Role of dopamine and arterial chemoreceptors in thermal tachypnea in conscious cats

1990 ◽  
Vol 69 (4) ◽  
pp. 1429-1434 ◽  
Author(s):  
M. Bonora ◽  
H. Gautier
Keyword(s):  
Heat Loss ◽  
Blood Brain Barrier ◽  
Intravenous Injection ◽  
Respiratory Frequency ◽  
Brain Barrier ◽  
Intracerebral Injection ◽  
Principal Mechanism ◽  
Warm Environment ◽  
Blood Brain ◽  
Loss Mechanisms

In mammals submitted to a warm environment, intracerebral injection of dopamine (DA) produces no change or an increase in body temperature accompanied by an increase in metabolic heat production, but its effect on heat loss mechanisms such as vasodilation and tachypnea is not clear. Because the principal mechanism of heat loss in the conscious cat is thermal tachypnea, we studied the influence of DA on thermal tachypnea in response to heat stress (ambient temperature = 33-36 degrees C) in five conscious cats. We first studied the steady-state response to a DA agonist, apomorphine, which crosses the blood-brain barrier. Intravenous injection of apomorphine greatly reduced thermal tachypnea by decreasing respiratory frequency (from 94.9 to 52.5 breaths/min) and increasing tidal volume (from 13.2 to 20.4 ml). The subsequent injection of the DA antagonist haloperidol, which also crosses the blood-brain barrier, restored the initial tachypnea. To further investigate the mechanism involved in thermal tachypnea, we studied the influence of peripheral chemoreceptors by transiently stimulating or inhibiting carotid body (CB) activity during tachypneic breathing. CB stimulation by intravenous injection of NaCN or domperidone reduced thermal tachypnea mainly by decreasing the respiratory frequency, whereas CB inhibition by DA tended to increase frequency and thus tachypnea. It is concluded that 1) in a warm environment, central DA receptors are also greatly involved in heat loss mechanisms, 2) arterial chemoreceptor input appears to counteract this tachypneic breathing, and 3) thermal and hypoxic tachypnea may be controlled by the same mechanism in which a DA-like system has a key role.

scholarly journals Intravenous injection of cyclophilin A realizes the transient and reversible opening of barrier of neural vasculature through basigin in endothelial cells

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Narumi Nakada-Honda ◽  
Dan Cui ◽  
Satoshi Matsuda ◽  
Eiji Ikeda
Keyword(s):  
Endothelial Cells ◽  
Single Dose ◽  
Blood Brain Barrier ◽  
Intravenous Injection ◽  
Cyclophilin A ◽  
Brain Barrier ◽  
Blood Brain ◽  
Neural Tissues ◽  
Neural Diseases

AbstractNeural vasculature forms the blood–brain barrier against the delivery of systemically administered therapeutic drugs into parenchyma of neural tissues. Therefore, procedures to open the blood–brain barrier with minimal damage to tissues would lead to the great progress in therapeutic strategy for intractable neural diseases. In this study, through analyses with mouse in vitro brain microvascular endothelial cells and in vivo neural vasculature, we demonstrate that the administration of cyclophilin A (CypA), a ligand of basigin which is expressed in barrier-forming endothelial cells, realizes the artificial opening of blood–brain barrier. Monolayers of endothelial cells lost their barrier properties through the disappearance of claudin-5, an integral tight junction molecule, from cell membranes in a transient and reversible manner. Furthermore, the intravenous injection of a single dose of CypA into mice resulted in the opening of blood–brain barrier for a certain period which enabled the enhanced delivery of systemically administered doxorubicin into the parenchyma of neural tissues. These findings that the pre-injection of a single dose of CypA realizes an artificial, transient as well as reversible opening of blood–brain barrier are considered to be a great step toward the establishment of therapeutic protocols to overcome the intractability of neural diseases.

Blut-Hirn-Schranke und Placentar-Schranke für H-Thymidin und H-Cytidin bei der Maus / Blood-Brain-Barrier and Placental-Barrier for H-Thymidine and H-Cytidine in the Mouse

1972 ◽  
Vol 27 (5) ◽  
pp. 554-558b ◽  
Author(s):  
B. Schultze ◽  
N. Hörning ◽  
W. Maurer
Keyword(s):  
Blood Brain Barrier ◽  
Intravenous Injection ◽  
Brain Barrier ◽  
Whole Body ◽  
Placental Barrier ◽  
Whole Body Autoradiography ◽  
Blood Brain ◽  
Pregnant Mice ◽  
Distribution In The Organism

The distribution in the organism of the mouse of free 3H-thymidine and 3H-cytidine was studied 1, 2½, 5 and 15 minutes after intravenous injection into normal and pregnant mice (20th day) using whole body autoradiography. The grain density measured over brain and fetus is 10 times smaller as compared to other tissues of the organism. This means that a blood brain barrier and placental barrier for thymidine and cytidine exists.

