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

The influence of a anesthetic, ethyl-ether, on arterial plasma levels of glucose, insulin and lipids was studied in starved Wistar rats. Ethyl-ether increased significantly (P < 0.05) glucose plasma levels, as a result not only of stress and of the release of catecholamines and glucocorticoids, but also of the decrease in the use of glucose by the tissues. Ethyl-ether did not change significantly the level of triglycerides, cholesterol and phospholipids. Insulin concentration was not increased, even when hyperglycemia was established. Ketonuria, acidosis and hypercapnia were increased. In these rats the administration of insulin produced a diminution in glycemia. The findings suggest that, under anesthesia with ether, the endocrine pancreas is incapable of recognizing glucose as a specific stimulus to promote the release of insulin.
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PMID:Effects of inhalation of ethyl-ether on glycemia and on some variables of intermediate metabolism in rats. 128 85

Diabetes has been reported to impair vasodilatory responses in the peripheral vascular tissue. However, little is known about vasodilatory function in the diabetic brain. We therefore studied, in the N2O-sedated, paralyzed, and artificially ventilated rat, the effects of chronic hyperglycemic diabetes on the cerebral blood flow (CBF) responses to 3 acutely imposed vasodilatory stimuli: hypoglycemia (HG) (plasma glucose = 1.6-1.9 mumol ml-1), hypoxia (HX) (PaO2 = 35-38 mm Hg), or hypercarbia HC) (PaCO2 = 75-78 mm Hg). In addition, we evaluated the somatosensory evoked potential (SSEP) and plasma catecholamine changes in rats exposed to acute glycemic reductions. Diabetes was induced via streptozotocin (STZ, 60 mg kg-1 i.p.). All results in diabetic rats were compared to those obtained in age-matched nondiabetic controls. The animals were studied at 6-8 weeks (HG experiments) or 4-6 months (HG, HX, and HC experiments) post-STZ. Values for CBF were obtained for the cortex (CX), subcortex (SC), brainstem (BS), and cerebellum (CE) employing radiolabeled microspheres. Up to three CBF determinations were made in each animal. In 6-8 week diabetics vs. controls, CBF increased to a lesser value in the CX, SC, and BS (p less than 0.05). Thus, in the diabetics, going from chronic hyperglycemia to acute hypoglycemia, CBF values (in ml 100 g-1 min-1 +/- SD) increased (p less than 0.05) from 89 +/- 22 to 221 +/- 57 in the CX, from 82 +/- 21 to 160 +/- 52 in the SC, and from 79 +/- 34 to 237 +/- 125 in the BS. In controls, going from normoglycemia to acute hypoglycemia, the CBF changes (p less than 0.05) were 128 +/- 27 to 350 +/- 219 (CX), 117 +/- 11 to 358 +/- 206 (SC), and 130 +/- 29 to 452 +/- 254 (BS). CBF changes and absolute values in the CE were similar in the two groups. At 4-6 months post-STZ, a complete loss of the hypoglycemic CBF response was found in the CX, SC, and CE. In the BS, a CBF response to hypoglycemia was seen in the diabetic rats, with the CBF increasing from 114 +/- 28 (hyperglycemia) to 270 +/- 204 ml 100 g-1 min-1 (p less than 0.05), compared to a change from 147 +/- 36 (normoglycemia) to 455 +/- 299 ml 100 g-1 min-1 (p less than 0.05) in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Chronic hyperglycemic diabetes in the rat is associated with a selective impairment of cerebral vasodilatory responses. 205 Jul 55

This study was undertaken to determine the differences (if any) in cerebral blood flow (CBF) between streptozotocin (STZ) diabetic and normal rats. CBF was studied in connection with episodes of hypoxia, hypercapnia and hypotension as compared to the basal condition. Overall basal CBF rates in streptozotocin diabetic rats were significantly higher than in normal animals. However, initial basal flow rates prior to the first challenge were insignificantly higher in the STZ diabetic group. The higher CBF rate in STZ diabetics was also seen during the peak flows of the hypoxic and hypercapnic challenges. Furthermore, although overall CBF decreased for both the normal and STZ diabetic groups during hypotension, higher CBFs were observed in the STZ diabetic group during this challenge. The percent increase in CBF above control resulting from hypoxia or hypercapnia and the changes in CBF resulting from hypotension were not significantly different in the STZ diabetic and normal groups. The results indicate that the STZ diabetic rat regulates CBF in the same manner as the normal rat in response to hypoxia, hypercapnia and hypertension. The STZ diabetic rat executes these CBF responses at a slightly higher CBF rate. In view of the finding that the regulation of CBF is unaltered in the STZ diabetic animal, it is hypothesized that the associated hyperglycemia may be the causative agent for the cerebral ischemic susceptibility associated with long-term diabetes mellitus rather than a failure of CBF regulation.
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PMID:A comparison of cerebral blood flow during basal, hypotensive, hypoxic and hypercapnic conditions between normal and streptozotocin diabetic rats. 212 71

