Constriction of Resistance Arteries Determines l-NAME-Induced Hypertension in a Conscious Hamster Model

Sakai, Hiromi; Hara, Hiroyuki; Tsai, Amy G.; Tsuchida, Eishun; Intaglietta, Marcos

doi:10.1006/mvre.2000.2240

Cited by 21 publications

(19 citation statements)

References 32 publications

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“…4). This result parallels previous observations by Sakai et al (31), who also found significant A1 arteriolar constriction after the administration of L-NAME. Nitrate/nitrite concentrations in the plasma were significantly lower compared with Hct augmented hamsters (4.88 Ϯ 1.64 mol vs. 7.54 Ϯ 2.76 mol; P Ͻ 0.05).…”

Section: Resultssupporting

confidence: 92%

“…Exchange transfusion with packed RBCs, increasing Hct between 8% and 19% (43 Ϯ 3% at baseline vs. 49 Ϯ 2% after exchange transfusion), did not produce the reduction in blood pressure found in the group with no L-NAME pretreatment. After 1 h, blood pressure tended to decrease according to the degradation of L-NAME (31). Blood pressure remained elevated from baseline (120 Ϯ 5 mmHg vs. 95 Ϯ 7 mmHg) 120 min after exchange transfusion and was significantly elevated compared with blood pressure levels of the hamster control group at 30, 60, 90, and 120 min after the exchange transfusion with packed RBCs (P Ͻ 0.05) (Fig.…”

Section: Resultsmentioning

confidence: 87%

“…Animals were suitable for the experiments if systemic parameters were within normal limits, namely, heart rate (HR) Ͼ340 beats/min, mean arterial blood pressure (MAP) Ͼ80 mmHg and Ͻ125 mmHg. The latter criterion did not apply for eNOS knockout mice, which are spontaneously hypertensive (31).…”

Section: Methodsmentioning

confidence: 99%

“…RBCs velocities in A1 arterioles were measured online by using the photodiode/cross-correlator system (16) Isovolemic exchange transfusion and pretreatment with L-NAME. L-NAME (Sigma) was dissolved in saline and infused through the jugular venous catheter within 1 min at a dosage of 30 mg/kg at a concentration of 20 mg/ml, previously shown to induce immediate hypertension after infusion (31). The volume of infusion was Ͻ5% of systemic blood volume.…”

Section: Methodsmentioning

confidence: 99%

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Paradoxical hypotension following increased hematocrit and blood viscosity

Martini¹,

Carpentier²,

Negrete³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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106

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-Hematocrit (Hct) of awake hamsters and CD-1 mice was acutely increased by isovolemic exchange transfusion of packed red blood cells (RBCs) to assess the relation between Hct and blood pressure. Increasing Hct 7-13% of baseline decreased mean arterial blood pressure (MAP) by 13 mmHg. Increasing Hct above 19% reversed this trend and caused MAP to rise above baseline. This relationship is described by a parabolic function (R 2 ϭ 0.57 and P Ͻ 0.05). Hamsters pretreated with the nitric oxide (NO) synthase (NOS) inhibitor N -nitro-L-arginine methyl ester (L-NAME) and endothelial NOS-deficient mice showed no change in MAP when Hct was increased by Ͻ19%. Nitrate/nitrite plasma levels of Hct-augmented hamsters increased relative to control and L-NAME treated animals. The blood pressure effect was stable 2 h after exchange transfusion. These findings suggest that increasing Hct increases blood viscosity, shear stress, and NO production, leading to vasodilation and mild hypotension. This was corroborated by measuring A1 arteriolar diameters (55.0 Ϯ 21.5 m) and blood flow in the hamster window chamber preparation, which showed statistically significant increased vessel diameter (1.04 Ϯ 0.1 relative to baseline) and microcirculatory blood flow (1.39 Ϯ 0.68 relative to baseline) after exchange transfusion with packed RBCs. Larger increases of Hct (Ͼ19% of baseline) led blood viscosity to increase Ͼ50%, overwhelming the NO effect through a significant viscosity-dependent increase in vascular resistance, causing MAP to rise above baseline values. nitric oxide; shear stress; vascular resistance; hypertension IT IS A GENERAL MEDICAL and clinical perception that an increase in blood viscosity may lead to short-and long-term negative physiological conditions, and there appears to be universal agreement that increased blood viscosity is a factor in hypertension. Lowering blood viscosity, however, is not advocated as a means for controlling hypertension with the exception of erythrocytosis, substantial Hct increases consequent to adaptation to high altitudes, and cardiovascular impairment in premature infants. These conditions represent extremes of an increase in blood viscosity and clearly must be corrected by lowering Hct, because the extreme excess of red blood cells (RBCs) is superfluous in providing adequate oxygen-carrying capacity and is in fact a hindrance to blood flow and therefore oxygen delivery.Clinical studies (14, 37) report a significant relationship between hypertension and high Hct levels. Hypertensive patients have higher Hct values than normotensive control individuals (23). Patients suffering from polycythemia vera or other erythrocytoses present with pathologically high Hcts leading to hypertension, thromboembolism, and other severe clinical complications (2, 15). There is evidence, however, that individuals, such as Peruvian miners, survive with Hct levels of 75-91% (18), suggesting the existence of an adaptive mechanism.Endothelial cells play a key role in the regulation of blood pressure and blood flow beca...

