Central role for angiotensin in control of adrenal catecholamine secretion

1985 ◽  
Vol 248 (3) ◽  
pp. R363-R370 ◽  
Author(s):  
E. J. Corwin ◽  
J. F. Seaton ◽  
M. Hamaji ◽  
T. S. Harrison
Keyword(s):  
Cerebrospinal Fluid ◽  
Catecholamine Secretion ◽  
Ang Ii ◽  
Artificial Cerebrospinal Fluid ◽  
Ventriculocisternal Perfusion ◽  
Before And After ◽  
Adrenal Response ◽  
Adrenal Secretion ◽  
Lateral Cerebral Ventricle

Angiotensin II (ANG II) is required for unimpaired adrenal reflex secretion of catecholamines after hemorrhage in the dog. To test if ANG II acts centrally, experiments were performed under general anesthesia on bilaterally or sham-nephrectomized dogs hemorrhaged at 25 ml/kg. Ventriculocisternal perfusion of ANG II or its antagonist saralasin was accomplished via needles inserted in the left lateral cerebral ventricle and cisterna magna. Mean arterial pressure and adrenal secretion of catecholamines were measured before and after hemorrhage. Nephrectomized dogs receiving only artificial cerebrospinal fluid (CSF) by ventriculocisternal perfusion had a very small adrenal response to hemorrhage compared with animals receiving ANG II intraventricularly (IVT) (at 10 and 100 pg . kg-1 . min-1). This effect of ANG II IVT also depended on the rate of IVT infusion. Peripheral infusion of ANG II (10 pg . kg-1 . min-1) had no effect on adrenal catecholamine secretion. Animals with intact kidneys given saralasin IVT (0.06 ng/min) responded similarly to nephrectomized dogs receiving only CSF IVT. Intravenous saralasin did not blunt the response to hemorrhage. Thus ANG II appears to support catecholamine secretion via a central mechanism. This mechanism is physiologically significant because either nephrectomy or functional elimination of ANG II by saralasin greatly attenuates the adrenal medullary response to hemorrhage in vivo.

The effect of intraventricular air on the rate of cerebrospinal fluid formation in dogs

1972 ◽  
Vol 37 (2) ◽  
pp. 177-181 ◽  
Author(s):  
Michael D. F. Deck ◽  
V. Deonarine ◽  
D. Gordon Potts
Keyword(s):  
Cerebrospinal Fluid ◽  
Statistical Analysis ◽  
Beagle Dogs ◽  
Content Type ◽  
Artificial Cerebrospinal Fluid ◽  
Ventriculocisternal Perfusion ◽  
Before And After ◽  
Fluid Formation ◽  
Fine Print

✓ Experiments were performed on dogs to estimate the effect of intraventricular air on the rate of cerebrospinal fluid formation. The rate of formation was measured satisfactorily in eight beagle dogs before and after the introduction of air using ventriculocisternal perfusion of artificial cerebrospinal fluid containing 14C-labelled inulin. Statistical analysis of rates of cerebrospinal fluid formation estimated half hourly indicated that there was little or no change after the introduction of air.

Creatinine, potassium, and calcium flux from chicken cerebrospinal fluid

1975 ◽  
Vol 228 (2) ◽  
pp. 415-419 ◽  
Author(s):  
DK Anderson ◽  
SR Heisey
Keyword(s):  
Cerebrospinal Fluid ◽  
Transport Process ◽  
Calcium Flux ◽  
Brain Blood Flow ◽  
Artificial Cerebrospinal Fluid ◽  
Bulk Absorption ◽  
Perfusion Time ◽  
Active Transport Process ◽  
Tracer Molecules ◽  
Lateral Cerebral Ventricle

