10 results on '"Nasir, Niaz"'
Search Results
2. A Review on Emerging Therapeutic Interventions for Corona Virus
- Author
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Qurban Ali, Zahid Manzoor, Shaukat Munawar, Muhammad Haseeb Khaliq, Muhammad Asif, Tanveer Ahmed, Muhammad Farrukh Nisar, Nasir Niaz, Qaiser Akram, Asim Faraz, Sheraz Ahmed Bhatti, Azhar Aslam, Muhammad Mudasser Nazir, Muhammad Arshad Javid, and Muhammad Yasir Waqas
- Abstract
The Coronavirus (SARS-CoV-2) is one of the deadliest viruses of current era and is identified as the causative agent of novel coronavirus disease-2019 (COVID-19). This disease stances a severe risk to mankind due to its unexplored pathologies. It was declared as a COVID-19 pandemic by the world health organization. This outbreak has challenged the public health concerns at large, killing the most vulnerable person, causing generalized panic and become a top debate among scientists, clinicians, physicians, pathologists, economists, athletes and politicians. Anti-viral vaccines and target drugs to treat this virus are unavailable due to its diverse genetic instability. Currently, its prevention, control and treatment are questionable as no proven remedies have been effective for its cure so far. From a research assessment, many number of drugs or medicines are being manufactured and tested at fast pace, goals and objectives are being celebrated on daily basis, and also many drugs are be subjected to clinical tests. Scientists are interested about how to provide the better care to everyone before a vaccine can be made available to common community. To stop COVID-19, effective solutions (i.e., personal protection elements, vaccines, drugs, etc.) are needed urgently. Red bells are ringing but there is no way out. Current review focuses on the ongoing regimes and therapeutic interventions for better combat with COVID-19.
- Published
- 2021
3. Intracerebroventricular injection of histamine induces the hypothalamic-pituitary-gonadal axis activation in male rats
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Burcu Üstüner, Gokcen Guvenc, Duygu Udum-Kucuksen, Elif Gokce, Begum Aydin, Burcin Altinbas, Murat Yalcin, Selim Alcay, Nasir Niaz, and Mehmed Berk Toker
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Male ,0301 basic medicine ,endocrine system ,medicine.medical_specialty ,Hypothalamus ,Hypothalamic–pituitary–gonadal axis ,Rats, Sprague-Dawley ,03 medical and health sciences ,Histamine receptor ,chemistry.chemical_compound ,Follicle-stimulating hormone ,0302 clinical medicine ,Histamine Agents ,Histamine H2 receptor ,Internal medicine ,Testis ,medicine ,Animals ,Histamine H4 receptor ,Molecular Biology ,Thioperamide ,General Neuroscience ,Histaminergic ,Spermatozoa ,Hormones ,030104 developmental biology ,Endocrinology ,chemistry ,Pituitary Gland ,Injections, Intravenous ,Receptors, Histamine ,Neurology (clinical) ,030217 neurology & neurosurgery ,Histamine ,Developmental Biology ,medicine.drug - Abstract
Brain histamine holds a key position in the regulation of behavioral states, biological rhythms, body weight, energy metabolism, thermoregulation, fluid balance, stress and reproduction in female animals. However, it is not clear whether central histamine exerts any effect on hypothalamic-pituitary-testicular in male rats and if so, the involvement of type of central histamine receptors. The current study was designed to determine the effect of centrally administrated histamine on plasma gonadotropin hormone-releasing hormone (GnRH), luteinizing hormone (LH), follicle stimulating hormone (FSH) and testosterone level, and sperm parameters, and to show the mediation of the central histaminergic H1, H2 and H3/H4 receptors on histamine-evoked hormonal and sperm parameters’ effects. Studies were performed in male Sprague-Dawley rats. A total of 50 or 100 nmol doses of histamine were injected intracerebroventricularly (icv). 100 nmol dose of histamine significantly caused increases in plasma GnRH, LH, FSH and testosterone levels of animals, but not 50 nmol dose of histamine. Moreover, central pretreatment with chlorpheniramine, histaminergic H1 receptor antagonist (100 nmol), ranitidine and histaminergic H2 receptor antagonist (100 nmol) completely prevented histamine evoked increase in plasma GnRH, LH, FSH and testosterone levels, while thioperamide, histaminergic H3/H4 receptor antagonist (100 nmol) pretreatment failed to reverse sex hormones responses to histamine. Both central histamine treatment alone and central histamine treatment after central histaminergic receptors antagonists’ pretreatments did not alter any sperm parameters in rats. In conclusion, our findings show that centrally administered histamine increases plasma GnRH, LH, FSH and testosterone levels of conscious male rats without change any sperm parameters. Moreover, according to our findings, central histaminergic H1, and H2 receptors mediate these histamine-induced effects.