Berberine Protects against Neurological Impairments and Blood-Brain Barrier Injury in Mouse Model of Intracerebral Hemorrhage

2021 ◽  
pp. 1-10
Author(s):  
Xiuwen Wu ◽  
Xiaopeng Liu ◽  
Liang Yang ◽  
Yuanyu Wang
Keyword(s):  
Intracerebral Hemorrhage ◽  
Blood Brain Barrier ◽  
Inflammatory Responses ◽  
Brain Barrier ◽  
Neurological Deficits ◽  
Peroxisome Proliferator ◽  
Intracerebral Injection ◽  
Neuroprotective Effects ◽  
Blood Brain ◽  
Autologous Whole Blood

<b><i>Background:</i></b> Elevation of AMP-activated protein kinase (AMPK)/peroxisome proliferator-activated receptor-γ coactivator-1α (PGC1α) signaling can suppress intracerebral hemorrhage (ICH)-induced neurological impairments. As an isoquinoline alkaloid, Berberine exerts neuroprotective effects in neurological disease models with activated AMPK/PGC1α signaling. <b><i>Aim:</i></b> We aim to study the effect of Berberine on ICH-induced brain injury and explore the potential molecular mechanism. <b><i>Methods:</i></b> ICH model was established in mice through intracerebral injection of autologous whole blood, followed by treatment with Berberine. Neurological impairments were assessed by the modified neurological severity score and behavioral assays. Brain edema and blood-brain barrier (BBB) integrity were assessed by water content in the brain, amount of extravasated Evans blue, and BBB tight junction components. Neuroinflammatory responses were assessed by inflammatory cytokine levels. AMPK/PGC1α signaling was examined by AMPK mRNA expression and phosphorylated AMPK and PGC1α protein levels. <b><i>Results:</i></b> Berberine (200 mg/kg) attenuated ICH-induced neurological deficits, motor and cognitive impairment, and BBB disruption. Berberine also suppressed ICH-induced inflammatory responses indicated by reduced production of inflammatory cytokines. Finally, Berberine drastically elevated AMPK/PGC1α signaling in the hemisphere of ICH mice. <b><i>Conclusion:</i></b> Our findings suggest that Berberine plays an important neuroprotective role against ICH-induced neurological impairments and BBB injury, probably by inhibition of inflammation and activation of AMPK/PGC1α signaling.

scholarly journals Safe long-term repeated disruption of the blood-brain barrier using an implantable ultrasound device: a multiparametric study in a primate model

2017 ◽  
Vol 126 (4) ◽  
pp. 1351-1361 ◽  
Author(s):  
Catherine Horodyckid ◽  
Michael Canney ◽  
Alexandre Vignot ◽  
Raphael Boisgard ◽  
Aurélie Drier ◽  
...  
Keyword(s):  
Blood Brain Barrier ◽  
Intravenous Injection ◽  
Cerebral Metabolism ◽  
Brain Barrier ◽  
Histopathological Analysis ◽  
Large Animal ◽  
Papio Anubis ◽  
Primate Model ◽  
Blood Brain ◽  
Bbb Opening

OBJECTIVE The main limitation to the efficacy of chemotherapy for brain tumors is the restricted access to the brain because of the limited permeability of the blood-brain barrier (BBB). Previous animal studies have shown that the application of pulsed ultrasound (US), in combination with the intravenous injection of microbubbles, can temporarily disrupt the BBB to deliver drugs that normally cannot reach brain tissue. Although many previous studies have been performed with external focused US transducers, the device described in the current work emits US energy using an unfocused transducer implanted in the skull thickness. This method avoids distortion of the US energy by the skull bone and allows for simple, repetitive, and broad disruption of the BBB without the need for MRI monitoring. The purpose of the present study was to determine if the BBB can be safely and repeatedly disrupted using such an implantable unfocused US device in a primate model. METHODS An 11.5-mm-diameter, 1-MHz, planar US device was implanted via a bur hole into the skull of 3 primates (2 Papio anubis [olive] baboons and 1 Macaca fascicularis [macaque]) for 4 months. Pulsed US sonications were applied together with the simultaneous intravenous injection of sulfur hexafluoride microbubbles (SonoVue) every 2 weeks to temporarily disrupt the BBB. In each primate, a total of 7 sonications were performed with a 23.2-msec burst length (25,000 cycles) and a 1-Hz pulse repetition frequency at acoustic pressure levels of 0.6–0.8 MPa. Potential toxicity induced by repeated BBB opening was analyzed using MRI, PET, electroencephalography (EEG), somatosensory evoked potential (SSEP) monitoring, behavioral scales, and histopathological analysis. RESULTS The T1-weighted contrast-enhanced MR images acquired after each sonication exhibited a zone of hypersignal underneath the transducer that persisted for more than 4 hours, indicating a broad region of BBB opening in the acoustic field of the implant. Positron emission tomography images with fluorine-18–labeled fluorodeoxyglucose (FDG) did not indicate any changes in the cerebral metabolism of glucose. Neither epileptic signs nor pathological central nerve conduction was observed on EEG and SSEP recordings, respectively. Behavior in all animals remained normal. Histological analysis showed no hemorrhagic processes, no petechia, and extravasation of only a few erythrocytes. CONCLUSIONS The studies performed confirm that an implantable, 1-MHz US device can be used to repeatedly open the BBB broadly in a large-animal model without inducing any acute, subacute, or chronic lesions.

