UMLS:C0406810 - FACTA Search

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Query: UMLS:C0406810 (NAME)
13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The heart, lungs and hemoglobin form the body's gas transport system, which links the atmosphere and its supply of O2 with tissue, while simultaneously providing for the elimination of the metabolic end-product, CO2, into the atmosphere. The transport of these respiratory gases must be in accordance with metabolic need. This is particularly evident during the physiologic stress of isotonic exercise, when the O2 requirements and CO2 production of skeletal muscle are increased. The monitoring of these respiratory gases during exercise, referred to as cardiopulmonary exercise testing (CAR-PET), can be used to assess heart and lung function in patients with cardiovascular or lung disease or both. Chronic cardiac failure (CCF) may be defined in physiologic terms as that circumstance in which the heart fails to provide tissue with O2 at a rate commensurate with aerobic requirements. In patients with CCF, CAR-PET represents a noninvasive means to determine aerobic capacity (that is, maximal O2 uptake) and anaerobic threshold during incremental treadmill exercise. It can also provide an objective measure of the severity of failure, the functional status of the patient and the heart's pump reserve. By using additional measurements of ventilation, arterial O2 saturation and, in selected cases, hemodynamic monitoring, the nature and severity of cardiovascular and pulmonary disease may be evaluated.
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PMID:Cardiopulmonary exercise testing for evaluation of chronic cardiac failure. 396 7

We compared the ability of human red blood cells (RBC) and a cell-free oxygen carrier to maintain isolated perfused kidney function under moderately hypoxic conditions. Recirculating perfusate was gassed initially with 93% air-7% CO2, and, after 30 min, the gas was changed to 12 O2-7 CO2-81% N2. Oxygen content of the perfusate was increased with RBC (30 g/l Hbg) or highly purified human hemoglobin Ao (HbAo) polymerized with O-raffinose (o-R-poly-Hb, 30 g/l Hbg). For comparison, kidneys were perfused with 60 g/l of bovine serum albumin (BSA) alone. The effects of unmodified hemoglobin were examined by adding 5 g/l of nonpolymerized HbAo to the BSA perfusate after 20 min. The effect of increasing oxygen delivery without hemoglobin was examined by switching to 93% O2 after 20 min during some BSA perfusions (BSA-HiO2). Vascular resistance decreased progressively in o-R-poly-Hb- and BSA-HiO2-perfused kidneys but remained constant in other experiments. Nitro-L-arginine methyl ester (L-NAME) prevented vasodilation and increased the filtration fraction of o-R-poly-Hb-perfused kidneys with no change in other functions. L-NAME also prevented the formation of methemoglobin. After a 70-min perfusion with BSA, Na reabsorption was 82 +/- 3% (means +/- SD), and inulin clearance [glomerular filtration rate (GFR)] was 0.66 +/- 0.33 ml.min-1.g-1. RBC increased reabsorption to 95% (85-98%) (median, 25th-75th percentile) but did not alter GFR (0.52 +/- 0.26 ml.min-1.g-1). o-R-poly-Hb increased Na reabsorption proportionately more than GFR, so that, while GFR was doubled to 1.04 +/- 0.40 ml.min-1.g-1, Na reabsorption increased to 98% (92-99.5%). HbAo increased GFR to 1.07 +/- 0.44 ml.min-1.g-1 and increased reabsorption to 89 +/- 6%.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cross-linked hemoglobin increases fractional reabsorption and GFR in hypoxic isolated perfused rat kidneys. 750 28

The role of nitric oxide (NO) in the mediation of cerebrovascular CO2 responsiveness was studied in 10 distinct brain and spinal cord regions of the anesthetized, ventilated, temperature-controlled, normoxic cat. Regional CBF was measured with 15-micron radiolabeled microspheres in hypocapnic, normocapnic, and hypercapnic conditions. CO2 responsiveness of each region was determined from the equation of the best-fit regression lines to the obtained flow values. The effect of altered endothelial and/or neuronal NO synthesis on CO2 responsiveness was studied following either selective blockade of the NO synthase enzyme by N omega-nitro-L-arginine methyl ester (L-NAME; 3 or 30 mg/kg i.v.) or simultaneous administration of L-NAME (3 mg/kg i.v.) and a large dose of the NO precursor L-arginine (30 mg/kg i.v.). Blockade of NO synthesis by 30 mg/kg L-NAME resulted in a significant reduction of the steady-state regional blood flow values and in an almost complete abolition of the CO2 sensitivity in each region studied. Changes of the basal flow values as well as the reduction of the regional CO2 sensitivity were dose dependent. Hypothalamic, sensorimotor cortical, and cerebellar regions were the areas most sensitive to the NO blockade. Impaired CO2 responsiveness following NO synthase inhibition, however, was reversed in these regions by simultaneous administration of a large dose of intravenously injected L-arginine. These findings suggest a major role of nitric oxide in the mediation of regional cerebrovascular CO2 responsiveness in cats.
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PMID:Major role of nitric oxide in the mediation of regional CO2 responsiveness of the cerebral and spinal cord vessels of the cat. 750 82

