Effects of CSF ANG II and AVP on sweating in the heat-stressed patas monkey

1989 ◽  
Vol 67 (1) ◽  
pp. 134-140 ◽  
Author(s):  
M. D. Owen ◽  
R. D. Matthes ◽  
C. V. Gisolfi
Keyword(s):  
Cerebrospinal Fluid ◽  
Rectal Temperature ◽  
Time Course ◽  
Potential Role ◽  
Sweat Rate ◽  
Ang Ii ◽  
Erythrocebus Patas ◽  
Patas Monkey ◽  
Artificial Cerebrospinal Fluid

Increasing cerebrospinal fluid [Na+] reduces sweat rate (msw) in the heat-stressed patas monkey (Erythrocebus patas). This study determined the potential role of two neuropeptides, angiotensin II (ANG II) and arginine vasopressin (AVP), in mediating this response. Artificial cerebrospinal fluid, containing either ANG II or AVP, was infused into the third cerebral ventricle of lenperone-tranquilized monkeys (n = 4) exposed to 41 +/- 2 degrees C. Solutions were infused at 16.5 microliters/min for 25 min (total vol approximately 413 microliters). ANG II (1.25, 2.5, 5, and 10 ng/microliters) tended to decrease .msw. However, during infusion, only the decline at 10 min associated with the 1.25-ng/microliters dose (26%) was different (P less than 0.004) from control. This dose elevated (P less than 0.004) core rectal temperature by 1.14 degrees C at 20 min postinfusion. In contrast, AVP (0.5 and 1.5 micrograms/microliters artificial cerebrospinal fluid) had no significant effect on .msw compared with control infusions. Both doses of AVP produced a slight but significant increase in rectal temperature of 0.14 and 0.22 degrees C, respectively, at 20 min postinfusion. In conclusion, the magnitude and time course of the change in .msw with central ANG II suggest that it does not act as the sole mediator of the decline in .msw observed with elevated cerebrospinal fluid [Na+]. The minimal effects produced by third ventricular AVP exclude this route as a means by which AVP could modulate .msw during dehydration.

Effect of cerebrospinal fluid hyperosmolality on sweating in the heat-stressed patas monkey

1989 ◽  
Vol 67 (1) ◽  
pp. 128-133 ◽  
Author(s):  
M. D. Owen ◽  
R. D. Matthes ◽  
C. V. Gisolfi
Keyword(s):  
Cerebrospinal Fluid ◽  
Rectal Temperature ◽  
Sweat Rate ◽  
Recovery Period ◽  
Erythrocebus Patas ◽  
Artificial Cerebrospinal Fluid ◽  
Skin Temperatures ◽  
Central Stimulation ◽  
Osmotic Stimuli

Dehydration increases the osmolality of body fluids and decreases the rate of sweating during thermal stress. By localizing osmotic stimuli to central nervous system tissues, this study assessed the role of central stimulation on sweating in a heat-stressed nonhuman primate. Lenperone-tranquilized patas monkeys (Erythrocebus patas n = 5), exposed to 41 +/- 2 degrees C, were monitored for calf sweat rate, rectal and mean skin temperatures, oxygen consumption, and heart rate during infusions (255–413 microliters) of hypertonic artificial cerebrospinal fluid (ACSF) into the third cerebral ventricle. ACSF made hypertonic with NaCl to yield osmolalities of 800 and 1,000 mosmol/kgH2O significantly decreased sweat rate compared with control ACSF (285 mosmol/kgH2O), achieving maximal reductions during infusion of 37 and 53%, respectively. Rectal temperature significantly increased during the recovery period, reaching elevations of 0.69 and 0.72 degrees C, respectively, at 20 min postinfusion. In contrast, ACSF made hypertonic with sucrose (800 mosmol/kgH2O) failed to change sweat rate or rectal temperature during infusion in three animals. Thus, intracerebroventricular infusions of hypertonic ACSF mimicked dehydration-induced effects on thermoregulation. The reduction in heat loss during infusion appeared to depend on an elevation in cerebrospinal fluid [Na+] and not osmolality per se.