- Published
- 2018
4. Extracellular vesicles and exosome: insight from physiological regulatory perspectives
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Muhammad Yasir Waqas, Muhammad Arshad Javid, Muhammad Mudasser Nazir, Nasir Niaz, Muhammad Farrukh Nisar, Zahid Manzoor, Sheraz Ahmed Bhatti, Sajid Hameed, and Muhammad Haseeb Khaliq
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Extracellular Vesicles ,Physiology ,Biological Transport ,General Medicine ,Exosomes ,Biochemistry ,Biomarkers ,Signal Transduction - Abstract
The current study highlights prospective mechanisms of biogenesis of extracellular vesicles (EVs) and potential involvement in cellular signaling and transport with great emphasis to illustrate their role as biomarkers in certain pathologies. The current review highlights EVs, the heterogeneous entities secreted by cells in highly conserved manner. A series of consensus terminologies for various types is yet to be organized. Exosomes, microvesicles and apoptotic bodies are major populations among EVs. EVs are key regulators in cellular physiological homeostasis, disease progression and evolve either from plasma membrane (microvesicles) or fusion of endosomes with exosomes. However, how vesicular inclusions elicit a plethora of biological responses is still not much clear. However, how these vesicular inclusions get packaged and delivered by these EVs shows great involvement in inter- and intracellular cellular signaling and channeling of multiple proteins, variety of RNAs and certain fat molecules. It's worth to mention that EVs carry small non-coding RNAs (snRNAs) which are involved in multiple cellular molecular events at targeted sites. Moreover, snRNA trafficking through exosomes and microvesicles depicts remarkable potential as non-invasive biomarkers in different clinical disorders especially immune system pathologies, cardiovascular issues, and metabolic syndromes.
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- 2021
5. The acute cardiorespiratory effects of centrally injected arachidonic acid; the mediation of prostaglandin E, D and F 2α
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Murat Yalcin, Leman Gizem Erkan, Nasir Niaz, Gokcen Guvenc, Begum Aydin, Burcin Altinbas, Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı., Erkan, Leman Gizem, Altınbaş, Burçin, Güvenç, Gökçen, Aydın, Begüm, Niaz, Nasir, Yalçın, Murat, AAR-6815-2021, AAC-4975-2022, and AAG-6956-2021
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Male ,Central histaminergic system ,Thromboxane ,medicine.medical_treatment ,Prostaglandins D ,Partial oxygen pressure ,Antagonists and inhibitors ,Time factor ,Cardiovascular agent ,0302 clinical medicine ,Partial carbon dioxide pressure ,Histamine H4 Receptors ,Thioperamide ,Intracerebroventricular Drug Administration ,Intracerebroventricular drug administration ,Neurotransmitter ,Respiratory rate ,Respiration ,Cardiovascular effect ,Prostaglandins E ,Thromboxane signaling pathway ,Breathing ,Intracerebroventricular ,Hemorrhaged hypotensive rats ,Arachidonic acid ,Prostaglandin E ,Pulmonary and Respiratory Medicine ,medicine.medical_specialty ,Xanthones ,Heart rate ,Prostaglandin ,Prostaglandins F ,Article ,Thromboxane A2 ,03 medical and health sciences ,Infusions, intraventricular ,6-isopropoxy-9-oxoxanthene-2-carboxylic acid ,Animal model ,Animal experiment ,Animal ,Time factors ,Peripheral mechanisms ,6 isopropoxy 9 oxo 2 xanthenecarboxylic acid ,Mean blood pressure ,030104 developmental biology ,Endocrinology ,Xanthone derivative ,chemistry ,Rat ,Prostaglandin F ,030217 neurology & neurosurgery ,Respiratory function ,0301 basic medicine ,Respiratory system agents ,Phospholipase a(2) activator ,Rats, sprague-dawley ,Physiology ,Blood gas ,Tidal volume ,chemistry.chemical_compound ,Hyperventilation ,Prostaglandin receptor ,Priority journal ,PGD ,Normotensive rats ,PGE ,General Neuroscience ,Cardiovascular regulation ,Receptor antagonist ,Respiratory tract agent ,Sprague dawley rat ,PGF2α ,Blood pressure ,Prostaglandin D ,lipids (amino acids, peptides, and proteins) ,Breathing movements ,medicine.symptom ,Respiratory minute ventilation ,Adult ,Carbon dioxide tension ,medicine.drug_class ,Receptors, prostaglandin ,Respiratory system ,Prostaglandin F2 alpha ,Blood gas analysis ,Internal medicine ,Bradycardia ,medicine ,Animals ,Oxygen tension ,Dimethylamine ,Drug effects ,Prostanoid ,Cardiovascular agents ,Nonhuman ,Metabolism ,Fetal sheep ,Controlled study - Abstract
