Norepinephrine release during autoregulatory escape: effects of alpha 2-receptor blockade

1991 ◽  
Vol 260 (2) ◽  
pp. H400-H408 ◽  
Author(s):  
L. Q. Chen ◽  
G. L. Riedel ◽  
A. P. Shepherd
Keyword(s):  
Blood Flow ◽  
Neural Control ◽  
Time Course ◽  
Venous Blood ◽  
Receptor Blockade ◽  
Control Mechanisms ◽  
Partial Recovery ◽  
Sympathetic Stimulation ◽  
Resistance Vessels ◽  
Autoregulatory Escape

The partial recovery that intestinal blood flow undergoes during continued sympathetic nerve stimulation is termed autoregulatory escape. This study tested two hypotheses that might explain escape: 1) diminishing norepinephrine (NE) release during sustained stimulation and 2) an alpha 2-receptor-mediated competition between local and neural control mechanisms. The rates of NE release before and during stimulation of the perivascular sympathetic nerves were determined by measuring blood flow in isolated loops of canine small intestine and assaying the concentrations of NE in arterial and venous blood. The presence of functional alpha 2-receptors was demonstrated by clonidine injections, and the effects of alpha 2-receptor blockade were studied during yohimbine infusions. The time course of NE release was inconsistent with a cause-effect relationship; NE release was greatest during the phase when resistance had already escaped. Deliberately altering NE release by changing the stimulus duration did not affect escape. The study demonstrated 1) that diminished NE release during continued sympathetic stimulation does not occur and cannot account for escape, 2) that resistance vessels in the canine intestinal circulation possess functional alpha 2-receptors which are responsible for part of the vasoconstriction caused by sympathetic stimulation, 3) that blockade of presynaptic alpha 2-receptors significantly enhanced NE release during the initial 30-s period but not during the escape phase, and 4) that alpha 2-receptor blockade enhances autoregulatory escape. Altogether these findings indicate that the postsynaptic alpha 2-receptors on intestinal resistance vessels deserve further investigation as the possible site at which local and neural mechanisms compete to influence vascular resistance.

Role of H+ and alpha 2-receptors in escape from sympathetic vasoconstriction

1991 ◽  
Vol 261 (3) ◽  
pp. H868-H873 ◽  
Author(s):  
L. Q. Chen ◽  
A. P. Shepherd
Keyword(s):  
Blood Flow ◽  
Small Bowel ◽  
Release Rate ◽  
Partial Recovery ◽  
Sympathetic Stimulation ◽  
Vasoconstrictor Response ◽  
Sympathetic Vasoconstriction ◽  
Autoregulatory Escape

In a previous study, we noted that mesenteric venous pH falls during the reductions in intestinal blood flow caused by sympathetic stimulation and that alpha 2-receptor antagonists enhanced autoregulatory escape (the partial recovery that blood flow undergoes despite sustained sympathetic stimulation). In addition, other studies indicated that increased [H+] selectively inhibits the responsiveness of postjunctional alpha 2-receptors to norepinephrine (NE). Therefore, we investigated the role of H+ in escape by 1) measuring the rate of unbuffered H+ release during sympathetic stimulation in isolated loops of canine small bowel, 2) infusing acidic buffer intra-arterially and determining the effects of acidosis on sympathetic vasoconstriction and escape, 3) ascertaining the effects of acidosis on the release rate of endogenous NE during sympathetic stimulation, and 4) determining whether acidosis exerts effects in vivo on post-junctional responses to the selective alpha 1- and alpha 2-agonists, phenylephrine and clonidine, respectively. Our findings were that 1) the rate at which the gut released H+ into blood increased during sympathetic stimulation, 2) infusing acidic buffer to lower venous pH from 7.3 to 7.1 attenuated the initial vasoconstrictor response after 30 s of stimulation, 3) acidosis caused blood flow to return further toward control despite continued stimulation and thus enhanced escape, 4) acidosis did not impair NE release at either 30 s or 6 min of stimulation, and 5) acidosis inhibited the intestinal vasoconstrictor effects of selective alpha 2- but not alpha 1-agonists. The results support the hypothesis that escape from sympathetic vasoconstriction occurs, in part, because increased [H+] inhibits alpha 2-mediated postjunctional responses to neuronally released NE.

