turn resulted in greater metabolic acidemia (low pH, low bicarbonate), and higher glucose and lactate levels than occurred in open field or control animals. In contrast to immersion in deep water, immersion in shallow water resulted in an initial hypocapnia followed by a hypercapnia. Immersion in deep water also resulted in higher potassium levels, lower bicarbonate and total carbon dioxide levels, and a higher anion gap than immersion in shallow water, testing in the open field, or in controls. In a second study, lactate infusion resulted in a metabolic alkalemia (increased pH and bicarbonate levels) and an increase in total carbon dioxide levels. These results indicate that test parameters from forced swim testing (e.g., water depth) can significantly affect the rat's physiological response to testing. The effects of forced swim testing are not simply due to general stress; and the physiological changes seen in conjunction with forced swim testing (e.g., acidemia) are not due to lactate alone.
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PMID:A further analysis of physiological changes in rats in the forced swim test. 780 Jul 51

To test the capillary recruitment hypothesis in brain, cerebral blood flow was raised markedly in rats by exposure to 8% CO2 (hypercapnia), and capillary permeability-surface area (PS) products were measured. Local cerebral blood flow (LCBF), volume of radiolabeled blood in parenchymal microvessels (also referred to as the blood space or Vb), plus the local capillary influx rate constants (K1) and PS products of [14C]antipyrine and 3-O-[14C]methyl-D-glucose (3OMG) were estimated in 44 brain areas. Hypercapnia raised PaO2 to 140 mm Hg, elevated LCBF by two- to threefold through out the brain, and increased Vb from 5 to 33% (mean = 22%) in 42 of 44 brain areas; hypercapnia did not, however, alter microvessel hematocrit. With hypercapnia, the influx of antipyrine was increased by 40-65% in all brain areas, and the PS products of antipyrine were elevated from 0-35% (mean = 17%). The PS products of antipyrine plus the parenchymal blood spaces suggest modest (< 30%) capillary recruitment in most brain areas as well as some microvessel dilation, mainly in forebrain gray matter and white matter areas. In contrast, hypercapnia did not appreciably alter K1 nor PS of 3OMG; it slightly but not significantly raised the blood levels of glucose. In view of the blood space and antipyrine evidence for modest capillary recruitment and vasodilation, the lack of change in PS of 3OMG implies that glucose transporter activity was lowered by hypercapnia, an effect similar to that reported for high-dose pentobarbital. Finally, the microvessel hematocrit and 3OMG data suggest that cerebral capillary permeability (P) was not increased by hypercapnia. Overall, hypercapnia seems to increase LCBF mainly by raising the velocity of blood flow; capillary recruitment and dilation appear to play relatively minor roles in this flow increase.
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PMID:Slightly altered permeability-surface area products imply some cerebral capillary recruitment during hypercapnia. 785 5

Episodes of hypoxia often occur in hypoglycemic newborns, but it is not known whether dysfunctions in cerebrovascular regulation contribute to brain injury incurred by these affected neonates. We tested the hypotheses that 1) perinatal hypoglycemia impairs cerebrovascular responses to hypoxia and 2) a reduced vascular smooth muscle sensitivity to adenosine accounts for this impairment. Responses of 25- to 50-mu m-diam pial arterioles were determined using the cranial window technique in isoflurane-anesthetized newborn piglets < 5 days of age. Hypoxia (arterial PO2 = 28 +/- 1 mmHg) caused a 47 +/- 5% increase (P = 0.0008) in arteriolar diameter, 89% of which could be blocked by prior superfusion of the window space with the preferential A2-adenosine receptor antagonist 3,7-dimethyl-1-propargylxanthine (DMPX; 50 microM). Insulin-induced hypoglycemia (blood glucose = 18 +/- 1 mg/dl without isoelectric electroencephalogram) caused a 31 +/- 5% increase (P = 0.002) in arteriolar diameter; however, no additional dilatative response to hypoxia (arterial PO2 = 28 +/- 1 mmHg) could be elicited in these animals. Arteriolar dilation of 41 +/- 6% (P = 0.002) induced by superfusion of 20 microM adenosine under normoglycemic conditions was also completely abolished after the animals were rendered hypoglycemic. Unlike the response to hypoxia and adenosine, hypoglycemia only attenuated prostanoid-dependent dilations to hypercapnia (arterial PCO2 = 68 +/- 3 mmHg) by 55 +/- 9%. These results indicate that, in the newborn, hypoglycemia selectively abolishes hypoxic reactivity through an impairment in adenosine-mediated cerebrovascular dilation.
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PMID:Hypoglycemia selectively abolishes hypoxic reactivity of pial arterioles in piglets: role of adenosine. 786 14


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