Brains of methoxyflurane-anesthetized chickens were perfused from a lateral cerebral ventricle to cisterna magna with an artificial cerebrospinal fluid (CSF) containing trace quantities of radioiodinated human serum albumin (RIHSA) or inulin (1.0 mg/ml) to measure CSF bulk absorption. In addition, it contained either trace quantities of 22Na, 42K, 45Ca or [14C]creatinine; the concentrations of the latter three were varied to determine permeability coefficients (K-D's) as a function of concentration. A mass balance for the tracer molecules was calculated to determine their movement into brain or blood. K-D's for 45Ca, 42K, 22Na, and creatinine (Cr) were unaffected by perfusion time and the latter two were larger than previously reported (3). The lack of effect of time on K-D and the large values for K-D22Na and K-D-Cr are attributed to anesthetic effects on brain blood flow. K-D-Cr and K-D42K were larger than K-D22Na or K-D45Ca and K-D's for 45Ca, Cr, and 42K were independent of their inflow concentrations. An active transport process is suggested for potassium and creatinine, but one that is located at sites other than the ependymal wall. Bulk flow clearance accounted for RIHSA movement from CSF, whereas nonbulk clearance accounted for 50% of 22Na and 45Ca movement and 90% of 42K clearance. Fifty percent of 42K and 25% of 22Na and 45Ca were found in brain. The large recovery of 42K in brain supports the hypothesis that intracellular potassium serves as an exchangeable pool for the tracer.

Cerebrospinal fluid transients induced by hypercapnia

1983 ◽  
Vol 245 (5) ◽  
pp. R701-R705
Author(s):  
M. J. Fisher ◽  
S. R. Heisey ◽  
T. Adams ◽  
D. L. Traxinger
Keyword(s):  
Cerebrospinal Fluid ◽  
Formation Rate ◽  
Tracer Concentration ◽  
Perfusion Studies ◽  
Fluid Redistribution ◽  
Ventriculocisternal Perfusion ◽  
Before And After ◽  
Outflow Rate ◽  
The Times ◽  
Stop Flow

Ventriculocisternal perfusion studies using tracers have shown that hypercapnia causes a transient increase in cerebrospinal fluid (CSF) outflow rate (displaced CSF volume, Vd) and a decrease in CSF effluent tracer concentration (tracer-free CSF, CSFtf). This dilution could be due to an increase in CSF formation rate (Vf) and/or to displacement of unequilibrated CSFtf sequestered in poorly mixed compartments. To facilitate convection in the subarachnoid spaces, we used a “stop-flow” procedure (by clamping the cisternal outflow tube while infusion was constant) in anesthetized cats during ventriculocisternal perfusion with mock CSF containing [14C]dextran. Each animal spontaneously breathed air, then 5% CO2 both before and after stopflow. Although Vd and the times over which Vd and CSFtf were defined were unaffected, CSFtf was decreased by 50% after stop-flow. We conclude that during ventriculocisternal perfusion, mixing is incomplete in CSF spaces, and that unequilibrated CSF contributes significantly to the reduced tracer concentration in Vd during acute hypercapnia. To determine whether Vf transiently increases in response to CO2 breathing, or to any perturbation causing craniospinal fluid redistribution, homogeneity in CSF spaces must be verified.

Finite Element Analysis of Laser Fabricated Microjoint Performance in Cerebrospinal Fluid

2007 ◽  
Author(s):  
Ahsan Mian ◽  
Jesse Law
Keyword(s):  
Finite Element ◽  
Cerebrospinal Fluid ◽  
Mechanical Performance ◽  
Degradation Mechanism ◽  
Polyimide Film ◽  
Element Analysis ◽  
Critical Feature ◽  
Artificial Cerebrospinal Fluid ◽  
Bond Degradation ◽  
Before And After

Assessment of neural biocompatibility requires that materials be tested with exposure in neural fluids. Laser bonded microjoint samples made from titanium foil and polyimide film (TiPI) were evaluated for mechanical performance before and after exposure in artificial cerebrospinal fluid (CSF) for two, four and twelve weeks at 37°C. These samples represent a critical feature i.e., the microjoint — a major weakness in the bioencapsulation system. The laser microbonds showed initial degradation up to four weeks which then stabilized afterwards and retained similar strength until twelve weeks. To understand this bond degradation mechanism better, a finite element modeling approach was adopted. From the finite element results, it was revealed that the bond degradation was not owing to the hygroscopic expansion of polyimide. Rather, relaxation of the process induced residual stresses may have resulted in weakening of the bond strength as observed from experimental measurements.

