• Title/Summary/Keyword: autoregulation

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Myogenic Autoregulation of Coronary Vessels and Heterometric Autoregulation of the Myocardium

  • Doring, H.J.;Schlicht, I.;Hiller, V.;Jiang, X.R.
    • The Korean Journal of Physiology
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    • v.23 no.2
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    • pp.225-236
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    • 1989
  • 1) At the isolated perfused guinea-pig and rat heart heterometric autoregulation of the myocardium and myogenic autoregulation of the coronary vessels were induced by means of stepwise increases of perfusion pressure. 2) According to this loading test Frank-Starling function curves of the left ventricle and pressure-flow curves of the coronary vessels can be drawn. This graphic evaluation gives more information about the condition of the heart and the coronary vessels than simple evaluation under hemodynamic equilibrium. 3) There are significant differences in both curves between animal species and between different perfusate Mg concentration. 4) Myogenic autoregulation is not affected by the cyclooxygenase inhibitors indometacin and me- clofenamate. Thus it appears unlikely that prostanoides are involved in myogenic autoregulation. 5) Ca antagonists (Gallopamil, prenylamine) depress myogenic autoregulation dose-dependently. Enhanced myogenic autoregulation, induced by low extracellular magnesium, can be reduced effectively by Gallopamil. 6) Ginsenosides from Panax ginseng as well as the ginsenoside 'Rg' are effective inhibitors of myogenic autoregulation without major negative inotropic effects.

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Prostaglandin in Regulations of Renal Blood Flow during Partial Ureteral Obstruction in Dogs

  • Song, Hoo-Bin;Yang, Hun-Mo;Min, Young-Gi
    • The Korean Journal of Physiology and Pharmacology
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    • v.2 no.1
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    • pp.77-84
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    • 1998
  • Ureteral obstruction causes increase in renal blood flow (RBF) and partial impairment of the autoregulation of RBF. Although increased renal prostaglandin production is responsible for the former, it is not clear whether or not it is also responsible for the latter. Therefore, we investigated the role which prostaglandins play in the autoregulation of RBF during an ureteral pressure elevation (40 $cmH_2O$). Since the major mechanism of RBF autoregulation is the tubuloglomerular feedback, studying the interaction between ureteral pressure and RBF autoregulation may reveal the role of prostaglandin in tubuloglomerular feedback. To pursue the purpose, six anesthetized dogs were prepared for the measurements of RBF, mean sytemic and renal arterial pressure (RAP) and the manipulation of ureteral pressure. The autoregulation curves were determined during both control and elevation of the ureteral pressure, before and after the pretreatment with indomethacin, a cyclooxygenase inhibitor. The desired ureteral pressure was achieved by vertically elevating the water-filled reservoir connected to the ureteral catheter to 40 cm above the kidney level. In response to the elevation of the ureteral pressure, RBF increased from $170{\pm}8 ml{\cdot}min^{-1}\;to\;189{\pm}8$, and the systemic arterial pressure didn't change significantly. During spontaneous urine flow, RBF autoregulation was abolished when RAP was reduced to $59{\pm}3$ mmHg. On the other hand, during the ureteral pressure elevation, the autoregulation curves shifted upward and rightward from control, and the pressure when RBF autoregulation was abolished was $74{\pm}3$ mmHg. The pretreatment of the dogs with indomethacin failed to affect the lower limit of RBF autoregulaion during both control ($63{\pm}5$ mmHg) and the elevated ureteral pressure ($77{\pm}5$ mmHg). Since RBF failed to increase in response to the elevated ureteral pressure, RBF autoregulation curves obtained during the elevated ureteral pressure shifted only rightward from indomethacin control. The results indicate that the increased intrarenal level of prostaglandin or prostaglandin-induced vasodilation does not appear to bear any relation to the reduction in the autoregulatory capacity during partial ureteral obstruction. It seems that the partial impairment of the autoregulation during acute ureteral obstruction is due to the consumption of tubuloglomerular feedback mechanism at spontaneous RAP and that prostaglandin is neither mediator nor effector of tubuloglomerular feedback mechanism.

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Cerebral Hemodynamics in Premature Infants

  • Rhee, Christopher J.;Rios, Danielle R.;Kaiser, Jeffrey R.;Brady, Ken
    • Neonatal Medicine
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    • v.25 no.1
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    • pp.1-6
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    • 2018
  • Extremely low birth weight infants remain at increased risk of intraventricular hemorrhage from the fragile vascular bed of the germinal matrix; the roles of hypotension (ischemia) and reperfusion (hyperemia) in the development of intraventricular hemorrhage are still debated. Cerebrovascular pressure autoregulation protects the brain by maintaining constant cerebral blood flow despite changes in blood pressure. The ontogeny of cerebrovascular pressure autoregulation has not been well established and uncertainty remains about the optimal arterial blood pressure required to support brain perfusion. Another important aspect of premature cerebral hemodynamics is the critical closing pressure--the arterial blood pressure at which cerebral blood flow ceases. Interestingly, in premature infants, the critical closing pressure approximates the mean arterial blood pressure. Often in this unique population, cerebral blood flow occurs only during systole when the diastolic arterial blood pressure is equal to the critical closing pressure. Moreover, the diastolic closing margin, a metric of cerebral perfusion that normalizes diastolic arterial blood pressure to the critical closing pressure, may be a better measure than arterial blood pressure for defining cerebral perfusion in premature infants. Elevated diastolic closing margin has been associated with intraventricular hemorrhage. This review summarizes the current state of understanding of cerebral hemodynamics in premature infants.

