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

Previous work has shown that a 25-30% citric acid solution was the most effective concentration with which to demineralize dentin. The purpose of this investigation was to study the topography, using a scanning electron microscope, of root surfaces treated with a 30% citric acid solution using various application pressures. 20 freshly extracted human teeth were collected and stored in physiologic saline at room temperature. 3 root specimens, approximately 3x5x5 mm in size, were prepared from the coronal periodontally healthy area of each tooth. 30 specimens were root planed to expose dentin (dentin group) while the remaining 30 specimens were lightly scaled to remove periodontal soft tissue (cementum group). A freshly made 30% citric acid (CA) solution, (pH = 1.60), was applied to each of the experimental areas. Cotton pellets soaked in the citric acid solution were either placed (CAP), lightly rubbed (CAR) or heavily burnished (CAB) on the prepared root surface for 3 min. Pellets were resoaked every 30 s. The root sections were rinsed, fixed in glutaraldehyde, dehydrated in graded ethanol, critically point dried in liquid CO2 and sputter coated in gold. The treated surfaces were assessed for fibril tufting using scanning electron microscopy. Assessment was made of: (i) the % of surface area tufted; (ii) tufting depth (0-3); (iii) tufting density (1-3). Results of the study showed significantly more tufted surface area and greater tufting depth on both dentin and cementum for CAR and CAB compared to CAP. CAP produced a flat/mat fibril surface with no evidence of tufting.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Citric acid demineralization of cementum and dentin: the effect of application pressure. 756 Feb 21

The effects of aging and hypertension on contraction were examined in rat mesenteric resistance arteries of 12- and 74-wk-old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). The vessels were suspended in myographs (37 degrees C, 95% O2-5% CO2) filled with modified Krebs-Ringer bicarbonate solution. Isometric tension was measured. Contractions to KCl (100 mM) were similar in adult WKY and SHR; they increased in senescent WKY (P < 0.05) but decreased in senescent SHR (P < 0.05). Responses to norepinephrine (% of KCl) were comparable in all four groups. However, blockade of nitric oxide (NO) production with NG-nitro-L-arginine methyl ester (L-NAME) enhanced the sensitivity to norepinephrine in senescent animals, particularly in SHR. Inhibition of cyclooxygenase with indomethacin prevented increased sensitivity to norepinephrine after NO blockade. Responses to angiotensin (ANG) II were not affected by aging and hypertension, but the thromboxane receptor antagonist SQ-30741 reduced ANG II-induced contractions only in SHR of both ages (P < 0.05). Aging increased responses to ANG I in SHR but decreased it in WKY (P < 0.05). In quiescent rings with endothelium, acetylcholine caused contractions in the presence of L-NAME in adult and senescent SHR but not in WKY (P < 0.05). SQ-30741 prevented these contractions (P < 0.05). Contractions to the thromboxane analogue U-46619 were reduced only in senescent SHR (P < 0.05). Thus aging increases and hypertension decreases contractility of smooth muscle in rat mesenteric resistance arteries.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of aging and hypertension on contractility of resistance arteries: modulation by endothelial factors. 757 25