Neural mechanisms regulating neurohypophysial resistance arteries

1992 ◽  
Vol 263 (5) ◽  
pp. H1605-H1615
Author(s):  
D. F. Hanley ◽  
D. A. Wilson ◽  
M. A. Conway ◽  
R. J. Traystman ◽  
J. A. Bevan ◽  
...  
Keyword(s):  
Blood Flow ◽  
Vasoactive Intestinal Polypeptide ◽  
Neural Control ◽  
Neural Mechanisms ◽  
Resistance Arteries ◽  
Frequency Dependent ◽  
Arterial Circulation ◽  
Physiological Relevance ◽  
Resistance Vessels ◽  
Perivascular Nerves

We defined the extent of vasoactive intestinal polypeptide (VIP) and noradrenergic influences on isolated 100- to 200-microns-diameter vessels from the resistance arterial circulation of the neurohypophysis. A dual extracranial (inferior hypophysial) and intracranial (superior hypophysial) arterial supply to the neurohypophysis was confirmed. The inferior hypophysial artery demonstrates noradrenergic and VIP-like perivascular nerves, whereas the superior hypophysial artery shows primarily VIP-like innervation. Pharmacological sensitivity of the inferior hypophysial to VIP [mean effective dose (ED50) = 10(-8.2) M] and to norepinephrine (ED50 = 10(-5.7) M) was demonstrated. The superior hypophysial reacted only to VIP (ED50 = 10(-8.6) M). The physiological relevance of these findings was tested with transmural nerve stimulation. Frequency-dependent vasodilation of both inferior and superior hypophysial arteries was demonstrated. This dilation could not be blocked with atropine or propranolol. Frequency-dependent vasoconstriction was identified in extracranial vessels including the inferior hypophysial artery. This constriction is only partially blocked by prazosin, phentolamine, and guanethidine. When neurohypophysial resistance vessels are compared with larger circle of Willis arteries and similar-size pial vessels of other cerebral regions, they appear to have regionally unique neural mechanisms for regulating blood flow. Specifically whether controlled by periarterial nerves or other tissue influences, the inferior hypophysial artery appears to meet anatomic, pharmacological, and physiological definitions of neural control for both dilator and constrictor activities of flow to the neurohypophysis.

Sympathetic reflex control of subcutaneous blood flow in patients with congestive heart failure

1986 ◽  
Vol 70 (5) ◽  
pp. 513-522 ◽  
Author(s):  
Eli Kassis ◽  
Ole Amtorp ◽  
Knud Skagen
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Blood Flow ◽  
Left Ventricular ◽  
Transmural Pressure ◽  
Receptor Blockade ◽  
Sympathetic Stimulation ◽  
Nerve Blockade ◽  
Control Subjects ◽  
Β Receptor

1. Central and local regulation of forearm subcutaneous vascular resistance (FSVR) during postural changes were studied in congestive heart failure (CHF). Blood flow was measured by the local 133Xe-washout technique. Nine patients with severe CHF (baseline angiographic ejection fraction, 23 ± 2%, mean ± sem; cardiac index, 2.2 ± 0.2 litres min−1 m−2; increased left ventricular pressures and dimensions) were compared with seven control subjects who had normal cardiac performance. 2. Baseline FSVR and plasma concentrations of noradrenaline and adrenaline were substantially higher in patients with CHF than control subjects. However, the patients, like control subjects, increased FSVR by 46 ± 3% in response to increase in local venous transmural pressure and disclosed a normal response to decrease in forearm perfusion pressure. Both responses to changes in vascular transmural pressure were preserved after either proximal nervous blockade or local β-receptor blockade. 3. Central sympathetic stimulation was induced with use of 45° upright tilt. Control subjects developed vasoconstriction (FSVR increased by 59 ± 5%), which was completely abolished after proximal nerve blockade. Patients with CHF developed vasodilatation (FSVR decreased by 24 ± 8%), which was not only abolished but reversed after proximal nerve blockade (FSVR increased by 22 ± 7%), probably owing to the increased humoral vasoconstrictor activity. The paradoxical vasodilator response to central sympathetic stimulation in these patients was reversed after local β-receptor blockade (FSVR increased by 19 ± 9%). 4. The local vasoconstrictor reflex responsiveness and intrinsic vascular reactivity were not affected by the augmented baseline sympathetic vasoconstrictor activity in patients with CHF. Central sympathetic stimulation seems to elicit a β-adrenergic reflex effect intended to improve perfusion of the subcutaneous tissue in these patients.

