Page last updated: 2024-10-17

chlorine and Apoplexy

chlorine has been researched along with Apoplexy in 21 studies

chloride : A halide anion formed when chlorine picks up an electron to form an an anion.

Research Excerpts

ExcerptRelevanceReference
"Ferric chloride-induced distal middle cerebral artery occlusion (MCAO) model of stroke was described in mice several years ago, however it lacked in-depth evaluation of the post-stroke functional outcomes in the animals."7.96Motor deficit in the mouse ferric chloride-induced distal middle cerebral artery occlusion model of stroke. ( Alamri, FF; Arumugam, TV; Jayaraman, S; Karamyan, ST; Karamyan, VT; Lee, P; Syeara, N, 2020)
"0) had significantly higher odds of death within 90 days after adjustment for age, race and ethnicity, National Institutes of Health Stroke Scale score strata, hematoma volume, presence or absence of intraventricular hemorrhage, cigarette smoking, previous stroke, and maximum hourly dose of nicardipine."4.12Early Hyperchloremia is Independently Associated with Death or Disability in Patients with Intracerebral Hemorrhage. ( Hanley, DF; Hsu, CY; Huang, W; Malhotra, K; Martin, RH; Qureshi, AI; Steiner, T; Suarez, JI; Toyoda, K; Yamamoto, H, 2022)
"Ferric chloride-induced distal middle cerebral artery occlusion (MCAO) model of stroke was described in mice several years ago, however it lacked in-depth evaluation of the post-stroke functional outcomes in the animals."3.96Motor deficit in the mouse ferric chloride-induced distal middle cerebral artery occlusion model of stroke. ( Alamri, FF; Arumugam, TV; Jayaraman, S; Karamyan, ST; Karamyan, VT; Lee, P; Syeara, N, 2020)
"Stroke is one of the major causes of death and disability worldwide."2.55Chloride co-transporters as possible therapeutic targets for stroke. ( Darlison, MG; Martín-Aragón Baudel, MA; Poole, AV, 2017)
"SLC26A11 inhibition ameliorates infarct formation and improves functional recovery."1.91SLC26A11 Inhibition Reduces Oncotic Neuronal Death and Attenuates Stroke Reperfusion Injury. ( Chen, B; Gao, Y; Liao, P; Low, SW; Nilius, B; Poore, CP; Wei, S, 2023)
"Ischaemic stroke is very rarely reported in osteopetrosis, resulting from vascular impingement."1.72Haemodynamic stroke in a rare adult presentation of osteopetrosis. ( Benjamin, RN; Jasper, A; Lionel, SA; Ninan, GA, 2022)
"Dual treatment with aspirin (5 mg kg(-1) ) and clopidogel (0."1.43A rabbit model of cerebral microembolic signals for translational research: preclinical validation for aspirin and clopidogrel. ( Chu, L; Desai, K; Gutstein, DE; Kurowski, S; Seiffert, D; Wang, X; Wu, W; Zhou, X, 2016)

Research

Studies (21)

TimeframeStudies, this research(%)All Research%
pre-19901 (4.76)18.7374
1990's0 (0.00)18.2507
2000's7 (33.33)29.6817
2010's7 (33.33)24.3611
2020's6 (28.57)2.80