The study was designed to check the role of endogenous NO in maintaining the vasodilatory tone and in mediation of local cerebral blood flow (CBF) responses to CO2 in rostral ventrolateral medulla (RVLM) in the rat. The ventral surface of the medulla was exposed and CBF in the RVLM continuously recorded with a laser-Doppler flowmeter. Local vascular resistance (CVR) was estimated as the ratio of mean arterial pressure (MAP) to CBF. During 1 min exposure to 10% CO2 in oxygen PaCO2 rose from 39.9 +/- 2 mm Hg to 89.7 +/- 4.6 mm Hg and pH fell from 7.4 +/- 0.04 to 7.1 +/- 0.03. After intravenous administration of 15 mg/kg L-NAME (Nitro-L-arginine-methyl ester) MAP increased by 43 +/- 2.9 mm Hg (p < 0.001), local CBF increased by 33 +/- 6% (p < 0.001) and CVR increased by 17 +/- 6% (p < 0.01). L-NAME significantly reduced CBF flow response to 60 s hypercapnia from 47 +/- 9% (p < 0.001) before administration of L-NAME to 14 +/- 5% (p < 0.001). This effect was due to reversal by L-NAME of a pressor response to hypercapnia to a depressor response. The attenuation of CVR response to CO2 by L-NAME was too small to account alone for the significant reduction of local CBF responsiveness to hypercapnia. We conclude that endogenous NO plays a role in maintaining a local vasodilatory tone in RVLM, but it is less significant than in the cortical microcirculation. NO is not a major mediator in the increase in local CBF in RVLM during brief hypercapnia. Endogenous NO is critical for the neurogenic pressor response to brief hypercapnia.
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PMID:Role of the endogenous nitric oxide in the vasodilatory tone and CO2 responsiveness of the rostral ventrolateral medulla microcirculation in the rat. 767 Jan 22

Hypercapnia induces initial constriction and prolonged relaxation of rat small mesenteric arteries. The mechanism of the relaxation is unknown, but has been attributed to lowering of pHi in the vascular smooth muscle. In this study we have investigated the response to raised PCO2 at constant pHo, in mesenteric small arteries precontracted with noradrenaline. 10% CO2 led to a fall in pHi associated with acute potentiation of tension, and subsequent relaxation. The relaxation did not occur in arteries in which the endothelium had been removed, nor in arteries pretreated with the nitric oxide synthase inhibitor, L-NAME (10(-4)M, NG-nitro-L-arginine methyl ester). The D-enantiomer, D-NAME, was without effect. We conclude that hypercapnic-induced vasodilatation in this circulation occurs via endothelium derived nitric oxide production.
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PMID:Carbon dioxide induced vasorelaxation in rat mesenteric small arteries precontracted with noradrenaline is endothelium dependent and mediated by nitric oxide. 768 47

The response of porcine pulmonary arteries to hypoxia depended on their location in the vasculature and the degree and duration of the hypoxic challenge. In rings of pulmonary artery suspended for isometric tension recording (37 degrees C, 16% O2 and 5% CO2), moderate hypoxia (10% and 4% O2) caused endothelium-dependent relaxation in distal arteries but transient endothelium-dependent contraction in proximal arteries. In both proximal and distal arteries, the initial response to anoxia (0% O2) was a transient endothelium-dependent contraction. This was followed by a slowly developing, sustained endothelium-dependent contraction in proximal arteries, or by an endothelium-independent relaxation in distal arteries. The endothelium-dependent relaxation to moderate hypoxia in distal arteries was inhibited only by combined inhibition of endothelium-derived relaxing factor (EDRF)-nitric oxide (NO) synthase [N omega-nitro-L-arginine methyl ester (L-NAME)] and cyclooxygenase (indomethacin), suggesting mediation by EDRF-NO and prostacyclin. Transient endothelium-dependent contractions to moderate hypoxia (proximal arteries) or anoxia (all arteries) were abolished by L-NAME, but the late endothelium-dependent anoxic contraction observed in proximal arteries was not reduced by L-NAME and/or indomethacin. Therefore, hypoxia/anoxia may initiate contraction of pulmonary arteries by decreasing the activity of EDRF-NO, but the contractions appear to be maintained by an increased activity of an endothelium-derived contracting factor.
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PMID:Endothelium-derived contracting and relaxing factors contribute to hypoxic responses of pulmonary arteries. 769 84