Gastric oxygen uptake during autoregulatory escape from sympathetic stimulation

1989 ◽  
Vol 257 (4) ◽  
pp. G633-G636
Author(s):  
J. W. Kiel ◽  
A. P. Shepherd
Keyword(s):  
Blood Flow ◽  
Sympathetic Stimulation ◽  
Oxygen Utilization ◽  
Total Blood ◽  
Perivascular Nerves ◽  
Gastric Corpus ◽  
Autoregulatory Escape ◽  
Total Blood Flow ◽  
Frequency Of Stimulation ◽  
Oxygen Difference

To assess the effects of sympathetic stimulation on gastric blood flow and oxygen utilization, the perivascular nerves were stimulated at 2, 4, 6, and 8 Hz in chambered segments of canine gastric corpus perfused at constant pressure. Spectrophotometric arteriovenous oxygen difference and electromagnetic blood flow were recorded continuously. Except at the lowest frequency of stimulation (2 Hz), total blood flow exhibited autoregulatory escape, i.e., blood flow decreased initially but then returned toward control. The fall in total blood flow at the onset of sympathetic stimulation was smaller at 2 Hz than at 4 Hz, but stimulation at 6 and 8 Hz caused no further reductions in total blood flow. However, at all frequencies, total blood flow escaped to the same steady-state value (approximately 17 ml.min-1.100 g-1). Although total blood flow was still less than control (approximately 25 ml.min-1.100 g-1), oxygen extraction increased proportionately so that oxygen consumption was not significantly less than control at any frequency of stimulation. We conclude that autoregulatory escape from sympathetic stimulation is mediated by local mechanisms acting to maintain tissue oxygenation in the stomach.

Expression of vascular escape: conductance or resistance?

1992 ◽  
Vol 262 (4) ◽  
pp. H1191-H1196 ◽  
Author(s):  
Mark S. D'Almeida ◽  
W. Wayne Lautt
Keyword(s):  
Experimental Data ◽  
Blood Pressure ◽  
Blood Flow ◽  
Vascular Tone ◽  
Sympathetic Stimulation ◽  
Autoregulatory Escape ◽  
Escape Responses

Vascular escape is that phenomenon whereby a tachyphylaxis occurs in the vasoconstriction of an arteriole to a constant sympathetic stimulation. Vascular escape, in vivo, is primarily a blood flow event. Calculated resistance, as an index of vascular tone, does not consistently describe the responses of the arterioles undergoing vascular escape. Conductance, which is the inverse of resistance, obviates several of the errors produced by the use of resistance. In this study, we illustrate this issue using hypothetical and experimental data. Escape responses were calculated in terms of resistance and conductance and plotted against blood flow escape responses. Resistance escape responses were nonlinearly related to blood flow escapes and overestimated vascular escape with both hypothetical and experimental data. Conductance escape responses were linearly related to flow escape responses and consistently described vascular escape. We therefore conclude that conductance is a better index of vascular tone to express vascular escape. arterial vascular tone; vasoconstriction; autoregulatory escape; blood flow; blood pressure Submitted on July 18, 1991 Accepted on November 11, 1991

Intramural distribution of intestinal blood flow during sympathetic stimulation

1988 ◽  
Vol 255 (5) ◽  
pp. H1091-H1095 ◽  
Author(s):  
A. P. Shepherd ◽  
G. L. Riedel
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Reactive Hyperemia ◽  
Mucosal Blood Flow ◽  
Control Mechanisms ◽  
Sympathetic Stimulation ◽  
Total Blood ◽  
Circulatory Control ◽  
Neurogenic Vasoconstriction ◽  
Total Blood Flow