Long-Distance Control of Nodulation: Molecules and Models

  • Magori, Shimpei;Kawaguchi, Masayoshi
    • Molecules and Cells
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    • v.27 no.2
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    • pp.129-134
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    • 2009
  • Legume plants develop root nodules to recruit nitrogen-fixing bacteria called rhizobia. This symbiotic relationship allows the host plants to grow even under nitrogen limiting environment. Since nodule development is an energetically expensive process, the number of nodules should be tightly controlled by the host plants. For this purpose, legume plants utilize a long-distance signaling known as autoregulation of nodulation (AON). AON signaling in legumes has been extensively studied over decades but the underlying molecular mechanism had been largely unclear until recently. With the advent of the model legumes, L. japonicus and M. truncatula, we have been seeing a great progress including isolation of the AON-associated receptor kinase. Here, we summarize recent studies on AON and discuss an updated view of the long-distance control of nodulation.

Pharmacological Evidence that Calcitonin Gene-Related Peptide is Implicated in Cerebral Autoregulation

  • Hong, Ki-Whan;Pyo, Kwang-Min;Yu, Sung-Sook;Rhim, Byung-Yong
    • Proceedings of the Korean Society of Applied Pharmacology
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    • 1994.04a
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    • pp.287-287
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    • 1994
  • In the present study, it was aimed to asses the possibility that calcitonin gene-related peptide (CGRP) released in response to transient hypotension may contribute to the reflex autoregulation of cerebral blood flow as a putative modulator. Changes in pial arterial diameter (mean, 33.0 ${\pm}$ 1.1 $\mu\textrm{m}$) with changes in systemic arterial blood pressure (mean, 101.9 ${\pm}$ 2.7 mmHg) were observed directly through a closed cranial window in anesthetized normotensive rats. Image of the pial vessels was captured with a stereoscope connected to a CCD video camera and the diameter was measured with a microscaler. In the capsaicin-treated rats (one day prior to experiment, 50 nmol capsaicin injected intracisternally), both vasodilater and vasoconstrictor responses evoked by a transient hypotension and the reverse of blood pressure were markedly attenuated or almost abolished. When changes in pial arterial diameter were plotted as a function of changes in blood pressure, the slopes of both regression lines (for vasodilators and vasoconstrictors ) were markedly reduced. Similar reductions were evidenced under treatment wi th the CGRP antibody serum (1:1,000) and following CGRP receptor desensitization. However, the autoregulatory mechanics were neither affected by treatment wi th spantide (1 ${\mu}$M), substance P antagonist, nor by substance P receptor desensitization. Suffusion wi th mock cerebrospinal fluid containing CGRP and cromakalim caused a vasodilatation in a concentration-dependent manner, respectively and their effects were antagonized by glibenclamide. Substance P produced a vasodilatation, which was, however, little affected by glibenclamide. These observations indicate that the CGRP released from the perivascular sensory fibers in response to a hypotension is implicated in the modulation of the autoregulation of cerebral blood flow.

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Altered Cerebral Vasomotion with Decreased CGRP Level in Pial Arteries of Spontaneously Hypertensive Rats

  • Lee, Kwang-Ho;Choi, Jae-Moon;Hong, Ki-Whan
    • The Korean Journal of Physiology and Pharmacology
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    • v.2 no.5
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    • pp.573-580
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    • 1998
  • The study aims to identify the mechanism (s) underlying the altered vasodilatory responses of the pial artery of spontaneously hypertensive rats (SHR) under a hypothesis that calcitonin gene-related peptide (CGRP) exerts a modulator role in the autoregulation of cerebral blood flow (CBF). The animals were divided into four groups: 1) Sprague-Dawley rats (SDR), 2) Wistar rats (WR), 3) SHR with high blood pressure $(BP{\ge}150\;mmHg),$ and 4) SHR with normotensive BP $({\le}150\;mmHg).$ The lower limit of CBF autoregulation in SHR shifted to a higher BP $(82.8{\pm}9.3\'mmHg,\;P<0.05)$ than that in SDR $(58.9{\pm}5.7\;mmHg)$. In SHR, whether the BP levels were high or normotensive, the vasodilator responses to a stepwise hypotension were significantly attenuated unlike with SDR and WR. When artificial cerebrospinal fluid (CSF) containing capsaicin $(3{\times}10^{-7}\;M)$ was suffused over the cortical surface, a transient increase in pial arterial diameter was observed in the SHR with high or normotensive BP. In contrast, SDR and WR showed a large increase in diameter, and the increase was sustained for over 10 minutes. In line with these results, the basal releases of CGRP-like immunoreactivity (CGRP-LI) in the isolated pial arteries from SHR with high and normotensive BP were $12.5{\pm}1.4\;and\;9.8{\pm}2.8\;fmole/mm^2/60\;min\;(P<0.05)$, while those from SDR and WR were $25.5{\pm}3.1\;and\;24.6{\pm}3.1\;fmole/mm^2/60\;min,$ respectively. The isolated basilar arteries showed similar results to those of the pial arteries in SHR. Thus, it is summarized that, in the SHR, the reduced autoregulatory vasodilator responses to stepwise hypotension and capsaicin may be, in part, ascribed to the decreased release of CGRP from the perivascular sensory nerve fibers of the pial arteries, and that altered vasomotor activity in SHR may not be related with the hypertensive tone.