We studied the effect of nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, on the increases in cerebral blood flow (CBF) elicited by stepwise elevations in arterial partial pressure of CO2 (PaCO2) from normocapnia up to 204 mmHg. Rats were anesthetized with halothane and ventilated. CBF was monitored over the parietal cortex using a laser-Doppler flowmeter. Increasing levels of hypercapnia elicited graded elevations in CBF that reached a plateau at PaCO2 = 82 +/- 1 mmHg (CBF +215 +/- 25%; n = 8; P < 0.05, analysis of variance). L-NAME (40 mg/kg i.v.; n = 8), but not nitro-D-arginine methyl ester (n = 8), reduced resting CBF (-42 +/- 4%) and attenuated the increase in CBF elicited by hypercapnia. The attenuation occurred only at PaCO2 40-80 mmHg and was maximal (-75 +/- 8%; P < 0.05) at 54 +/- 2 mmHg. At PaCO2 > or = 100 mmHg, L-NAME (40-80 mg/kg) did not attenuate the response (P > 0.05). Reduction of resting CBF (-50 +/- 4%; n = 6) by administration of chloralose (20-40 mg/kg i.v.) did not attenuate the CBF response to hypercapnia (P > 0.05). We also found that the attenuation by L-NAME of resting CBF (n = 5) and of the cerebrovasodilation elicited by hypercapnia (n = 6) has a relatively slow time course, the effects reaching a maximum 45-60 min after intravenous administration of the drug. We conclude that L-NAME does not attenuate the CBF response to CO2 uniformly at all levels of hypercapnia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nitric oxide-dependent and -independent components of cerebrovasodilation elicited by hypercapnia. 751 52

We sought to determine whether the attenuation of the hypercapnic cerebrovasodilation associated with inhibition of nitric oxide synthase (NOS) can be reversed by exogenous NO. Rats were anesthetized (halothane) and ventilated. Neocortical cerebral blood flow (CBF) was monitored by a laser-Doppler probe. The NOS inhibitor N omega-nitro-L-arginine methyl ester (L-NAME; 40 mg/kg iv) reduced resting CBF [-36 +/- 5% (SE); P < 0.01, analysis of variance] and attenuated the increase in CBF elicited by hypercapnia (partial pressure of CO2 = 50-60 mmHg) by 66% (P < 0.01). L-NAME reduced forebrain NOS catalytic activity by 64 +/- 3% (n = 10; P < 0.001). After L-NAME, intracarotid infusion of the NO donor 3-morpholinosydnonimine (SIN-1; n = 6) increased resting CBF and reestablished the CBF increase elicited by hypercapnia (P > 0.05 from before L-NAME). Similarly, infusion of the guanosine 3',5'-cyclic monophosphate (cGMP) analogue 8-bromo-cGMP (n = 6) reversed the L-NAME-induced attenuation of the hypercapnic cerebrovasodilation. The NO-independent vasodilator papaverine (n = 6) increased resting CBF but did not reverse the attenuation of the CO2 response. SIN-1 did not affect the attenuation of the CO2 response induced by indomethacin (n = 6). The observation that NO donors reverse the L-NAME-induced attenuation of the CO2 response suggests that a basal level of NO is required for the vasodilation to occur. The findings are consistent with the hypothesis that NO is not the final mediator of smooth muscle relaxation in hypercapnia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:SIN-1 reverses attenuation of hypercapnic cerebrovasodilation by nitric oxide synthase inhibitors. 751 10