The metabolic consequences of external hypercapnia (1% CO2) were assessed in rainbow trout (Salmo gairdneri) in the presence or absence of circulating levels of the beta adrenoceptor antagonist, propranolol. External hypercapnia caused a severe extracellular respiratory acidosis and a less pronounced reduction of hepatic intracellular pH (pHi). pHi was restored to prehypercapnic values after 48 hr of continuous hypercapnia due to elevation of bicarbonate levels. In the presence of propranolol, hypercapnia elicited a pronounced activation of pyruvate kinase (PyK) (measured at both low and high phosphoenolpyruvate (PEP) concentrations) and inactivation of both total glycogen phosphorylase (GPase) and glycogen phosphorylase a (GPase a). In the absence of propranolol, the changes in enzyme activities were significantly reduced (low PEP PyK activity) or totally absent (GPase inactivation). These results suggest that beta adrenoceptor-mediated phenomena offset disruptive effects of hypercapnia on PyK and GPase activities and may be important in the control of gluconeogenesis and glycogenolysis during this acid-base disturbance. The adrenergic effects were not related to modification of hepatic intracellular acid-base status. Hypercapnia induced a rapid depletion of liver glycogen and concomitant hyperglycemia. These effects were not prevented by pretreating fish with propranolol and appeared to be unrelated to changes in GPase a activity. These results suggest that factors other than adrenergic activation of GPase a are involved in the enhancement of liver glycogenolysis.
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PMID:Metabolic consequences of hypercapnia in the rainbow trout, Salmo gairdneri: beta-adrenergic effects. 283 62

Brain tissue acidosis is a result of either an increase in tissue PCO2 or an accumulation of acids produced by metabolism. Severe hypercapnia (arterial PCO2 around 300 mm Hg) may cause a fall in tissue pH to around 6.6 without any deterioration of the cerebral energy state or morphologic evidence of irreversible cell damage. In severe ischemia and tissue hypoxia, anaerobic glycolysis leads to lactic acid accumulation. This is aggravated by hyperglycemia and by a (trickling) residual blood flow. Under such circumstances lactate concentration in the tissue may increase to levels above 20 to 25 mumol/g (tissue wet weight), causing a decrease in pH to around 6.0. If lactic acidosis during ischemia or hypoxia reaches these excessive levels, metabolic and functional restitution is severely hampered upon subsequent recirculation and reoxygenation. In these circumstances cell morphology shows signs of irreversible damage. Conversely there is less damage if severe tissue lactic acidosis can be hindered. The deleterious effect of excessive lactic acidosis may be related to an influence on the following: synthesis and degradation of cellular constituents; mitochondrial function; cell volume control; postischemic blood flow; and stimulation of pathologic free radical reactions. Possibilities for therapeutic interventions include the avoidance of hyperglycemia, inhibition of glycolysis, and measures for increasing the buffer capacity of the brain.
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PMID:Brain acidosis. 392 94

Although the presence of fetal breathing movements (FBMs) has been suspected for almost a century, the major advances in the field were made during the last decade. Experimental animal techniques of detection include instrumentation of fetuses with electronic recording equipment. Human studies use more indirect, although no less accurate, A-mode or real-time B-scan ultrasonography in the recording of FBMs. The fetus does not make breathing movements continuously; however, there are periods of FBMs interspersed with periods of apnea. Inherent to FBMs is a diurnal variation. Hypoxia and hypoglycemia diminish FBMs, while hypercarbia and hyperglycemia have the opposite effect. Caffeine, barbiturates, and general anesthetics modify FBMs by their influence on the CNS. Preliminary studies have shown the presence of FBMs to indicate a state of fetal well-being. Possibly, in the future, testing for FBMs may become a useful clinical tool in the identification of the fetus at risk.
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PMID:Fetal breathing movements. An update for the pediatrician. 668 79

