Quantitation of rhythmic diameter changes in arterial microcirculation

Colantuoni, Antonio; Bertuglia, Silvia; Intaglietta, Marcos

doi:10.1152/ajpheart.1984.246.4.h508

Cited by 175 publications

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“…The study was approved by the local Animal Subjects Committee of the University of California, San Diego. The window chamber model is widely used for microvascular studies in the unanesthetized state, and the complete surgical technique is described in detail elsewhere (3,10). This model was used to maintain the catheters in place in the awake animals and to prevent them from chewing or pulling them.…”

Section: Methodsmentioning

confidence: 99%

Paradoxical hypotension following increased hematocrit and blood viscosity

Martini¹,

Carpentier²,

Negrete³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

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: Methodsmentioning

confidence: 99%

Paradoxical hypotension following increased hematocrit and blood viscosity

Martini¹,

Carpentier²,

Negrete³

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

106

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“…Spontaneous rhythmic oscillations in vessel diameter are known as vasomotion and occur primarily in small arteries and arterioles (Bertuglia et al, 1996;Colantuoni et al, 1984Colantuoni et al, , 1990Jackson et al, 1991;Meyer et al, 1988;Meyer & Intaglietta, 1987;Schmidt et al, 1993;Slaaf et al, 1987;Wiedeman, 1955). Generally, the frequencies of the oscillations are in the range 3-30 min −1 and the peak-peak amplitudes are large, 50-100% or more of the mean diameter (Tuma et al, 2008).…”

Section: The Phenomenon Of Vasomotionmentioning

confidence: 99%

“…The oscillations varied in frequency and duration and appeared independent of other vessels. Colantuoni et al (1984) studied vasomotion in several different vessel types in a hamster skin fold window preparation. They showed that the oscillations were independent of the nervous system and that the fundamental c The Author 2011.…”

Section: The Phenomenon Of Vasomotionmentioning

confidence: 99%

Spontaneous oscillations in a model for active control of microvessel diameters

Arciero

Secomb²

2011

Mathematical Medicine and Biology

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A new theory is presented for the origin of spontaneous oscillations in blood vessel diameters that are observed experimentally in the microcirculation. These oscillations, known as vasomotion, involve timevarying contractions of the vascular smooth muscle in the walls of arterioles. It is shown that such oscillations can arise as a result of interactions between the mechanics of the vessel wall and the dynamics of the active contraction of smooth muscle cells in response to circumferential tension in the wall. A theoretical model is developed in which the diameter and the degree of activation in a vessel are dynamic variables. The model includes effects of wall shear stress and oxygen-dependent metabolic signals on smooth muscle activation and is applied to a single vessel and to simplified network structures. The model equations predict limit cycle oscillations for certain ranges of parameters such as wall shear stress, arterial pressure and oxygen consumption rate. Predicted characteristics of the oscillations, including their sensitivity to arterial pressure, are consistent with experimental observations.

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“…The hamster window chamber model is widely used for microvascular studies in the unanesthetized state, and the complete surgical technique is described in detail elsewhere. 15,16 Catheters were tunneled under the skin, exteriorized at the dorsal side of the neck, and securely attached to the window frame.…”

Section: Animal Preparationmentioning

confidence: 99%

Increased plasma viscosity prolongs microhemodynamic conditions during small volume resuscitation from hemorrhagic shock

2008

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Systemic and microvascular hemodynamic responses to hemorrhagic shock resuscitation with hypertonic saline (HTS, 7.5% NaCl) followed with a small volume of plasma expander were studied in the hamster window chamber model to determine the role of plasma expander viscosity in the acute resuscitation outcome. Moderate hemorrhagic shock was induced by arterial controlled bleeding of 50% of blood volume (BV) and the hypovolemic state was maintained for one hour. Volume restitution was performed by infusion of HTS, 3.5% of BV followed by 10% of BV plasma expanders. Resuscitation was followed for 90 min. The experimental groups were named based on the plasma expanders infused after the HTS, namely: [Hextend], Hextend® (6% Hetastarch 670 kDa in lactated electrolyte solution, 4 cp), [Hextend+V], Hextend® with viscosity enhanced by the addition of 0.4% alginate, 8 cp, and [NVR] no volume resuscitation as control group. Measurement of systemic parameters, microvascular hemodynamics and capillary perfusion were performed during hemorrhage, shock and resuscitation. Restitution with Hextend yielded the higher mean arterial pressure (MAP), followed by Hextend+V and NVR. Increasing plasma viscosity did not increase peripheral vascular resistance. Functional capillary density (FCD) was higher for Hextend+V than Hextend and NVR. The level of restoration of acid-base balance correlated with microvascular perfusion and was significantly improved with Hextend+V when compared to Hextend and NVR. These results suggest the importance of restoration of blood rheological properties through enhancing plasma viscosity, influencing the re-establishment of microvascular perfusion during small volume resuscitation from hemorrhagic shock.

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Quantitation of rhythmic diameter changes in arterial microcirculation

Cited by 175 publications

References 0 publications

Paradoxical hypotension following increased hematocrit and blood viscosity

Paradoxical hypotension following increased hematocrit and blood viscosity

Spontaneous oscillations in a model for active control of microvessel diameters

Increased plasma viscosity prolongs microhemodynamic conditions during small volume resuscitation from hemorrhagic shock

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