Recent studies indicate that the mucosal circulation of the small intestine possesses more potent local circulatory control mechanisms than the muscularis. Several lines of evidence support this assertion: the absence of reactive hyperemia in the muscularis, the confinement of glucose-induced hyperemia to the mucosal circulation, and the more effective autoregulation of villus blood flow in comparison with total blood flow. Therefore, we postulated that the mucosal circulation would exhibit a more pronounced ability to escape the vasoconstrictor influence of sympathetic nerve stimulation. To test this hypothesis, we used laser-Doppler velocimetry (LDV) to study the effects of perivascular nerve stimulation on blood flow in the muscularis and mucosa of isolated dog intestine. In two series of experiments, we measured total blood flow to a gut loop with an electromagnetic flow probe on the supply artery, while LDV measurements were made either on the mucosa or on the muscularis. Sympathetic stimulation (10 Hz) transiently reduced total blood flow to approximately 10% of control in both studies. Muscularis and mucosal blood flow both reached minimal values. Subsequently, total blood flow and the two regional perfusions exhibited "autoregulatory escape," but the propensity for blood flow to escape from sympathetic vasoconstriction was significantly greater in the mucosa than in the muscularis. These data provide more evidence that, compared with the muscularis, the intestinal mucosa possesses more potent local control mechanisms that oppose neurogenic vasoconstriction.

scholarly journals Role of adenosine in the regulation of coronary blood flow in swine at rest and during treadmill exercise

1998 ◽  
Vol 275 (5) ◽  
pp. H1663-H1672 ◽  
Author(s):  
Dirk J. Duncker ◽  
René Stubenitsky ◽  
Pieter D. Verdouw
Keyword(s):  
Blood Flow ◽  
Coronary Blood Flow ◽  
Treadmill Exercise ◽  
Receptor Blockade ◽  
Coronary Resistance ◽  
Vasomotor Tone ◽  
Coronary Vasodilation ◽  
Resistance Vessels ◽  
Exercise Induced

A pivotal role for adenosine in the regulation of coronary blood flow is still controversial. Consequently, we investigated its role in the regulation of coronary vasomotor tone in swine at rest and during graded treadmill exercise. During exercise, myocardial O2 consumption increased from 167 ± 18 μmol/min at rest to 399 ± 27 μmol/min at 5 km/h ( P ≤ 0.05), which was paralleled by an increase in O2 delivery, so that myocardial O2 extraction (76 ± 1 and 78 ± 1% at rest and 5 km/h, respectively) and coronary venous[Formula: see text] (24.5 ± 1.0 and 22.8 ± 0.3 mmHg at rest and 5 km/h, respectively) remained unchanged. After adenosine receptor blockade with 8-phenyltheophylline (5 mg/kg iv), the relation between myocardial O2consumption and coronary vascular resistance was shifted toward higher resistance, whereas myocardial O2extraction rose to 81 ± 1 and 83 ± 1% at rest and 5 km/h and coronary venous [Formula: see text] fell to 19.2 ± 0.8 and 18.9 ± 0.8 mmHg at rest and 5 km/h, respectively (all P ≤ 0.05). Thus, although adenosine is not mandatory for the exercise-induced coronary vasodilation, it exerts a vasodilator influence on the coronary resistance vessels in swine at rest and during exercise.

Progressive hypoxia until brain electrical silence: a useful model for studying protective interventions

1988 ◽  
Vol 66 (11) ◽  
pp. 1398-1406 ◽  
Author(s):  
Carl F. Cartheuser
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Time Course ◽  
Venous Blood ◽  
Hypoxia Tolerance ◽  
Sagittal Sinus ◽  
Progressive Hypoxia ◽  
Time Courses ◽  
Blood Data

Anesthetized spontaneously breathing rats, fitted with epicortical electrodes and catheters for sampling arterial, venous, and cerebral venous blood, were exposed to standardized progressive hypoxia. Three minutes of hypoxia sequentially caused hyperpnea, hypopnea, apnea, and cessation of electrocorticogram "spiking," of synchronization, and of background in electroencephalogram (EEG). Blood data and cerebral blood flow and metabolism were measured throughout and at "insults," i.e., at apnea and cessation events, to clarify their interdependence. Arterial and brain venous Po2 fell linearly with inspired oxygen (final value of 2% at 280 s). Hyperpnea induced arterial alkalosis; subsequent hypopnea led to near-normal Pco2 and pH when EEG ceased. Hypercapnia was more pronounced in cerebral than in systemic venous blood; time courses of pH changes were similar. Sagittal sinus blood pressure and outflow were linearly related and resembled the time course of local cerebral blood flow. Blood flow increased by 25% at apnea and only 60% at EEG silence. Cerebral metabolic rate of O2 rose during the hyperpnea phase and fell exponentially thereafter. Cerebral glucose uptake and lactate release increased within the first 3 min but fell abruptly when cortico-electric spiking ceased. Time courses of cerebral O2 consumption and spike rate were linearly related; both showed inverse linear relations to cerebral perfusion. The hypoxic insults were well defined by blood data; critical Po2 values were lower than previously assumed. This model is proving to be a useful, controlled method by which mechanisms of cerebral hypoxia tolerance may be studied in vivo.