Arachidonic acid (AA), which is released from synaptic membrane phospholipid by neuroreceptor-initiated activation of phospholipase A(2), is abundant in the brain and works as a neurotransmitter and/or neuromodulator in the central nervous system. Recently we reported that centrally injected AA generated pressor and hyperventilation effects by activating thromboxane A(2) (TXA(2)) signaling pathway. The present study was designed to investigate the mediation of other metabolites of AA such as prostaglandin (PG) D, PGE and PGF(2 alpha), alongside TXA(2) in the AA-evoked cardiorespiratory effects in anaesthetized rats. Intracerebroventricular (i.c.v.) administration of AA caused pressor, bradycardic and hyperventilation responses by increasing pO(2) and decreasing pCO(2) in adult male anaesthetized Sprague Dawley rats. Pretreatment (i.c.v) with different doses of DP/EP prostanoid receptor antagonist, AH6809 or FP prostanoid receptor antagonist, PGF(2 alpha), dimethylamine partially blocked the cardiorespiratory and blood gas changes induced by AA. In conclusion, these data plainly report that central PGD, PGE or PGF(2 alpha) might mediate, at least partly, centrally administered AA-evoked cardiorespiratory and blood gas responses.
- Published
- 2017
6. Contingent role of phoenixin and nesfatin‐1 on secretions of the male reproductive hormones
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Ebru Ozyurt, Aysenur Bas, Gokcen Guvenc, Murat Yalcin, Duygu Udum, Esra Kasikci, Burcin Altinbas, and Nasir Niaz
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Male ,Pituitary gland ,medicine.medical_specialty ,Peptide Hormones ,Urology ,Neuropeptide ,Hypothalamic–pituitary–gonadal axis ,Male sex hormones ,Biology ,Gonadotropin-Releasing Hormone ,Endocrinology ,Internal medicine ,medicine ,Animals ,Nucleobindins ,Testosterone ,Rats, Wistar ,Hypothalamic Hormones ,Reproductive hormones ,General Medicine ,medicine.anatomical_structure ,Hypothalamus ,Gonadotropins, Pituitary ,Hormone - Abstract
Phoenixin (PNX) and nesfatin-1 are localised in the hypothalamus and the pituitary gland. Moreover, the most of the PNX-expressing neurons in the hypothalamus also co-express nesfatin-1. These outcomes may suggest that there is an interaction between PNX and nesfatin-1, at least in terms of neuroendocrine-mediated regulations. Hence, the study was planned to find out the effects of centrally delivered PNX and nesfatin-1 on male sex hormones or to show the interactive association of intracerebroventricularly (ICV) injected PNX+nesfatin-1 combination on the release of male hormones. PNX and nesfatin-1, single or together, were delivered ICV to different male Wistar Albino rat groups. Both PNX and nesfatin-1 induced a significant enhancement in plasma FSH, LH and testosterone without inducing any alteration in plasma GnRH in the rats. The central combinatorial treatment of both the neuropeptides produced a more potent rise in male plasma hormone levels than treating with single neuropeptide. In summary, our preliminary data show that centrally delivered PNX and nesfatin-1 can affect plasma male hormone levels. Moreover, that the combinatorial treatment with both the neuropeptides in male rats leading to a more potent effect on the plasma male hormone levels might suggest that both these neuropeptides act synergistically in terms of regulation of male HPGA.
