Blood Flow Control Mechanisms Research Articles

ATP-induced cochlear blood flow changes involve the nitric oxide pathway

Although control mechanisms of cochlear blood flow (CBF) have been intensively studied since laser Doppler flowmetry was introduced for CBF measurement in animals and humans, the role of adenosine 5′-trophosphate (ATP) in CBF regulation is not known. Since ATP is a potent vasoactive agent in other organs, the aim of this study is to examine ATP-induced changes in CBF and to test whether the nitric oxide pathway is involved in ATP-induced CBF changes. The anterior inferior cerebellar artery (RICA) of anesthetized pigmented guinea pigs was exposed, and ATP was perfused into the AICA. For CBF measurement, the bulla was opened and the 0.7 mm laser probe of a Perimed PF2B flowmeter was positioned on the basal turn of the cochlea. AICA perfusion of an ATP solution caused dose-dependent transient CBF increases. The maximum CBF increase induced was 220% of the baseline. In some animals, CBF showed a dual effect; a transient decrease followed by a longer-lasting increase. The perfusions of sodium nitroprusside (SNP) also resulted in dose-dependent CBF changes. The intravenous application of N ω-nitro- l-arginine methyl ester (L-NAME) significantly attenuated ATP-induced CBF increases, and enhanced ATP-induced decreases, but did not affect SNP-induced CBF changes. The ATP-induced CBF responses indicate that ATP plays a role in CBF regulation. The biphasic characteristic of the ATP-induced CBF change suggests the involvement of both P 2x- and P 2y-subtype purinoceptors. That L-NAME caused attenuation of the ATP-induced CBF increase implies that the ATP-induced CBF increase is mediated by the release of endothelium-derived relaxing factor, nitric oxide, following activation of endothelial P 2y-purinoceptors in the cochlear vascular bed and/or cochlear supplying vessels.

THE MESENTERIC CIRCULATION: Anatomy and Physiology

The purpose of this article is to review the angiographic appearance of the major visceral arteries, the more common variants, their embryologic origins, and some of the most common sources of collateral flow. A brief review of the physiology of the mesenteric circulation is also provided, including a discussion of the intrinsic and extrinsic mechanisms of splanchnic blood flow control.

Intraretinal oxygen distribution in rats as a function of systemic blood pressure

Differential responses to induced changes in systemic blood pressure (BP) at different layers of both the retinal and choroidal vasculature were observed, by monitoring localized PO2 as a function of depth, in the retina and choroid of the rat eye using oxygen-sensitive recessed microelectrodes. Visual and electrophysiological localization of the microelectrode tip allowed the oxygen distribution to be related to the positions of the vascular beds of the retina and choroid. Highly reproducible intraretinal PO2 profiles were achieved. The relationship between PO2 and systemic BP was linear in the deep capillary layer of the retina (PO2 = 0.17 x BP - 2.63) and in the choriocapillaris (PO2 = 0.21 x BP + 2.95), whereas it was nonlinear in the superficial retinal capillary layer [PO2 = 40.01/[1 + (BP/66.22)-1.22]] and deep choroid [PO2 = 83.82/[1 + (BP/124.61)-0.87]]. The minimum PO2 occurred between the two retinal capillary beds, and a PO2 gradient was evident in the choroid. The contrasting responses of different layers of the two circulations reflect different blood flow control mechanisms not evident when studying the circulations as a whole.

Adrenergic control mechanisms of blood flow in a vascularized canine tibial allograft

A vascularized canine tibial allograft was used to study the alpha-adrenoreceptor subtypes of the microcirculation of bone. Bone transplantation was performed on six dogs, and the bone blood flow was estimated with the use of serial injections of radiolabeled 15 microns microspheres. After microvascular anastomosis, the mean cortical blood flow in the allografted tibia was 3.6 +/- 2.1 ml/100 g/min. Alpha 1-adrenoreceptor blockade, with prazosin, caused an increase in normalized blood flow in five allografts and a slight decrease in one allograft. The mean increase was 32 +/- 48%, but this was not statistically significant (p < 0.2). The addition of an alpha 2-adrenoreceptor blockade, with rauwolszin, resulted in a significant increase (132 +/- 88%) in normalized blood flow in all allografts (p < 0.02). This ex vivo experiment confirms that both alpha 1 and alpha 2 adrenergic mechanisms play a role in controlling bone blood flow in centrally denervated allografts.