The effects of chronic therapy with the angiotensin-converting enzyme (ACE) inhibitor trandolapril and/or Ca2+ antagonist verapamil on endothelial and vascular smooth muscle (VSM) function were studied in spontaneously hypertensive, stroke-prone rats (SHRSP). Dosages decreasing systolic blood pressure (SBP) by 20% were administered orally (p.o.) by gavage as monotherapy or combination therapy for 8 weeks, beginning at age 6 weeks. Combination therapy dosages were the same as those used in monotherapy (trandolapril 0.7 mg/kg/day verapamil 20 mg/kg/day) in one group; the second group received only half the monotherapy dosage. The study was placebo-controlled and performed in parallel groups. Isometric tension was measured in aortic rings suspended in organ chambers (95% C2/5% CO2; 37 degrees C). SBP decreased in all groups, as compared with placebo [30-47 mm Hg, analysis of variance (ANOVA), p < 0.05], but decrease was more pronounced in rats receiving high-dose combination (76 mm Hg, ANOVA, p < 0.05). In norepinephrine (NE)-contracted rings, endothelium-dependent relaxation to acetylcholine (ACh) was augmented similarly with all forms of therapy (maximal relaxations 89-94%) as compared with placebo (64 +/- 6%, p < 0.05). In contrast, the response to sodium nitroprusside (SNP) was similar in all groups (NS). In quiescent rings, ACh elicited endothelium-dependent contractions (in the presence of N omega-monomethyl-L-arginine, L-NAME) that were not affected by therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Endothelial dysfunction in aorta of the spontaneously hypertensive, stroke-prone rat: effects of therapy with verapamil and trandolapril alone and in combination. 789 83

We studied the effect of endothelium on the flow-induced response of conductance arteries and the resistance arteriolar network in an in situ model of perfused mesenteric artery in normotensive Wistar-Kyoto and spontaneously hypertensive rats. The mesenteric network was perfused with a Tyrode's albumin solution. The diameter of a conductance mesenteric artery was measured using a video camera system, and mesenteric pressure was recorded in a collateral artery. The preparation was perfused at 0.2, 2, and 4 mL/min, and flow-diameter-pressure relations were established (1) under control conditions, (2) during local inhibition of nitric oxide synthesis by topical application of N omega-nitro-L-arginine methyl ester (L-NAME) (1 mmol/L), and (3) after endothelium removal (CO2 drying). In normotensive rats, L-NAME decreased conductance artery diameter by 12 +/- 2% (P < .01) at 0.2 mL/min and 3.3 +/- 1.9% (P < .05) at 2 mL/min. In hypertensive rats, L-NAME did not modify mesenteric diameter. Endothelium removal markedly increased arterial resistance in both strains and decreased conductance artery diameter in normotensive rats (10.3 +/- 3%, P < .05 at 0.2 mL/min and 4.2 +/- 2%, P < .05 at 2 mL/min) but not in hypertensive rats. The present study suggests that the endothelium plays a similar role in the control of mesenteric resistance in both strains and that there is a significant diameter-flow dependency affected by both endothelium removal and inhibition of nitric oxide synthesis in conductance mesenteric arteries from normotensive but not from hypertensive rats.
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PMID:Alterations in flow-dependent vasomotor tone in spontaneously hypertensive rats. 808 14

The role of nitric oxide in the cerebral circulation under basal conditions and when exposed to hypoxic, hypercapnic and hypotensive stimuli, was studied in mechanically ventilated rats using a venous outflow technique, by examining the effects of inhibition of nitric oxide synthase with N-nitro-L-arginine methyl ester (L-NAME). L-NAME (10 or 30 mg/kg injected intravenously) raised mean arterial blood pressure by 14% and 24%, and increased cerebrovascular resistance (CVR) by 20% and 24%, respectively. Cerebral blood flow (CBF) was unaltered, as were blood gases and pH. The increases in MABP and CVR were attenuated by L-arginine (300 mg/kg). Following the administration of L-NAME, the increases in CBF elicited by ventilation with 8% oxygen for 25 s were unaltered, in comparison to control responses. L-NAME attenuated the increases in CBF and reduced the time for recovery to basal flow rates evoked by ventilation with 10% carbon dioxide. These effects were reversed by L-, but not by D-, arginine. Autoregulation by CBF during hypotensive episodes, as measured by comparisons of CVR values, was unaffected by L-NAME. The results suggest that endogenous nitric oxide is involved in the responses of the cerebral vasculature to elevated levels of CO2 in the arterial blood. Nitric oxide does not appear to play a major role in autoregulation to increases or decreases in MABP, or in hypoxia-evoked vasodilation.
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PMID:The role of nitric oxide in the regulation of cerebral blood flow. 831 87