Despite the increasing number of publications devoted to the cerebrovascular role of NO, its precise influence in awake animals is still poorly characterized. The effect of nitric oxide synthase (NOS) inhibition on the cerebrovascular CO2 reactivity was therefore studied in conscious rats. Regional CBF was measured using the [14C]iodoantipyrine technique and brain tissue sampling. The CO2 reactivity was determined 60 min after administration of 30 mg kg-1 N omega-nitro-L-arginine methyl ester (L-NAME). Blockade of NOS by L-NAME significantly decreased CBF in all 11 brain regions studied (-17 to -49%) and increased arterial pressure from 117 +/- 12 to 147 +/- 11 mn Hg. In control conditions, CO2 responsiveness ranged from 1.3 +/- 0.4 in the hypophysis to 6.4 +/- 0.6 ml 100 g-1 min-1 mm Hg-1 in the parietal cortex. Following L-NAME injection, the reactivity to hypercapnia was significantly attenuated in all structures, the magnitude of the reduction ranging from 57% in the medulla to 74% in the cerebellum. This result shows that NO is an important mediator of the hypercapnic vasodilation in the conscious rat.
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PMID:Widespread attenuation of the cerebrovascular reactivity to hypercapnia following inhibition of nitric oxide synthase in the conscious rat. 752 Apr 50

We investigated the effect of hypoxia on acetylcholine (ACh) stimulated, endothelium-derived relaxing factor/nitric oxide (EDRF/NO)-dependent relaxation, and on basal tension in rat aortic rings. ACh (10(-9)-10(-6) M)-mediated relaxation at high [95%, Emax -76.2 +/- 4.5% of phenylephrine (PE)-induced constriction] and normal (20%, Emax -81.2 +/- 3.6%) O2 levels was inhibited by hypoxia (5%, Emax -36.2 +/- 7.2%); residual hypoxic relaxation was blocked by the K+ channel antagonist glibenclamide. To address whether O2 influenced EDRF/NO and K+ channel contributions to basal tone, the effect of stepwise reduction of available O2 (95, 20, 5, and 0%) was studied in intact and endothelial cell (EC)-denuded rings. The effects in these rings were compared with results of the same progressive reduction in O2 in the presence of the NO-synthase inhibitor N omega-nitro-L-arginine methyl ester (L-NAME) (10(-4) M) or glibenclamide (10(-4) M). EC-intact and EC-denuded rings constricted to 0.80 +/- 0.10 and 1.41 +/- 0.15 g, respectively. Reducing O2 to 20% had no significant effect on vascular tension, but 5% caused constriction (p < 0.05) in EC-intact rings (0.90 +/- 0.15 g). This hypoxic vasoconstriction was blocked by L-NAME, but not by glibenclamide, suggesting that hypoxic vasoconstriction was mediated by withdrawal of EDRF/NO. In contrast, EC-denuded rings showed a significant relaxant response at 5% O2. When O2 was then reduced further (95% N2/5% CO2), both EC-intact and EC-denuded rings relaxed, and this relaxation reached baseline tension (0.10 +/- 0.1 g).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of oxygen on endothelium-derived relaxing factor/nitric oxide and K(+)-dependent regulation of vascular tone. 752 42

The present study was performed to evaluate the role of nitric oxide (NO) in coronary vasodilation during hypercapnic acidosis (HC). The left anterior descending coronary arteries of 17 anesthetized, open-chest dogs were perfused with normal arterial blood or with arterial blood equilibrated in an extracorporeal circuit with 90% O2-10% CO2 [arterial carbon dioxide tension (PaCO2) 72 +/- 3 mmHg, arterial pH 7.16 +/- 0.02]. Coronary perfusion pressure (CPP) was initially set at 100 mmHg. Coronary blood flow (CBF) was measured with a Doppler transducer. Studies were conducted under constant-pressure (variable CBF; n = 13) and constant-flow (variable CPP) conditions (n = 4). Steady-state changes in CBF (or CPP) during HC and during intracoronary infusions of acetylcholine (ACh, 20 micrograms/min), an endothelium-dependent vasodilator, and sodium nitroprusside (SNP, 80 micrograms/min), an endothelium-independent vasodilator, were compared before and after intracoronary infusion of a NO synthase inhibitor, either NG-nitro-L-arginine methyl ester (L-NAME, 4.5 mg) or NG-monomethyl-L-arginine (L-NMMA, 30 mg). Under constant pressure, L-NAME blunted increases in CBF by HC (274 +/- 32 vs. 113 +/- 24%) and ACh (400 +/- 43 vs. 68 +/- 17%), whereas increases in CBF by SNP were not significantly affected (207 +/- 34 vs. 186 +/- 18%). Results with L-NMMA were similar. Under constant flow, L-NAME attenuated decreases in CPP by HC and ACh, whereas it had no significant effect on decreases in CPP by SNP. In conclusion, HC elicits release of NO from coronary vascular endothelium via a direct effect rather than secondary to an increased flow rate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of nitric oxide to coronary vasodilation during hypercapnic acidosis. 753 Sep 20