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- 2019
7. Modulation of nesfatin-1-induced cardiovascular effects by the central cholinergic system
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Murat Yalcin, Burcin Altinbas, Nasir Niaz, Gokcen Guvenc, and Begum Aydin
- Subjects
0301 basic medicine ,Male ,Vasopressin ,medicine.medical_specialty ,Vasopressins ,Cholinergic Agents ,Blood Pressure ,Nerve Tissue Proteins ,Mecamylamine ,Rats, Sprague-Dawley ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Endocrinology ,Catecholamines ,Heart Rate ,Internal medicine ,Renin–angiotensin system ,Muscarinic acetylcholine receptor ,medicine ,Animals ,Nucleobindins ,Vasoconstrictor Agents ,Endocrine and Autonomic Systems ,business.industry ,Calcium-Binding Proteins ,Brain ,General Medicine ,Acetylcholine ,DNA-Binding Proteins ,030104 developmental biology ,Nicotinic agonist ,Neurology ,Catecholamine ,Cholinergic ,Hypotension ,business ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Nesfatin-1, a peptide whose receptor is yet to be identified, has been shown to be involved in the modulation of feeding, stress, and metabolic responses. Recently, increasing evidence has supported a modulatory role of nesfatin-1 in cardiovascular activity. We have previously reported that nesfatin-1 causes an increase in blood pressure in normotensive and hypotensive rats by increasing plasma catecholamine, vasopressin, and renin levels. Recent reports suggest that nesfatin-1 may activate the central cholinergic system. However, there is no evidence showing an interaction between central nesfatin-1 and the cholinergic system. Therefore, this study aimed to determine whether the central cholinergic system may have a functional role in the nesfatin-1-induced cardiovascular effect observed in normotensive rats. Intracerebroventricular injection of nesfatin-1 caused short-term increases in mean arterial pressure and heart rate responses including bradycardic/tachycardic phases in normotensive animals. Central injection of nesfatin-1 increased the acetylcholine and choline levels in the posterior hypothalamus, as shown in microdialysis studies. Central pretreatment with the cholinergic muscarinic receptor antagonist atropine and/or nicotinic receptor antagonist mecamylamine blocked nesfatin-1-induced cardiovascular effects. In conclusion, the results show that centrally administered nesfatin-1 produces a pressor effect on blood pressure and heart rate responses including bradycardic/tachycardic phases in normotensive rats. Moreover, according to our findings, the central cholinergic system can modulate nesfatin-1-evoked cardiovascular activity.