Experiments were designed to determine the role of the L-arginine pathway in endothelium-dependent relaxations to vasopressin. The effects of L-arginine analogues NG-nitro-L-arginine (L-NNA), NG-nitro-L-arginine methyl ester (L-NAME), and NG-monomethyl-L-arginine (L-NMMA) on basal and vasopressin-induced activity of nitric oxide synthase were studied in isolated canine basilar arteries. Rings with and without endothelium were suspended for isometric tension recording in Krebs-Ringer bicarbonate solution bubbled with 94% O2-6% CO2 (37 degrees C, pH 7.4). Radioimmunoassay was used to determine the level of guanosine 3',5'-cyclic monophosphate (cGMP). All experiments were performed in the presence of indomethacin, a cyclooxygenase inhibitor. L-NAME and L-NMMA caused endothelium-dependent contractions and inhibited basal production of cGMP. In contrast, L-NNA did not affect basal tone or basal production of cGMP. L-Arginine analogues inhibited relaxations to vasopressin but did not affect relaxations to a nitric oxide donor, molsidomine (SIN-1). The effects of L-NNA, L-NAME, and L-NMMA were reversed in the presence of L-arginine. The relaxations to vasopressin were associated with an increase of cGMP levels in the arterial wall. This effect of vasopressin was inhibited in the presence of L-NNA. These studies suggest that the relaxations to vasopressin are mediated by activation of the endothelial L-arginine pathway, leading to increased production of nitric oxide, with subsequent activation of guanylate cyclase in smooth muscle cells. In canine basilar artery, L-NAME and L-NMMA are nonselective inhibitors of both basal and stimulated production of nitric oxide, whereas L-NNA selectively inhibits vasopressin-induced activation of the L-arginine pathway.
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PMID:Endothelial L-arginine pathway and relaxations to vasopressin in canine basilar artery. 838 55

The vascular effects of endothelin-1 (ET-1; ETA/ETB agonist), sarafotoxin 6b (S6b; ETA agonist), and IRL 1620 (ETB agonist) were investigated in the isolated canine liver arterial circuit before and after infusions of indomethacin (cyclo-oxygenase inhibitor) and N omega L-nitro arginine methyl ester (L-NAME; nitric oxide synthesis inhibitor). Norepinephrine (NE) was used as vasconstrictor control agent. The portal vein, hepatic artery, and vena cava were cannulated in vitro and the liver was perfused via the hepatic artery and portal vein with oxygenated (95%) O2/5% CO2) Krebs solution at 37 degrees C. Intra-arterial bolus injections of either ET-1 (0.4-400 pmol) or S6b (0.4-400 pmol) induced dose-dependent and long-lasting vasoconstriction accompanied by significant prostacyclin release. The vasoconstrictor responses to these peptides were slightly increased during infusion of indomethacin. Subsequent infusion of L-NAME potentiated both ET-1- and S6b-induced vasoconstriction (p < 0.05). IRL 1620 (up to 1.2 nmol) had no effect on the hepatic arterial vascular resistance even during indomethacin and L-NAME infusions. Infusion of the ETA receptor antagonist FR-139317 (0.3 microM) markedly reduced both ET-1- and S6b-induced vasoconstriction without affecting that evoked by NE. Our results indicate that pressor responses to ET-1 and S6b in the isolated canine liver are modulated by concomitant release of vasodilator mediators, including prostacyclin and nitric oxide. These effects appear to depend primarily on the activation of ETA receptor subtypes. IRL 1620 (but not ET-1) induced a significant release of hemoglobin into the venous effluent, suggesting that ETB receptors are located in the venous side of the intrahepatic circulation.
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PMID:Role of endothelin ETA and ETB receptors in the arterial vasculature of the isolated canine liver. 858 63


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