We investigated whether nitric oxide (NO) played a role in the generation of cerebrocortical flow oscillations and their modification by hypocapnia, hypercapnia, and halothane administration. Parietal cortical laser-Doppler flow (LDF) was monitored transcranially in anesthetized (barbiturate + 0-1.0% halothane), artificially ventilated, adult male Sprague-Dawley rats. Thirty minutes after infusion of N omega-nitro-L-arginine methyl ester (L-NAME, 20 mg/kg i.v.) mean arterial pressure (MAP) increased from 105 +/- 10 to 132 +/- 15 mmHg (P < 0.02), while mean LDF decreased from 159 +/- 36 to 135 +/- 30 perfusion units (PU, P < 0.05). Oscillations in LDF at a frequency of 6.3-7.8 cycles/min and amplitude of 10% were induced or augmented by L-NAME but not by D-NAME or indomethacin (2 mg/kg i.p.). L-arginine (200 mg/kg) abolished the oscillations post-L-NAME at constant MAP. Sodium nitroprusside infusion (10(-5) M, 5-50 microliters/min) reversed the L-NAME-induced increase in MAP and decrease in mean LDF but did not attenuate the flow oscillations. Hypocapnia post-L-NAME decreased LDF to 110 +/- 20 PU (P < 0.001) and augmented the flow oscillations (amplitude: 11-31%). Hypercapnia (5% CO2) or halothane (0.4-1.0%) suspended the oscillations in the presence of L-NAME. The results suggest that NO synthase activity inhibits cerebrocortical flow oscillations, and NO is not an obligatory mediator of the effects of halothane, hypocapnia, and hypercapnia on oscillatory activity.
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PMID:Modification of cerebral laser-Doppler flow oscillations by halothane, PCO2, and nitric oxide synthase blockade. 754 53

Inhibition of nitric oxide synthase (NOS) by Nitro-L-arginine-methyl-ester (L-NAME 15 mg and 70 mg/kg i.v.) in 16 male Wistar rats anaesthetized with urethane, paralysed and artificially ventilated, increased significantly local peripheral vascular resistance in the parietal cortex (CVR) along with augmentation of the mean arterial blood pressure (MAP) and no change of the local cerebrocortical blood flow (CBF) recorded with a Laser-Doppler-Flowmeter. In 11 rats L-NAME reversed a pressor effect of brief hypercapnia induced by 10% CO2/air mixture (PaCO2 84.1 +/- 5 mm Hg) into a depressor response, reduced CBF response proportionally to the reduction of MAP and did not influence CVR response to CO2. In 5 rats L-NAME did not abolish the central pressor effect of a CO2-stimulus and significantly augmented CO2-induced vasodilatatory response in the cortex (43.4 +/- 24% before L-NAME and 137.8 +/- 38.8% after L-NAME) by a larger reduction of CVR (-11 +/- 8% before L-NAME and -47.1 +/- 7.6% after L-NAME). It is concluded that NO does not mediate the vasodilatatory effect of brief hypercapnia in the cortex. NO appears critical for the central pressor effect of CO2. In those rats in which the central pressor effect of a CO2-stimulus was not abolished by an NOS blocker, an increased CBF and augmented decrease in CVR was observed during brief hypercapnia. Possible mechanisms of this dual responsiveness of cortical blood flow and arterial blood pressure to CO2, induced by inhibition of NOS, are discussed.
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PMID:Dual response of cerebrocortical blood flow and arterial blood pressure to transient CO2 stimulus after inhibition of nitric oxide synthesis in rats. 754 47

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