Authors

AuthorsStudies
Qureshi, AI1
Huang, W1
Hanley, DF1
Hsu, CY1
Martin, RH1
Malhotra, K1
Steiner, T1
Suarez, JI1
Yamamoto, H1
Toyoda, K1
Wang, L1
Sheng, G1
Cui, J1
Yao, Y1
Bai, X1
Chen, F1
Yu, W1
Ninan, GA1
Benjamin, RN1
Jasper, A1
Lionel, SA1
Hugues, N1
Pin-Barre, C1
Brioche, T1
Pellegrino, C1
Berton, E1
Rivera, C1
Laurin, J1
Wei, S1
Chen, B1
Low, SW1
Poore, CP1
Gao, Y1
Nilius, B1
Liao, P1
Syeara, N1
Alamri, FF1
Jayaraman, S1
Lee, P1
Karamyan, ST1
Arumugam, TV1
Karamyan, VT1
Bei, HZ1
You, SJ1
Zheng, D1
Zhong, CK1
Du, HP1
Zhang, Y1
Lu, TS1
Cao, LD1
Dong, XF1
Cao, YJ1
Liu, CF1
Yang, J1
Chen, J1
Del Carmen Vitery, M1
Osei-Owusu, J1
Chu, J1
Yu, H1
Sun, S1
Qiu, Z1
Pan, R1
Timmins, GS1
Liu, W1
Liu, KJ1
Zhou, X1
Kurowski, S1
Wu, W1
Desai, K1
Chu, L1
Gutstein, DE1
Seiffert, D1
Wang, X1
Martín-Aragón Baudel, MA1
Poole, AV1
Darlison, MG1
STENNING, JC1
Zhang, YP1
Zhang, H1
Duan, DD1
Alam, MN1
Uddin, MJ1
Rahman, KM1
Ahmed, S1
Akhter, M1
Nahar, N1
Swapan, MK1
Alam, MM2
Sultana, N1
Hallaz, MM1
Uddin, MM1
Bari, MS1
Israil, MA1
Limbrick, DD2
Sombati, S2
DeLorenzo, RJ2
Music, M1
Schmidlin, O2
Tanaka, M2
Bollen, AW1
Yi, SL2
Morris, RC2
Solini, A1
Zamboni, P1
Passaro, A1
Fellin, R1
Ferrannini, E1
Deshpande, LS1
Ahmad, S1
Olson, JL1

Clinical Trials (1)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Antihypertensive Treatment of Acute Cerebral Hemorrhage (ATACH)-II: A Phase III Randomized Multicenter Clinical Trial of Blood Pressure Reduction for Hypertension in Acute Intracerebral Hemorrhage[NCT01176565]Phase 31,000 participants (Actual)Interventional2011-05-15Terminated (stopped due to Planned interim analysis: no significant outcome differences between groups)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Any Serious Adverse Event Within the 90-day Study Period

The complete count of all subjects who experienced any serious adverse events throughout their participation in the trial was included in this tabulation. Adverse events (AEs) and serious adverse events (SAEs) were assessed by the site investigators for all patients. Potential relatedness to the study treatment was a required reporting element for all adverse events but was not considered in this count. Terminology from the Medical Dictionary for Regulatory Activities (MedDRA) and severity criteria from the Common Terminology Criteria for Adverse Events (CTCAE v. 4.03) were used as a basis for reporting adverse events. Serious adverse events are defined as being fatal, life-threatening, resulting in hospitalization or prolonged hospitalization, resulting in disability or congenital anomaly, or requiring intervention to prevent permanent impairment or damage and were required to be reported promptly. An Independent Oversight Committee (IOC) reviewed and adjudicated adverse event data. (NCT01176565)
Timeframe: From randomization through the 90 day visit (90 ± 14 days per protocol window; up to ± 30 days data is used) or until known death, withdrawal, or loss to follow-up.

InterventionParticipants (Count of Participants)
Standard SBP Reduction Arm100
Intensive SBP Reduction Arm128

Hematoma Expansion (Number of Patients With Hematoma Expansion of 33% or Greater Between the Baseline and 24 +/- 6 Hours Head CTs, as Measured by the Central Reader for Patients With Readable Scans for Both Time Points Submitted by Data Lock.)

Hematoma expansion as determined by serial CT scans: Hematoma expansion was defined as an increase in the volume of intraparenchymal hemorrhage of 33% or greater as measured by a central imaging analyst who was was unaware of the treatment assignments, clinical findings, and time points of image acquisition. The area of the hematoma was delineated by image analysis software with the use of density thresholds on each slice, followed by manual correction. To ensure accuracy and consistency of the readings, images were coded randomly and independently of subject numbers and manual correction was also done without awareness of treatment assignments, clinical findings, or time points of image acquisition. This data point is defined as being present (hematoma expansion of 33% or more was calculated between the baseline scan hematoma volume and the 24 +/- 6 hours hematoma volume measures at data analysis), meaning that hematoma expansion as defined must have occurred or it was not counted. (NCT01176565)
Timeframe: From the baseline head CT to the 24 +/- 6 hours from randomization head CT

InterventionParticipants (Count of Participants)
Standard SBP Reduction Arm104
Intensive SBP Reduction Arm85