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Section: Resultssupporting

confidence: 92%

Section: Resultsmentioning

confidence: 87%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 2 more Smart Citations

Paradoxical hypotension following increased hematocrit and blood viscosity

Martini¹,

Carpentier²,

Negrete³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

Self Cite

106

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show abstract

“…The dorsal skinfold chamber is a widely used and well-accepted model in microcirculatory research in hamsters and mice. [12][13][14][15][16][17][18] Scaffold manufacturing and characteristics A block-copolymer polymer composed of alternating soft blocks of polyethylene glycol terephthalate (PEGT) and hard blocks of polybutylene terephthalate (PBT) was used. Polymer composition can be modified by varying the weight percentages of PEGT and PBT or by changing the molecular weight (MW) of the PEG.…”

Section: Surgical Proceduresmentioning

confidence: 99%

Neovascularization of poly(ether ester) block‐copolymer scaffolds in vivo: Long‐term investigations using intravital fluorescent microscopy

Druecke

Langer

Lamme³

et al. 2003

J Biomedical Materials Res

167

138

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Poly(ether ester) block-copolymer scaffolds of different pore size were implanted into the dorsal skinfold chamber of balb/c mice. Using intravital fluorescent microscopy, the temporal course of neovascularization into these scaffolds was quantitatively analyzed. Three scaffold groups (diameter, 5 mm; 220 -260 thickness, m; n ϭ 30) were implanted. Different pore sizes were evaluated: small (20 -75 m), medium (75-212 m) and large pores (250 -300 m). Measurements were performed on days 8, 12, 16, and 20 in the surrounding normal tissue, in the border zone, and in the center of the scaffold. Standard microcirculatory parameters were assessed (plasma leakage, vessel diameter, red blood cell velocity, and functional vessel density). The largepored scaffolds showed significantly higher functional vessel density in the border zone and in the center (days 8 and 12) compared with the scaffold with the small and mediumsized pores. These data correlated with a larger vessel diameter and a higher red blood cell velocity in the largepored scaffold group. Interestingly, during the evaluation period the microcirculatory parameters on the edge of the scaffolds returned to values similar to those found in the surrounding tissue. In the center of the scaffold, however, neovascularization was still active 20 days after implantation. Plasma leakage and vessel diameter were higher in the center of the scaffold. Red blood cell velocity and functional vessel density were 50% lower than in the surrounding tissue. In conclusion, the dorsal skinfold chamber model in mice allows long-term study of blood vessel growth and remodeling in porous biomedical materials. The rate of vessel ingrowth into poly(ether ester) block-copolymer scaffolds is influenced by pore size and was highest in the scaffold with the largest pores. The data generated with this model contribute to knowledge about the development of functional vessels and tissue ingrowth into biomaterials.

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Introduction

Johnson

2008

Comprehensive Physiology

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Constriction of Resistance Arteries Determines l-NAME-Induced Hypertension in a Conscious Hamster Model

Cited by 21 publications

References 32 publications

Paradoxical hypotension following increased hematocrit and blood viscosity

Paradoxical hypotension following increased hematocrit and blood viscosity

Neovascularization of poly(ether ester) block‐copolymer scaffolds in vivo: Long‐term investigations using intravital fluorescent microscopy

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