Abnormal renal function and autoregulation in essential hypertension.

The goal of this presentation has been to emphasize two fundamental mechanisms in the development of essential hypertension. These are: 1) The basic cause of essential hypertension is the inability of the kidneys to excrete an adequate volume of urine at normal arterial pressure. Therefore, fluid accumulates in the body until the pressure rises high enough to balance fluid output with fluid intake. This fluid balancing act is an infinite gain feedback system for controlling arterial pressure to a very precise level determined by the kidneys. Furthermore, this infinite gain allows the kidney mechanism to dominate the other pressure control mechanisms for long-term pressure control. Because of this domination, as long as a person has normal intake of water and electrolytes, essential hypertension cannot develop without an elevated pressure setting of the kidneys. 2) An increase in total peripheral resistance will not cause hypertension as long as the kidneys can still excrete normal amounts of water and electrolytes at normal arterial pressure, because loss of excess fluid volume at high pressures will simply reduce the cardiac output until the pressure falls back to normal. Therefore, what is the cause of the very high total peripheral resistance found in almost all patients with essential hypertension? The answer is likely the long-term blood flow autoregulation mechanism that occurs in virtually all tissues of the body. That is, when the pressure rises too high for whatever reason, this in turn forces too much blood flow through the tissues. In response, the local blood flow control mechanisms all over the body increase the vascular resistances until the flows return to normal.(ABSTRACT TRUNCATED AT 250 WORDS)

Heart rate and blood pressure changes during sleep-waking cycles and cataplexy in narcoleptic dogs.

Cataplexy is the abrupt loss of muscle tone experienced by narcoleptics. It is usually precipitated by strong emotions or athletic activity. It has been hypothesized that cardiovascular variables have a role in the triggering of cataplexy. In the present study, we have utilized the narcoleptic canine model to directly investigate changes in heart rate and blood pressure in relation to cataplectic episodes. We found that heart rate increased 18% on average in the 20 s preceding cataplexy onset and then fell during cataplexy. Thus, from a cardiovascular standpoint, cataplexy can be subdivided into two very different periods, the cataplexy onset period with very high and declining heart rate, and the period greater than or equal to 10 s after onset, with greatly reduced heart rate. Heart rate at cataplexy onset was significantly higher than heart rate in rapid-eye-movement (REM) sleep, non-REM sleep, and quiet waking. Blood pressure did not markedly change before the onset of spontaneous cataplexies but decreased significantly during cataplexy. Although blood pressure increases did not precede spontaneous cataplexies, sudden increases in blood pressure, induced pharmacologically or by obstruction of the descending aorta, triggered cataplexy in the most severely affected subjects. A hypothesized role for cataplexy as a homeostatic reflex, triggered by interactions between blood flow, central chemoreceptors, and atonia control mechanisms in the medial medulla, is discussed.

Recent Advances in Cochlear Blood Flow Measurements

Changes in blood flow to the inner ear have been thought to influence or underlie a number of cochlear diseases, including some forms of noise-induced hearing loss, sudden hearing loss, and Meniere's disease. Recently, important advances have been made in two technologies for the study of cochlear blood flow. The first is in the area of vital microscopic studies of cochlear microcirculation, and the second is based on the introduction of laser technology in the form of laser Doppler flowmetry. In this report, measurements are given of changes in cochlear circulation caused by carbon dioxide breathing, intravenous phenylephrine injection, systemic hemodilution, positive end expiratory pressure, and direct electrical stimulation of the cochlea. From these changes, we observe that cochlear blood circulation responds to systemic blood pressure alterations and is subject to local flow control mechanisms. Linearity and speed of response of the laser Doppler instrumentation also are shown. These advances show promise for contributing to our knowledge of control mechanisms of inner ear blood flow and for revealing the influence of various pharmacologic agents of potential clinical value.