Peripheral venous catecholamines versus adrenal secretory rates after brain stem stimulation in cats

1986 ◽  
Vol 251 (1) ◽  
pp. E14-E20 ◽  
Author(s):  
D. A. Bereiter ◽  
W. C. Engeland ◽  
D. S. Gann
Keyword(s):  
Blood Flow ◽  
Electrical Stimulation ◽  
Brain Stem ◽  
Catecholamine Secretion ◽  
Wide Range ◽  
Before And After ◽  
Alpha Chloralose ◽  
The Relationship ◽  
Adrenal Secretion ◽  
Catecholamine Concentration

The relationship between adrenal catecholamine secretion and peripheral venous catecholamine concentration was assessed in samples collected before and after brief (15-s) periods of brain stem electrical stimulation in cats anesthetized with alpha-chloralose-urethan. Adrenal blood flow from the left lumboadrenal vein averaged 0.75 +/- 0.05 ml/min (means +/- SE, n = 56). Peripheral norepinephrine (NE) concentration (1.19 +/- 0.07 ng/ml) was not well correlated with adrenal NE secretion (38.18 +/- 3.99 ng/min) before stimulation (r = 0.334, P less than 0.025). Although brain stem sites that evoked large increases in adrenal NE secretion often caused an increase in peripheral NE, sites that evoked significant decreases in adrenal NE secretion were not accompanied by decreases in peripheral NE. Peripheral epinephrine (E) concentration (0.11 +/- 0.01 ng/ml) was well correlated with adrenal E secretion (23.72 +/- 2.33 ng/min) before stimulation (r = 0.468, P less than 0.001). Brain stem stimulation-evoked changes in adrenal E secretion were generally reflected in changes of peripheral E concentration, although many exceptions were seen. Peripheral dopamine (DA) concentration (0.23 +/- 0.02 ng/ml) was well correlated with adrenal DA secretion (0.94 +/- 0.11 ng/min) before stimulation (r = 0.505, P less than 0.001). However, stimulus-evoked changes in adrenal DA secretion were not reflected in changes of peripheral DA concentration. The data indicate that, whereas brief periods of brain stem stimulation evoke a wide range of adrenal secretory responses, peripheral catecholamine responses best reflected adrenal secretion only when large increases in adrenal secretion were evoked and were poor indicators of decreased adrenal catecholamine secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventriculocisternal cerebrospinal perfusion in unanesthetized fetal lambs

1981 ◽  
Vol 50 (4) ◽  
pp. 880-883 ◽  
Author(s):  
J. M. Bissonnette ◽  
A. R. Hohimer ◽  
B. S. Richardson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cerebrospinal Fluid ◽  
Arterial Blood Pressure ◽  
Mean Arterial Blood Pressure ◽  
Ionic Composition ◽  
Arterial Blood ◽  
Artificial Cerebrospinal Fluid ◽  
Fetal Lamb ◽  
Lateral Cerebral Ventricle

Methods have been developed for the placement of cannulas in the lateral cerebral ventricle and cisternum magnum of the fetal lamb. Three to seven days after surgery, perfusion of the cerebral ventricular system was carried out in unanesthetized lambs in utero. Artificial cerebrospinal fluid (CSF) was perfused at 123 microliter/min for 4-5 h with no change in fetal arterial O2 pressure, CO2 pressure, pH, mean arterial blood pressure, or heart rate. The preparation is suitable for measurements of net formation of fetal central CSF and also for producing changes in the ionic composition of the fetal CSF.