PVN lesions prevent the endothelin 1-induced increase in arterial pressure and vasopressin

2001 ◽  
Vol 280 (2) ◽  
pp. E349-E356 ◽  
Author(s):  
Noreen F. Rossi ◽  
Haiping Chen
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Arterial Pressure ◽  
Paraventricular Nuclei ◽  
Artificial Cerebrospinal Fluid ◽  
Electrolytic Lesions ◽  
The Central Nervous System ◽  
Baseline Values ◽  
Long Evans

Endothelin (ET) acts within the central nervous system to increase arterial pressure and arginine vasopressin (AVP) secretion. This study assessed the role of the paraventricular nuclei (PVN) in these actions. Intracerebroventricular ET-1 (10 pmol) or the ETA antagonist BQ-123 (40 nmol) was administered in conscious intact or sinoaortic-denervated (SAD) Long-Evans rats with sham or bilateral electrolytic lesions of the magnocellular region of the PVN. Baseline values did not differ among groups, and artificial cerebrospinal fluid (CSF) induced no significant changes. In sham-lesioned rats, ET-1 increased mean arterial pressure (MAP) 15.9 ± 1.3 mmHg in intact and 22.3 ± 2.7 mmHg in SAD ( P < 0.001 ET-1 vs. CSF) rats. PVN lesions abolished the rise in MAP: −0.1 ± 2.8 mmHg in intact and 0.0 ± 2.9 mmHg in SAD. AVP increased in only in the sham-lesioned SAD group 8.6 ± 3.5 pg/ml ( P < 0.001 ET-1 vs. CSF). BQ-123 blocked the responses. Thus the integrity of the PVN is required for intracerebroventricularly administered ET-1 to exert pressor and AVP secretory effects.

Regeneration of vascular tissue through redifferentiation of interxylary phloem after complete girdling in Aquilaria sinensis

IAWA Journal ◽  
2021 ◽  
pp. 1-16
Author(s):  
Bei Luo ◽  
Arata Yoshinaga ◽  
Tatsuya Awano ◽  
Keiji Takabe ◽  
Takao Itoh
Keyword(s):  
Time Course ◽  
Potential Role ◽  
Vascular Tissue ◽  
Secondary Xylem ◽  
Vascular Cambium ◽  
Aquilaria Sinensis ◽  
Phloem Fibers ◽  
Interxylary Phloem ◽  
Time Course Study

Abstract We studied the time-course of stem response for six months following complete girdling in branches of Aquilaria sinensis to determine the potential role of interxylary phloem (IP) in this response. It was found that the vascular cambium, as well as its derivative secondary xylem and phloem, regenerated fully through redifferentiation of IP. We confirmed that vascular cambium regenerated within one month after girdling based on observation of new vessels, IP, and secondary phloem fibers. The time-course study showed that IPs made connections with each other, merged, and became larger through the proliferation of IPs parenchyma cells and the cleaving of secondary xylem in a narrow zone 400 to 1000 μm deep inside the girdled edge. This led to the formation of a complete circular sheath of vascular cambium, followed by the regeneration of vascular tissue. It is worth noting that the secondary xylem is regenerated always following the formation of a thick belt of wound xylem.

Abstract 105: Platelet-Neutrophil Aggregates play a crucial role in regulating vasculitis in Kawasaki Disease

Circulation ◽  
2015 ◽  
Vol 131 (suppl_2) ◽  
Author(s):  
Kentaro Ueno
Keyword(s):  
Kawasaki Disease ◽  
Crucial Role ◽  
Bacterial Infections ◽  
Time Course ◽  
Acute Inflammation ◽  
Potential Role ◽  
Platelet Factor ◽  
Normal Volunteers ◽  
Inflammatory Activation

Objective: Circulating platelet-neutrophil aggregates play a crucial role in amplifying acute inflammation and could promote adverse effects involving vascular injury. The aim of this study was to clarify the role of platelet-neutrophil aggregates in patients with Kawasaki disease (KD). Methods: We analyzed 40 patients with KD (30 intravenous immunoglobulin [IVIG] responders and 10 IVIG non-responders), 7 febrile patients with bacterial infections, and 9 normal volunteers. Thirty-three patients with KD were treated with IVIG alone, and remaining seven were treated with IVIG plus prednisolone. We evaluated the rate of platelet-neutrophil aggregates and measured the platelet factor 4 (PF4) and β-thromboglobulin (β-TG) levels in patients with KD. Results: The rate of platelet-neutrophil aggregates was significantly higher in patients with KD than in both patients with bacterial infection and normal volunteers. There was a trend toward increased rate of platelet-neutrophil aggregates within 2 or 3 days after IVIG than before IVIG. The rate of platelet-neutrophil aggregates was significantly higher in patients who showed coronary artery abnormalities (CAA) than in those who showed without CAA and was correlated with PF4 and β-TG levels in patients with KD. Comparing time course analysis, the rate of platelet-neutrophil aggregates was significantly decreased in patients treated with IVIG plus prednisolone than in those treated with IVIG alone. Conclusions: Our findings demonstrate that platelet-neutrophil aggregates play a crucial role in regulating vasculitis, and are involved in the development of CAA. Additional prednisolone treatment in the acute phase of KD might have a potential role in inhibiting amplified reciprocal inflammatory activation by suppressing platelet-neutrophil aggregates.