Hypotension Within 72 Hours

Hypotension (abnormally low blood pressure) was the most likely adverse event that could be associated with the study treatment, and is the primary basis (risk) on which neurological deterioration or other untoward effects of the study treatment could occur. It is therefore examined as a numerically-measured occurrence in addition to monitoring patients closely for neurological deterioration or other symptoms. Hypotension, when named as an adverse event, was defined as the syndrome of low blood pressure with SBP < 85 mmHg. Instances of hypotension were to be avoided through close monitoring, and administration of fluid bolus for SBP < 110 mmHg. If hypotension did occur, it was to be reversed as quickly as possible through discontinuation of intravenous nicardipine and intravenous fluid administration, which can be accomplished readily in a variety of settings where patients with intracerebral hemorrhage are routinely housed during early hospitalization. (NCT01176565)
Timeframe: From randomization through 72 hours from randomization

InterventionParticipants (Count of Participants)
Standard SBP Reduction Arm3
Intensive SBP Reduction Arm6

Neurological Deterioration Within 24 Hours, Defined by a Decrease of 2 or More Points on the GCS Score or an Increase of 4 or More Points on the NIHSS Score From Baseline, Not Related to Sedation or Hypnotic-agent Use and Sustained for at Least 8 Hours.

Neurologic deterioration was measured using two scales. The Glasgow Coma Scale (GCS) score measures of level of consciousness in eye, motor, and verbal components. At least one point is given in each category. The scale ranges from 3 to 15, with 3 indicating deep unconsciousness and 15 indicating consciousness is not impaired. The National Institutes of Health Stroke Scale (NIHSS) quantifies neurologic deficits in 11 categories. Level of consciousness, horizontal eye movement, visual fields, facial palsy, movement in each limb, sensation, language & speech, and extinction or inattention on one side of the body are tested. Scores range from 0 to 42, with 0 indicating normal function and higher scores indicating greater deficit severity. Neurological status was checked per ICU standards through 24 hours, recommended as hourly GCS and full assessment every 2 hours. NIHSS assessment at baseline and 24 +/- 3 hours was pre-specified. Assessments were added for suspected neurological change. (NCT01176565)
Timeframe: From randomization through the 24-hour treatment period

InterventionParticipants (Count of Participants)
Standard SBP Reduction Arm40
Intensive SBP Reduction Arm55

Treatment-related Serious Adverse Event Within 72 Hours of Randomization

Adverse events (AEs) and serious adverse events (SAEs) were assessed by the site investigators for all patients, including for their potential relatedness to the study treatment. An Independent Oversight Committee (IOC) reviewed and adjudicated all adverse event data. The 72-hours-from-randomization time window was considered the most likely time frame during which treatment-related adverse events or serious adverse events would be observed. Terminology from the Medical Dictionary for Regulatory Activities (MedDRA) and severity criteria from the Common Terminology Criteria for Adverse Events (CTCAE v. 4.03) were used as a basis for reporting adverse events. Serious adverse events are defined as being fatal, life-threatening, resulting in hospitalization or prolonged hospitalization, resulting in disability or congenital anomaly, or requiring intervention to prevent permanent impairment or damage and were required to be reported promptly. (NCT01176565)
Timeframe: From randomization through 72 hours (3 days)

InterventionParticipants (Count of Participants)
Standard SBP Reduction Arm6
Intensive SBP Reduction Arm8

Death or Disability According to Modified Rankin Scale Score at 90 Days (3 Months) From Randomization

The primary outcome was death or disability, defined by modified Rankin scale (mRS) of 4-6 at 90 days following treatment. The modified Rankin Scale score ranges from 0, indicating no symptoms, to 6, indicating death. A score of 4 indicates moderately severe disability including the inability to walk or attend to one's own bodily needs. A score of 5 indicates severe disability; bedridden, incontinent, and requiring constant nursing care. To score a 3 or lower on the mRS, a person must at least be able to walk without the assistance of another person. We chose the mRS because of its high inter-observer reliability, superiority to other indices, and consistency with previous trials in patients with ICH. Reliability was further increased by use of a structured interview template and by requiring mRS assessors to pass a certification test. Persons conducting the 90-day mRS assessment were to be unaware of the treatment arm or clinical course of the patients they assessed. (NCT01176565)
Timeframe: 90 days (± 14 days per protocol window; up to ± 30 days data is used) from randomization

,
InterventionParticipants (Count of Participants)
Death or disability at 90 days (mRS = 4 - 6)Known death at or before 90 days
Intensive SBP Reduction Arm18633
Standard SBP Reduction Arm18134