Central V1 AVP receptors are involved in cardiovascular adaptation to hypovolemia in WKY but not in SHR

1996 ◽  
Vol 271 (3) ◽  
pp. H1057-H1064 ◽  
Author(s):  
A. S. Budzikowski ◽  
P. Paczwa ◽  
E. Szczepanska-Sadowska
Keyword(s):  
Cardiovascular Responses ◽  
Receptor Antagonists ◽  
Question Mark ◽  
Spontaneously Hypertensive ◽  
Arterial Bleeding ◽  
Artificial Cerebrospinal Fluid ◽  
Before And After ◽  
Wistar Kyoto ◽  
Lateral Cerebral Ventricle

The present study was designed to determine the role of centrally released arginine vasopressin (AVP) in cardiovascular adaptation to hypotensive hypovolemia in conscious normotensive Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR). Three groups of experiments were performed on WKY and SHR chronically implanted with lateral cerebral ventricle (LCV) cannulas and with femoral artery catheters. Mean arterial pressure (MAP) and heart rate (HR) were monitored before and after arterial bleeding (1.3% body weight) performed during LCV infusion 1) artificial cerebrospinal fluid (control), 2) V1 AVP-receptor antagonists inverted question mark[d(Et2)Tyr(Me)]DAVP, 5 ng/min inverted question mark, and 3) V2 AVP-receptor antagonists inverted question mark[d(CH2)5-D-Ile2, Ile4, AlaNH2]AVP, 5 ng/min inverted question mark. In control experiments hemorrhage caused similar significant decreases of MAP in both strains and bradycardia in WKY. Blockade of central V1 AVP receptors abolished hemorrhagic bradycardia and significantly reduced hypotension in WKY, with no effect on HR and MAP responses to hypovolemia in SHR. Neither in WKY nor in SHR were the cardiovascular responses to hemorrhage altered by blockade of central V2 receptors. The results suggest that the central V1 AVP system plays a significant role in eliciting hypovolemic bradycardia and hypotension in WKY and that this function is significantly impaired in SHR.

Cerebrospinal fluid hydrodynamics after placement of a shunt with an antisiphon device: a long-term study

2001 ◽  
Vol 94 (5) ◽  
pp. 750-756 ◽  
Author(s):  
Bo Lundkvist ◽  
Anders Eklund ◽  
Bo Kristensen ◽  
Markku Fagerlund ◽  
Lars-Owe D. Koskinen ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Csf Shunt ◽  
Content Type ◽  
Long Term Study ◽  
Before And After ◽  
Cerebrospinal Fluid Hydrodynamics ◽  
Antisiphon Device ◽  
Fine Print

Object. Few studies have been performed to investigate the cerebrospinal fluid (CSF) hydrodynamic profile in patients with idiopathic adult hydrocephalus syndrome (IAHS) before and after shunt implantation. The authors compared the in vivo CSF hydrodynamic properties, including the degree of gravity-induced CSF flow, of a shunt with an antisiphon device with a standard shunt. Methods. Twelve patients with IAHS underwent insertion of shunts with Delta valves. Clinical testing, magnetic resonance imaging, and CSF hydrodynamic investigations were conducted with intracranial pressure (ICP), gravity effect, and pressure—flow curve of the shunt estimated at baseline and at 3 and 12 months postoperatively. No shunt was revised. Despite postoperative clinical improvement in all patients who received Delta valves, the mean ICP was only moderately reduced (mean decrease at 3 months 0.3 kPa [p = 0.02], at 12 months 0.2 kPa [not significant]). Patients with the greatest increase in ICP preoperatively had the most pronounced decrease postoperatively. The hydrostatic effect of the Delta valves was significantly lower than with the Hakim shunts (0.1–0.2 kPa compared with 0.6 kPa). The increased conductance (that is, lowered resistance) was up to 14 times higher with the Delta valves compared with preoperative levels. Conclusions. The function of a CSF shunt may be more complicated than previously thought; the subcutaneous pressure acting on the antisiphon device can modify the shunt characteristics. A compensatory increase in CSF production may counteract the increased outflow through the shunt. The improved CSF outflow conductance may increase the intracranial compliance and thereby dampen a pathological ICP waveform.