Effects of peripheral CCK receptor blockade on gastric emptying in rats

2003 ◽  
Vol 284 (1) ◽  
pp. R66-R75 ◽  
Author(s):  
Roger D. Reidelberger ◽  
Linda Kelsey ◽  
Dean Heimann ◽  
Martin Hulce
Keyword(s):  
Gastric Emptying ◽  
Blood Brain Barrier ◽  
Intravenous Injection ◽  
Intravenous Infusion ◽  
Brain Barrier ◽  
Receptor Blockade ◽  
Induced Responses ◽  
Barrier Permeability ◽  
Blood Brain ◽  
Brain Barrier Permeability

Type A CCK receptor (CCKAR) antagonists differing in blood-brain barrier permeability [devazepide penetrates; the dicyclohexylammonium salt of Nα-3-quinolinoyl-d-Glu- N,N-dipentylamide (A-70104) does not] were used to test the hypothesis that duodenal nutrient-induced inhibition of gastric emptying is mediated by CCKARs located peripheral to the blood-brain barrier. Rats received A-70104 (700 or 3,000 nmol · kg−1· h−1iv) or devazepide (2.5 μmol/kg iv) and either a 15-min intravenous infusion of CCK-8 (3 nmol · kg−1· h−1) or duodenal infusion of casein, peptone, Intralipid, or maltose. Gastric emptying of saline was measured during the last 5 min of each infusion. A-70104 and devazepide abolished the gastric emptying response to a maximal inhibitory dose of CCK-8. Each of the macronutrients inhibited gastric emptying. A-70104 and devazepide attenuated inhibitory responses to each macronutrient. Intravenous injection of a CCK antibody to immunoneutralize circulating CCK had no effect on peptone or Intralipid-induced responses. Thus endogenous CCK appears to act in part by a paracrine or neurocrine mechanism at CCKARs peripheral to the blood-brain barrier to inhibit gastric emptying.

scholarly journals Recruitment of Neutrophils across the Blood–Brain Barrier: The Role of E- and P-selectins

2001 ◽  
Vol 21 (9) ◽  
pp. 1115-1124 ◽  
Author(s):  
Martine Bernardes-Silva ◽  
Daniel C. Anthony ◽  
Andrew C. Issekutz ◽  
V. Hugh Perry
Keyword(s):  
Blood Brain Barrier ◽  
Acute Inflammation ◽  
Brain Parenchyma ◽  
Neutrophil Recruitment ◽  
Brain Barrier ◽  
Intracerebral Injection ◽  
Juvenile Rats ◽  
Blood Brain ◽  
Barrier Breakdown ◽  
The Brain

The adult central nervous system parenchyma is resistant to inflammation, but in juvenile rats the injection of inflammatory mediators, interleukin-1β for example, gives rise to extensive neutrophil recruitment and neutrophil-dependent blood–brain barrier breakdown. The factors that confer this resistant phenotype are unknown. In this study, the authors demonstrate that E- and P-selectin expression is increased to a similar extent in adult and juvenile brain after the intracerebral injection of IL-1β. Thus, the refractory nature of the brain parenchyma cannot be attributed to an absence of selectin expression. However, in injuries where the resistant characteristic of the brain parenchyma is compromised, and neutrophil recruitment occurs, selectin blockade may be an advantage. The authors investigated the contribution that selectins make to neutrophil recruitment during acute inflammation in the brain. The authors examined neutrophil recruitment by immunohistochemistry on brain sections of juvenile rats killed four hours after the intracerebral injection of IL-1β and the intravenous injection of neutralizing anti-selectin monoclonal antibodies (mAb). The administration of the P-selectin blocking mAb inhibited neutrophil recruitment by 85% compared with controls. Surprisingly, E-selectin blockade had no effect on neutrophil recruitment to the brain parenchyma. Thus, P-selectin appears to play a pivotal role in mediating neutrophil recruitment to the brain parenchyma during acute inflammation.

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