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.

scholarly journals TRH microdialysis into the RTN of the conscious rat increases breathing, metabolism, and temperature

1999 ◽  
Vol 87 (2) ◽  
pp. 673-682 ◽  
Author(s):  
Carlos Cream ◽  
Eugene Nattie ◽  
Aihua Li
Keyword(s):  
Cerebrospinal Fluid ◽  
Rectal Temperature ◽  
Random Order ◽  
Conscious Rat ◽  
Tissue Volume ◽  
Retrotrapezoid Nucleus ◽  
Sustained Effects ◽  
Artificial Cerebrospinal Fluid ◽  
E 32 ◽  
Stimulation Of

Thyrotropin-releasing hormone (TRH) injected into the retrotrapezoid nucleus (RTN) of anesthetized rats produces a large, prolonged stimulation of ventilatory output (C. L. Cream, A. Li, and E. E. Nattie. J. Appl. Physiol. 83: 792–799, 1997). Here we inject or dialyze TRH into the RTN of conscious rats. In 6 of 17 injections (200 nl, 3.1 ± 1.7 mM), ventilation (V˙e) increased 31% by 10 min, with recovery by 60 min. With dialysis, each animal of one group ( n = 5) received, in random order, 10 mM TRH, 10 mM TRHOH (a metabolite of TRH), and artificial cerebrospinal fluid (aCSF); each animal of a second group ( n = 5) received aCSF and 1 mM TRH. TRHOH and aCSF had no sustained effects. TRH (1 mM) increasedV˙e (32%, P < 0.02, by 10 min, with recovery by 60 min), O2 consumption (V˙o 2; 19%, P < 0.03), and body (rectal) temperature (Tre; 0.5°C, P < 0.09). TRH (10 mM) increasedV˙e (78%, P < 0.01, by 10 min, with no recovery at 60 min), V˙o 2(48%, P < 0.01), and Tre (1.0°C, P < 0.01). TRH also induced arousal. The tissue volume affected in dialysis, estimated by spread of dialyzed fluorescein (332.3 mol wt, mol wt of TRH = 362.4), was 1,580 ± 256 nl for 10 mM ( n = 5) and 590 ± 128 nl for 1 mM ( n = 5). We conclude that 1) the RTN is involved in the integration ofV˙e,V˙o 2, Tre, and arousal and 2) TRH may establish the responsiveness of RTN neurons.

scholarly journals The Potential Role of Matrix Metalloproteinases 8 and 9 and Myeloperoxidase in Predicting Outcomes of Bacterial Meningitis of Childhood

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Okko Savonius ◽  
Irmeli Roine ◽  
Saeed Alassiri ◽  
Taina Tervahartiala ◽  
Otto Helve ◽  
...  
Keyword(s):  
Clinical Trial ◽  
Cerebrospinal Fluid ◽  
Matrix Metalloproteinases ◽  
Bacterial Meningitis ◽  
Confidence Interval ◽  
Potential Role ◽  
Tissue Inhibitor Of Metalloproteinase ◽  
Inflammatory Cascade ◽  
Disease Outcomes

Background. Matrix metalloproteinases (MMPs) and myeloperoxidase (MPO) contribute to the inflammatory cascade in the cerebrospinal fluid (CSF) during bacterial meningitis. We determined levels of MPO, MMP-8, MMP-9, and tissue inhibitor of metalloproteinase- (TIMP-) 1 in the CSF of children with bacterial meningitis and investigated how these inflammatory mediators relate to each other and to the disease outcomes. Methods. Clinical data and the diagnostic CSF samples from 245 children (median age eight months) with bacterial meningitis were obtained from a clinical trial in Latin America in 1996–2003. MMP-9 levels in the CSF were assessed by zymography, while MMP-8, MPO, and TIMP-1 concentrations were determined with immunofluorometric and enzyme-linked immunosorbent assays. Results. MPO correlated positively with MMP-8 (rho 0.496, P<0.001) and MMP-9 (rho 0.153, P=0.02) but negatively with TIMP-1 (rho -0.361, P<0.001). MMP-8 emerged as the best predictor of disease outcomes: a CSF MMP-8 concentration above the median increased the odds of death 4.9-fold (95% confidence interval 1.8–12.9). Conclusions. CSF MMP-8 presented as an attractive prognostic marker in children with bacterial meningitis.