- Published
- 2018
8. The acute cardiorespiratory effects of centrally injected arachidonic acid; the mediation of prostaglandin E, D and F
- Author
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Leman Gizem, Erkan, Burcin, Altinbas, Gokcen, Guvenc, Begum, Aydin, Nasir, Niaz, and Murat, Yalcin
- Subjects
Male ,Arachidonic Acid ,Time Factors ,Prostaglandins D ,Prostaglandins E ,Respiration ,Xanthones ,Prostaglandins F ,Receptors, Prostaglandin ,Respiratory System Agents ,Blood Pressure ,Cardiovascular Agents ,Rats, Sprague-Dawley ,Thromboxane A2 ,Infusions, Intraventricular ,Animals ,Blood Gas Analysis - Abstract
Arachidonic acid (AA), which is released from synaptic membrane phospholipid by neuroreceptor-initiated activation of phospholipase A
- Published
- 2016
9. Histamine restores hemorrhage induced hypotension by activating cholinergic neurons in nucleus tractus solitarius
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Leman Gizem Erkan, Gokcen Guvenc, Burcin Altinbas, Nasir Niaz, Murat Yalcin, Tuncay Ilhan, Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı., Uludağ Üniversitesi/Veteriner Fakültesi/Histoloji ve Embriyoloji Anabilim Dalı., Altınbaş, Burçin, Güvenç, Gökçen, Erkan, Leman G., İlhan, Tuncay, Niaz, Nasir, Yalçın, Murat, AAG-6956-2021, AAH-8859-2021, AAR-6815-2021, and AAC-4975-2022
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Male ,0301 basic medicine ,Injection ,Hemorrhagic hypotension ,Microdialysis ,Freely moving rat ,Arachidonic-acid ,Functional connectivity ,chemistry.chemical_compound ,Immunoreactivity ,0302 clinical medicine ,Histamine H2 receptor ,Histamine H4 Receptors ,Thioperamide ,Intracerebroventricular Drug Administration ,Priority journal ,Cholinergic stimulation ,Histamine H1 receptor ,Chemistry ,General Neuroscience ,Cardiovascular regulation ,Nucleus tractus solitarius ,Injected melittin ,Cardiovascular effect ,Cholinergic nerve cell ,Modulate acetylcholine-release ,Extracellular matrix ,Immunohistochemistry ,Mean arterial pressure ,Cardiovascular system ,Endogenous central histamine ,Acetylcholinesterase ,Hypotension ,Histamine H3 receptor ,Animal cell ,Histamine ,medicine.drug ,Adult ,Chlorpheniramine ,medicine.medical_specialty ,Sodium chloride ,Heart rate ,Central cholinergic system ,Neurosciences & neurology ,Ranitidine ,Article ,03 medical and health sciences ,Internal medicine ,medicine ,Animal experiment ,Histamine H4 receptor ,Molecular Biology ,Thromboxane A(2) ,Neurosciences ,Hemodynamics ,Histaminergic ,Cholinergic system ,Induced reversal ,Cholinesterase ,Nonhuman ,Solitary tract nucleus ,Drug efficacy ,030104 developmental biology ,Endocrinology ,nervous system ,Dual-probe microdialysis ,Rat ,Cholinergic ,Neurology (clinical) ,Ventral striatum ,Controlled study ,030217 neurology & neurosurgery ,Developmental Biology - Abstract
The purpose of the current study is to investigate the functional connections between the central histaminergic and cholinergic systems at NTS level in hypotensive condition. Experiments were carried out in male Wistar Albino rats. The hypotension was achieved by withdrawing a total volume of 1.5 ml blood/100 g bodyweight over a period of 10 min. A microdialysis study was performed in NTS area to measure extracellular ACh and Ch levels. The hemorrhage produced a severe and long-lasting decrease in mean arterial blood pressure (MAP) and increase in extracellular ACh and Ch levels in NTS. Administration of histamine intracerebroventricularly (i.c.v.) or into the NTS reversed the hemorrhagic hypotension by increasing MAP and heart rate. I.c.v. injection of histamine also caused the additional increase in extracellular ACh and Ch levels. Moreover, central histamine injection augmented intracytoplasmic AChE immunoreactivity in NTS. These changes were completely blocked by histaminergic H1 receptor antagonist chlorpheniramine, but histaminergic H2 receptor blocker ranitidine and histaminergic H3/H4 receptor antagonist thioperamide failed to produce these effects. In conclusion, these findings are interpreted that brain histaminergic H1 receptor activation by central histamine injection may promote cholinergic stimulation in the NTS and subsequently reverses the hypotension.