Patterns of Cerebral Blood Flow and Systemic Hemodynamics During Arithmetic Processing

2008 ◽  
Vol 22 (2) ◽  
pp. 81-90 ◽  
Author(s):  
Natalie Werner ◽  
Neval Kapan ◽  
Gustavo A. Reyes del Paso
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Time Course ◽  
Doppler Sonography ◽  
Transcranial Doppler Sonography ◽  
Systemic Hemodynamics ◽  
Heart Period ◽  
Blood Flow Velocities ◽  
Flow Velocities

The present study explored modulations in cerebral blood flow and systemic hemodynamics during the execution of a mental calculation task in 41 healthy subjects. Time course and lateralization of blood flow velocities in the medial cerebral arteries of both hemispheres were assessed using functional transcranial Doppler sonography. Indices of systemic hemodynamics were obtained using continuous blood pressure recordings. Doppler sonography revealed a biphasic left dominant rise in cerebral blood flow velocities during task execution. Systemic blood pressure increased, whereas heart period, heart period variability, and baroreflex sensitivity declined. Blood pressure and heart period proved predictive of the magnitude of the cerebral blood flow response, particularly of its initial component. Various physiological mechanisms may be assumed to be involved in cardiovascular adjustment to cognitive demands. While specific contributions of the sympathetic and parasympathetic systems may account for the observed pattern of systemic hemodynamics, flow metabolism coupling, fast neurogenic vasodilation, and cerebral autoregulation may be involved in mediating cerebral blood flow modulations. Furthermore, during conditions of high cardiovascular reactivity, systemic hemodynamic changes exert a marked influence on cerebral blood perfusion.

Assessment of the incorporation of revascularized fibula grafts used for mandibular reconstruction with F-18-PET

2001 ◽  
Vol 40 (02) ◽  
pp. 51-58 ◽  
Author(s):  
H. Schliephake ◽  
van den Hoff ◽  
W. H. Knapp ◽  
G. Berding
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Venous Blood ◽  
Mandibular Reconstruction ◽  
Reference Region ◽  
Osteoblastic Activity ◽  
Non Union ◽  
Range Of Values ◽  
Measured Input

Summary Aim: Determination of the range of regional blood flow and fluoride influx during normal incorporation of revascularized fibula grafts used for mandibular reconstruction. Evaluation, if healing complications are preceded by typical deviations of these parameters from the normal range. Assessment of the potential influence of using “scaled population-derived” instead of “individually measured” input functions in quantitative analysis. Methods: Dynamic F-l 8-PET images and arterialized venous blood samples were obtained in 11 patients early and late after surgery. Based on kinetic modeling regional blood flow (K1) and fluoride influx (Kmlf) were determined. Results: In uncomplicated cases, early postoperative graft K1 - but not Kmlf -exceeded that of vertebrae as reference region. Kmn values obtained in graft necrosis (n = 2) were below the ranges of values observed in uncomplicated healing (0.01 13-0.0745 ml/min/ml) as well as that of the reference region (0.0154-0.0748). Knf values in mobile non-union were in the lower range - and those in rigid non-union in the upper range of values obtained in stable union (0.021 1-0.0694). If scaled population-derived instead of measured input functions were used for quantification, mean deviations of 23 ± 17% in K1 and 12 ± 16% in Kmlf were observed. Conclusions: Normal healing of predominantly cortical bone transplants is characterized by relatively low osteoblastic activity together with increased perfusion. It may be anticipated that transplant necrosis can be identified by showing markedly reduced F− influx. In case that measured input functions are not available, quantification with scaled population-derived input functions is appropriate if expected differences in quantitative parameters exceed 70%.

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