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Cerebral Blood Flow Velocity of Young People in Their Twenties

  • Choi Seok-Cheol;Kwon Heun-Young;Kim Tae-Un;Kim Jai-Young
    • Biomedical Science Letters
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    • v.10 no.4
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    • pp.467-472
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    • 2004
  • Transcranial Doppler sonography (TCD) is a useful diagnostic method to measure cerebral blood flow velocity in various cerebral disorders. However, we haven't data enough to be available for young persons, especially in the twenties in Korea. This study was performed to collect the basic data of the cerebral blood flow velocity and to understand the cerebral physiology in the twenties. We determined the mean velocities of middle, anterior, and posterior cerebral artery, and vertebral and basilar artery (MCA-V, ACA-V, PCA-V, VA-V, and BA-V, respectively) in eighty-two healthy volunteers. For evaluating cerebral autoregulation, only the MCA- V was measured under various conditions such as stable, apnea, and hyperventilation state. Right and left MCA-V were 80.66±14.03 and 83.22±14.40 cm/sec at stable state, 90.13±17.47 and 90.26±16.38 cm/sec at apnea, and 54.83±11.09 and 55.33±10.74 cm/sec at hyperventilation. Right and left ACA-V were 49.11±15.71 and 48.19±13.75 cm/sec. Right and left PCA-V were 39.44±9.12 and 37.91±6.74 cm/sec. Right and left VA-V were 33.65±9.26 and 36.l8±10.39 cm/sec. BA-V was 48.49±11.16 cm/sec. Right and left MCA- V, V A-V, and right ACA- V and PCA- V in women were higher than those of men (P<0.05). No significant differences were found between men and women in the others. These findings indicate that cerebral hemodynamics and autoregulation were normal in young people in their twenties. The velocities of MCA, ACA, PCA, and BA were high values in women as compared with men.

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The Effect of Systemic Hypertension on the Pediatric Brain (중추신경계에 미치는 소아 고혈압의 영향)

  • Hur, Yun-Jung
    • Childhood Kidney Diseases
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    • v.15 no.1
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    • pp.22-28
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    • 2011
  • Hypertension is one of the most common chronic diseases in childhood and adolescence. Untreated hypertension adversely affects many organs including heart, brain, kidney and peripheral arteries. We reviewed the complication of central nervous system caused by pediatric hypertension. Cerebral blood flows are maintained constantly in response to changes in blood pressure by cerebral autoregulation. Severe hypertension which destructs cerebral autoregulation results in acute hypertensive encephalopathy syndrome, ischemic or hemorrhagic stroke. Chronic pediatric hypertension induces learning disability and cognitive defect which are subclinical symptom prior to brain damage caused by severe hypertension. We should consider the effect of hypertension on pediatric brain because appropriate antihypertensive drugs could prevent these complications.

Electrohydraulic Pump-Driven Closed-Loop Blood Pressure Regulatory System

  • Ahn, Jae-Mok
    • Journal of Biomedical Engineering Research
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    • v.28 no.4
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    • pp.449-454
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    • 2007
  • An electrohydraulic (EH) pump-driven closed-loop blood pressure regulatory system was developed based on flow-mediated vascular occlusion using the vascular occlusive cuff technique. It is very useful for investigating blood pressure-dependant physiological variability, in particular, that could identify the principal mediators of renal autoregulation, such as tubuloglomerular feedback (TGF) and myogenic (MYO), during blood pressure regulation. To address this issue, renal perfusion pressure (RPP) should be well regulated under various experimental conditions. In this paper, we designed a new EH pump-driven RPP regulatory system capable of implementing precise and rapid RPP regulation. A closed-loop servo-controlwas developed with an optimal proportional plus integral (PI) compensation using the dynamic feedback RPP signal from animals. An in vivo performance was evaluated in terms of flow-mediated RPP occlusion, maintenance, and release responses. Step change to 80 mmHg reference from normal RPP revealed steady state error of ${\pm}3%$ during the RPP regulatory period after PI action. We obtained rapid RPP release time of approximately 300 ms. It is concluded that the proposed EH RPP regulatory system could be utilized in in vivo performance to study various pressure-flow relationships in diverse fields of physiology, and in particular, in renal autoregulation mechanisms.