Potential Role of Sponge Spicules in Influencing the Silicon Biogeochemistry of Florida Lakes

1993 ◽  
Vol 50 (2) ◽  
pp. 296-302 ◽  
Author(s):  
Daniel J. Conley ◽  
Claire L. Schelske
Keyword(s):  
Amorphous Silica ◽  
Biogenic Silica ◽  
Time Course ◽  
Potential Role ◽  
Complete Dissolution ◽  
Sediment Samples ◽  
Florida Lakes ◽  
Sponge Spicules ◽  
Time Required

Amorphous silica, e.g. biogenic silica (BSi), contained in diatoms and in sponge spicules was estimated by time course extraction from surficial sediment samples of 82 Florida lakes. Separation of diatom BSi from sponge BSi was based on the observation that diatoms completely dissolve within 2 h of digestion at 85 °C in 1% Na2CO3 whereas sponge spicules, which are generally larger than diatoms, take longer to dissolve. Sponge samples from four lakes in northern Wisconsin ranged widely in the time required to dissolve completely (1.5–12 h), but no significant differences were observed in the rates of dissolution among the lakes. In Florida lake sediments, diatom BSi averaged 49.2 (± 48.4) mg∙g−1 and sponge BSi averaged 31.5 (± 35.8) mg∙g−1, with sponge BSi comprising on average 40% of the total amorphous silica extracted. The procedure for separating diatom BSi from sponge BSi underestimates sponge BSi because smaller and/or lightly silicified components of sponges are completely dissolved early in the digestion. However, because sponge spicules comprise a significant fraction of total amorphous silica extracted, we hypothesize that sponge spicules, which on average are larger than diatoms and require a longer time for complete dissolution, may constitute an important sink for BSi in Florida lakes.

scholarly journals Noradrenergic control of central oxytocin release during lactation in rats

1998 ◽  
Vol 274 (3) ◽  
pp. E453-E458 ◽  
Author(s):  
Steven L. Bealer ◽  
William R. Crowley
Keyword(s):  
Cerebrospinal Fluid ◽  
Adrenergic Receptors ◽  
Adrenergic Receptor ◽  
Additional Experiment ◽  
Adrenergic Agonist ◽  
Magnocellular Nuclei ◽  
Artificial Cerebrospinal Fluid ◽  
Oxytocin Release ◽  
Stimulation Of

Noradrenergic systems regulate the systemic release of oxytocin (OT) in lactating rats. However, a role for norepinephrine (NE) in release of OT within the magnocellular nuclei during suckling has not been established. These studies were designed to determine 1) if suckling induces NE release in the supraoptic (SON) and paraventricular (PVN) nuclei of conscious rats and 2) the role of NE in the central, intranuclear release of OT within these nuclei. Female Holtzman rats were implanted with microdialysis probes adjacent to the PVN or SON on lactation days 8- 12. The following day, the pups were isolated from the dams for 4 h. Microdialysis probes were perfused with artificial cerebrospinal fluid (ACSF) or with ACSF containing an α- or a β-adrenergic receptor antagonist. Dialysate was collected before, during, and after suckling and analyzed for NE or OT. In an additional experiment, an α- or β-adrenergic agonist was administered via the microdialysis probes into the PVN in nonsuckled, lactating rats. Extracellular NE increased in the PVN during suckling but was not detectable in the SON. OT concentrations in dialysates from the PVN and SON significantly increased during suckling. Blockade of either α- (in both PVN and SON) or β- (PVN) adrenergic receptors prevented the suckling-induced increase in central OT release. OT release was increased in nonsuckled, lactating rats by central application of either an α- or β-adrenergic agonist. These data demonstrate that intranuclear NE release is increased in the PVN by suckling and that subsequent stimulation of both α- and β-noradrenergic receptors mediates intranuclear OT release.

Microinjection of a cyclooxygenase inhibitor into the anteroventral preoptic region attenuates LPS fever

1998 ◽  
Vol 274 (3) ◽  
pp. R783-R789 ◽  
Author(s):  
Thomas E. Scammell ◽  
John D. Griffin ◽  
Joel K. Elmquist ◽  
Clifford B. Saper
Keyword(s):  
Cerebrospinal Fluid ◽  
Body Temperature ◽  
Preoptic Area ◽  
Prostaglandin Synthesis ◽  
Cyclooxygenase Inhibitor ◽  
Preoptic Region ◽  
Considerable Evidence ◽  
Artificial Cerebrospinal Fluid ◽  
Intravenous Ketorolac

Considerable evidence supports the role of prostaglandins in fever production, but the neuroanatomic sites of prostaglandin synthesis that produce fever remain unknown. With the use of a novel microinjection technique, we injected the cyclooxygenase inhibitor ketorolac into the preoptic area (POA) to determine which preoptic regions produce the prostaglandins required for fever. Initial experiments demonstrated that intravenous ketorolac blocked the fever normally produced by lipopolysaccharide (LPS) 5 μg/kg iv. Microinjection of ketorolac into the POA had no effect on body temperature, and injection of artificial cerebrospinal fluid into the POA did not alter LPS fever. Injection of ketorolac into the anteroventral POA markedly decreased the fever produced by LPS, compared with injections into more rostral, caudal, or dorsal locations. These observations indicate that prostaglandin synthesis in the anteroventral preoptic region is necessary for the production of fever.

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