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

Ten splenectomized and ten nonsplenectomized conscious dogs were subjected to hemorrhage of 41% of their blood volume over a 15-minute period. Hemodynamic and metabolic variables were monitored for 4 hours after hemorrhage. Mortality (100%) occurred in the splenectomized group. Significant (P < 0.001) hemodynamic responses after hemorrhage included hypotension, tachycardia, low central venous pressure, and decreased ECG voltage of the R wave. Tachypnea was noted in the absence of hypoxia, hypercapnia, and acidosis inthe nonsplenectomized dogs. Significant (P < 0.001) hypocapnia and mean PCO2 values of 13.9 MM of Hg and 23.5 mm of Hg in splenectomized and nonssplenectomized dogs, respectively, was noted. Mean hemoglobin levels were significantly (P < 0.001) decreased after hemorrhage in the splenectomized dogs. The absence of a change in hemoglobin in thenonsplenectomized dogs was attributed to the translocationof extracellular fluid into the vascular space which diluted the high concentration of RBC from splenic contraction. Other changes noted after hemorrhage were hyperglycemia, increased blood cortisol, and increased pyruvate and lacte levels. Changes were not noted in pyruvate-to-lactate ratios.
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PMID:Experimental hemorrhage in splenectomized and nonsplenectomized dogs. 740 89

The object of the study was to find out how preischemic hyperglycemia (in normocapnic animals) or excessive hypercapnia (in normoglycemic animals) affect the calcium transient during ischemia, as this can be assessed by measurements of the extracellular calcium concentration ([Ca2+]e). To that extent, normocapnic-normoglycemic control animals were compared with animals with induced hyperglycemia or hypercapnia, all being subjected to 10 min of forebrain ischemia, the [Ca2+]e and d.c. potential being measured with ion-sensitive glass microelectrodes. Hyperglycemia and hypercapnia delayed the loss of ion homeostasis following induction of ischemia. Furthermore, both hyperglycemia and hypercapnia reduced the delay of Ca2+ extrusion upon recirculation. As a result, both hyperglycemia and hypercapnia significantly reduced the ischemic calcium transient, as this was assessed by calculating the duration of maximal calcium load of cells. The results make it less likely that aggravation of brain damage by hyperglycemia or excessive hypercapnia is related to a further derangement of cell calcium homeostasis.
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PMID:Influence of hyperglycemia and of hypercapnia on cellular calcium transients during reversible brain ischemia. 758 97

The tumor interstitial pH and its modification play a significant role in cancer treatment. Current in vivo pH measurement techniques are invasive and/or provide poor spatial resolution. Therefore, there are no data on perivascular interstitial pH gradients in normal or tumor tissue. We have optically measured interstitial pH gradients with high resolution in normal and tumor (VX2 carcinoma) tissue in vivo by combining a fluorescence ratio imaging microscopy technique and the rabbit ear chamber preparation. The strengths of our approach include the ability to follow pH in the same location for several weeks and to relate these measurements to local blood flow and vascular architecture. Our results show: (a) tumor interstitial pH (6.75 units; N = 6 animals, n = 324 measurements) is significantly (P < 0.001) less than normal interstitial pH (7.23; N = 5, n = 274). This increased acidity in the tumor interstitium is in agreement with the previously reported data on this tumor; (b) with respect to pH spatial gradients in normal tissue, the interstitial pH decreased by approximately 0.32 pH units over a distance of 50 microns away from the blood vessel, while in tumor tissue, interstitial pH decreased by approximately 0.13 units over the same distance. Although the pH gradient near the vessel wall was steeper in normal tissue compared to tumor, the proton concentration gradient in normal tissue was less than that in the tumor. The approximate increase in proton concentration from 0-50 microns from the vessel was 4.5 x 10(-8)M in normal versus 5.7 x 10(-8)M in tumor tissue; (c) a simple one-dimensional diffusion-reaction model suggested that tumor tissue was producing protons at a rat 65-100% greater than normal tissue; (d) feasibility studies of temporal dynamics resulting from hyperglycemia (6 g/kg) or hypercapnia (10% CO2) led to significant (P < 0.05) interstitial pH reductions. During hyperglycemia, pH dropped by more than 0.2 pH units in about 90 min in tumor tissue but remained constant in normal tissue. Hypercapnia dramatically reduced pH by approximately 0.3 pH units in tumor tissue. Our limited studies on hyperglycemia and hypercapnia are in agreement with the previously published studies and demonstrate the capability of fluorescence ratio imaging microscopy to measure spatial as well as temporal changes in interstitial pH. Fluorescence ratio imaging microscopy should permit noninvasive evaluation of new pH-modifying agents and offer unique mechanistic information about tumor pathophysiology in tissue preparations where the surface of the tissue can be observed.
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PMID:Noninvasive measurement of interstitial pH profiles in normal and neoplastic tissue using fluorescence ratio imaging microscopy. 792 15


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