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- 2016
10. The Effects Of Centrally Injected Arachidonic Acid On Respiratory System: Involvement Of Cyclooxygenase To Thromboxane Signaling Pathway
- Author
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Leman Gizem Erkan, Murat Yalcin, Gokcen Guvenc, Nasir Niaz, Burcin Altinbas, Uludağ Üniversitesi/Veteriner Fakültesi/Fizyoloji Anabilim Dalı., Erkan, Leman Gizem, Güvenç, Gökçen, Altınbaş, Burçin, Niaz, Nasır, Yalçın, Murat, AAR-6815-2021, and AAG-6956-2021
- Subjects
0301 basic medicine ,Male ,Time Factors ,Thromboxane ,Physiology ,Central histaminergic system ,Respiratory System ,Respiratory System Agents ,Peripheral mechanism ,Ibuprofen ,Partial oxygen pressure ,Pharmacology ,Signal transduction ,Time factor ,Pressor ,Blood gas ,Rats, Sprague-Dawley ,Thromboxane A2 ,chemistry.chemical_compound ,0302 clinical medicine ,Lung minute volume ,Partial carbon dioxide pressure ,Histamine H4 Receptors ,Thioperamide ,Intracerebroventricular Drug Administration ,Hyperventilation ,Anesthesia ,Intracerebroventricular drug administration ,Respiratory system ,Enzyme Inhibitors ,Priority journal ,Arachidonic Acid ,biology ,Chemistry ,General Neuroscience ,Respiratory rate ,Respiration ,Fetal lambs ,Enzyme inhibitor ,Prostaglandin synthase ,Respiratory tract agent ,Cyclooxygenase ,Sprague dawley rat ,Blood ,Biochemistry ,Breathing ,Intracerebroventricular ,Cascade ,Arachidonic acid ,Hemorrhaged hypotensive rats ,medicine.symptom ,Breathing movements ,Respiratory minute ventilation ,circulatory and respiratory physiology ,Pulmonary and Respiratory Medicine ,Adult ,Gas analysis equipment ,Carbon dioxide tension ,Breathing rate ,Article ,03 medical and health sciences ,Dose response ,medicine ,Tidal Volume ,Animals ,Animal experiment ,Oxygen tension ,Benzofurans ,Injections, Intraventricular ,Chronotherapy ,Drug effects ,Dose-Response Relationship, Drug ,Animal ,Phospholipase A(2) activator ,Melittin ,Carbon Dioxide ,Nonhuman ,Oxygen ,030104 developmental biology ,Metabolism ,Prostaglandin-Endoperoxide Synthases ,biology.protein ,Benzofuran derivative ,Enzymology ,Rat ,Furegrelate ,Controlled study ,030217 neurology & neurosurgery ,Respiratory minute volume ,Respiratory function - Abstract
Arachidonic acid (AA) is a polyunsaturated fatty acid that is present in the phospholipids of the cell membranes of the body and is abundant in the brain. Exogenously administered AA has been shown to affect brain metabolism and to exhibit cardiovascular and neuroendocrine actions. However, little is known regarding its respiratory actions and/or central mechanism of its respiratory effects. Therefore, the present study was designed to investigate the possible effects of centrally injected AA on respiratory system and the mediation of the central cyclooxygenase (COX) to thromboxane A2 (TXA2) signaling pathway on AA-induced respiratory effects in anaesthetized rats. Intracerebroventricular (i.c.v.) administration of AA induced dose- and time-dependent increase in tidal volume, respiratory rates and respiratory minute ventilation and also caused an increase in partial oxygen pressure (pO2) and decrease in partial carbon dioxide pressure (pCO2) in male anaesthetized Sprague Dawley rats. I.c.v. pretreatment with ibuprofen, a non-selective COX inhibitor, completely blocked the hyperventilation and blood gases changes induced by AA. In addition, central pretreatment with different doses of furegrelate, a TXA2 synthesis inhibitor, also partially prevented AA-evoked hyperventilation and blood gases effects. These data explicitly show that centrally administered AA induces hyperventilation with increasing pO2 and decreasing pCO2 levels which are mediated by the activation of central COX to TXA(2) signaling pathway. (C) 2016 Elsevier B.V. All rights reserved.
- Published
- 2016
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