Functional evidence for L-type Ca2+ channels controlling ANG II-induced adrenal catecholamine release in vivo

1996 ◽  
Vol 271 (6) ◽  
pp. R1713-R1719
Author(s):  
D. Martineau ◽  
R. Briand ◽  
N. Yamaguchi
Keyword(s):  
Catecholamine Release ◽  
Bay K 8644 ◽  
Catecholamine Secretion ◽  
Dependent Manner ◽  
Ang Ii ◽  
Catecholamine Response ◽  
Series Of Experiments ◽  
Plasma Catecholamine Concentrations ◽  
Ca2 Channels

The aim of the present study was to investigate the functional involvement of L- and/or N-type Ca2+ channels in adrenal catecholamine secretion in response to exogenous angiotensin II (ANG II) in anesthetized dogs. Plasma catecholamine concentrations in adrenal venous and aortic blood were determined by a high-performance liquid chromatography-electrochemical method. In the first series of experiments, repeated infusions of BAY K 8644 locally into the left adrenal gland at 15-min intervals resulted in significant and reproducible increases in adrenal catecholamine secretion. Nifedipine, similarly administered 5 min before BAY K 8644, diminished BAY K 8644-induced catecholamine secretion in a dose-dependent manner and completely blocked the catecholamine response at the highest dose tested. In the second series of experiments, local infusion of ANG II resulted in a significant increase in adrenal catecholamine secretion. The maximum catecholamine response to ANG II was attenuated by approximately 65% in the presence of nifedipine at the dose that abolished the BAY K 8644-induced catecholamine release. This inhibition by nifedipine remained unchanged in the presence of omega-conotoxin. The present study shows that dihydropyridine-sensitive L-type Ca2+ channels are operative in the adrenal medulla of the dog in vivo. The results indicate that the L-type Ca2+ channels are only partially implicated in the local regulation of ANG II-induced adrenal catecholamine secretion, suggesting the existence of another mechanism. However, omega-conotoxin-sensitive N-type Ca2+ channels are unlikely to be functionally involved in postsynaptic mechanisms mediating adrenal catecholamine secretion in response to exogenous ANG II under in vivo conditions.

Responses of pial arterioles after prolonged hypercapnia and hypoxia in the awake rabbit

1979 ◽  
Vol 46 (1) ◽  
pp. 89-95 ◽  
Author(s):  
J. E. Levasseur ◽  
E. P. Wei ◽  
H. A. Kontos ◽  
J. L. Patterson
Keyword(s):  
Cerebrospinal Fluid ◽  
Chemical Composition ◽  
Bicarbonate Concentration ◽  
Vasodilator Response ◽  
Brain Surface ◽  
Bicarbonate Ions ◽  
Artificial Cerebrospinal Fluid ◽  
Before And After ◽  
Pial Arterioles ◽  
The Brain

The changes in the responsiveness of pial arterioles to CO2 and in the composition of cortical cerebrospinal fluid bathing these vessels were studied in the awake rabbit before and after 6 days exposure to hypercapnia (7% CO2) or hypoxia (10% O2). The vasodilator response of pial arterioles to inhalation of 3--10% CO2 was diminished after prolonged hypercapnia and enhanced after prolonged hypoxia. After both hypoxia and hypercapnia, pial arteriolar responsiveness to CO2 was immediately returned toward control levels by washing the brain surface with normal artificial cerebrospinal fluid. The bicarbonate concentration of cerebrospinal fluid bathing the pial vasculature showed a significant decrease after hypoxia and a significant increase after hypercapnia, whereas CSF pH remained unaltered. We conclude that the alteration in responsiveness of pial arterioles to CO2 is due to a change in the chemical composition of the CSF bathing these vessels, involving an adjustment in the concentration of bicarbonate ions.

Sign in / Sign up

Export Citation Format

Share Document