Hemodynamic Interactions between Intrinsic Blood Flow Control Mechanisms in the Rat Kidney

In order to reconcile the controversial concepts of myogenically and tubuloglomerular-feedback (TGF)-mediated control of renal vascular resistance, a hypothesis is advanced according to which both mechanisms interact hemodynamically because of their serial arrangement. Whereas the myogenic mechanism is suggested to be localized in the more upstream segments of the preglomerular resistance vessels, the TGF mechanism is assumed to control the pre- and/or postglomerular vascular segment(s), close to the glomerular vascular pole. The efferent vascular resistance, however, is assumed to function generally akin to a 'passive' flow resistor. These assumptions together with elementary hemodynamic considerations, allow formulation of a simple renal hemodynamic model whose quantitative predications regarding the characteristics of RBF, GFR and TGF control are remarkably consistent with the literature: (1) the magnitude of TGF response is mainly dependent upon the myogenic cooperative amplification and (2) although the TGF mechanism is not involved in the autoregulative control of RBF and GFR, changes of the TGF function may shift the autoregulation curve to higher or lower RBF and blood pressure levels.

Muscle Blood Flow During Locomotory Exercise

Mammalian skeletal muscles are composed of three primary muscle fiber types, FOG, FG, and SO. These fiber types are distributed within and among muscles in predictable patterns. Current data indicate that blood flows to inactive muscles composed of the various fiber types are approximately equal. Total muscle blood flow increases when the animal stands up. When maintaining posture (standing), the muscular force is provided by the SO fibers. These fibers receive the highest blood flows under these conditions. When the animal walks the SO fibers remain active and the additional muscular force is provided by FOG fibers. The increased muscle blood flow during exercise is primarily directed to the active FOG fibers. At fast running speeds, FG fibers are additionally recruited and blood flow increases in muscle areas composed of FG fibers. However, the FG blood flows per gram of tissue are much less than in the oxidative muscles. Thus, muscle blood flow is primarily directed to the active high oxidative muscle fibers within and among the muscles during normal activities. Much is known about factors believed to link blood flow to metabolism in skeletal muscle and about the reflex control of skeletal muscle vascular beds. However, the mechanisms responsible for blood flow control during locomotory exercise are yet to be established. It appears that the different muscle fiber types may have qualitatively similar blood flow control mechanisms with quantitative differences in relation to each fiber type. The capacity for blood flow in skeletal muscle is related to the oxidative potential of the muscles. Blood flows in high-oxidative muscles may reach 400-600 ml/min/100 g, which is considerably higher than the commonly accepted values for maximal muscle blood flow. Also, muscle blood flows are higher during locomotory exercise in conscious animals than in in situ electrical stimulation experiments. Chronic exercise training does not appear to change total muscle blood flow during locomotory exercise. However, the distribution of blood flow within and among muscles changes so that the deep red muscle fibers have higher flows during exercise. While data exist suggesting that blood flow capacity is increased with exercise training, this remains controversial.

4. Regulation of pulpal blood flow

It can be concluded that the sympathetic vasoconstrictor regulation is dominant among the remote control mechanisms of pulpal blood flow. The local systems, neurogenic and humoral, probably act by modulating t h e sympathetic vasoconstrictor tone. The basal vascular tone, of fundamental importance in other vascular beds, has not been analyzed in the dental pulp. It can be concluded that the sympathetic vasoconstrictor regulation is dominant among the remote control mechanisms of pulpal blood flow. The local systems, neurogenic and humoral, probably act by modulating t h e sympathetic vasoconstrictor tone. The basal vascular tone, of fundamental importance in other vascular beds, has not been analyzed in the dental pulp.