Quality of Life at 90 Days Using EuroQol (EQ) Measures: EQ-5D (EuroQol Five Dimension), Consisting of Standardized EQ-5D-3L (EuroQol Five Dimension, Three-Level) Questionnaire and EQ VAS (EuroQol Visual Analog Scale) Scores

Standardized scales developed by the EuroQol Research Foundation were used as a secondary outcome measure in addition to the mRS scale score. The EQ-5D is a simple, standardized non-disease-specific instrument for describing and valuating health-related quality of life. The EQ-5D-3L questionnaire consists of 5 questions in 5 different domains and allows for responses from 1 (the best outcome) to 3 (the worst outcome) in each of five categories (mobility, self-care, usual activities, pain/discomfort, and anxiety/depression). Total scores range from 5 to 15, with lower scores indicating better quality of life and a higher score indicating a worse quality of life. A second component of EuroQol outcome measurements is a printed 20 cm visual analogue scale (EQ VAS) that appears somewhat like a thermometer, on which a score from 0 (worst imaginable health state or death) to 100 (best imaginable health state) is marked by the patient (or, when necessary, their proxy) with the scale in view. (NCT01176565)
Timeframe: 90 days (± 14 days per protocol window; up to ± 30 days data is used) from randomization

,
Interventionunits on a scale (Median)
EQ-5D utility scale questionnaireEQ VAS (visual analog scale)
Intensive SBP Reduction Arm0.762.5
Standard SBP Reduction Arm0.770

Reviews

2 reviews available for chlorine and Apoplexy

ArticleYear
Chloride co-transporters as possible therapeutic targets for stroke.
    Journal of neurochemistry, 2017, Volume: 140, Issue:2

    Topics: Animals; Brain; Cell Death; Chlorides; Humans; Neuroprotective Agents; Stroke; Symporters

2017
Chloride channels in stroke.
    Acta pharmacologica Sinica, 2013, Volume: 34, Issue:1

    Topics: Animals; Chloride Channels; Chlorides; Humans; Muscle, Smooth, Vascular; Oxidative Stress; Stroke

2013

Other Studies

19 other studies available for chlorine and Apoplexy

ArticleYear
Early Hyperchloremia is Independently Associated with Death or Disability in Patients with Intracerebral Hemorrhage.
    Neurocritical care, 2022, Volume: 37, Issue:2

    Topics: Antihypertensive Agents; Cerebral Hemorrhage; Chlorides; Humans; Nicardipine; Stroke

2022
Electroacupuncture attenuates ischemic injury after stroke and promotes angiogenesis via activation of EPO mediated Src and VEGF signaling pathways.
    PloS one, 2022, Volume: 17, Issue:9

    Topics: Animals; Chlorides; Electroacupuncture; Endothelial Cells; Erythropoietin; Glucose; Ischemia; Oxygen

2022
Haemodynamic stroke in a rare adult presentation of osteopetrosis.
    BMJ case reports, 2022, Sep-26, Volume: 15, Issue:9

    Topics: Brain Ischemia; Chloride Channels; Chlorides; Female; Hemodynamics; Humans; Ischemic Stroke; Osteope

2022
High-intensity training with short and long intervals regulate cortical neurotrophic factors, apoptosis markers and chloride homeostasis in rats with stroke.
    Physiology & behavior, 2023, 07-01, Volume: 266

    Topics: Animals; Apoptosis; Chlorides; High-Intensity Interval Training; Homeostasis; Humans; Nerve Growth F

2023
SLC26A11 Inhibition Reduces Oncotic Neuronal Death and Attenuates Stroke Reperfusion Injury.
    Molecular neurobiology, 2023, Volume: 60, Issue:10

    Topics: Animals; Brain Ischemia; Chlorides; Edema; Glucose; Hypoxia; Infarction; Rats; Reperfusion Injury; S

2023
Motor deficit in the mouse ferric chloride-induced distal middle cerebral artery occlusion model of stroke.
    Behavioural brain research, 2020, 02-17, Volume: 380

    Topics: Animals; Behavior, Animal; Cerebral Cortex; Cerebral Infarction; Chlorides; Disease Models, Animal;

2020
Prognostic role of hypochloremia in acute ischemic stroke patients.
    Acta neurologica Scandinavica, 2017, Volume: 136, Issue:6

    Topics: Aged; Biomarkers; Chlorides; Female; Humans; Hyponatremia; Male; Middle Aged; Prognosis; Sodium; Str

2017
PAC, an evolutionarily conserved membrane protein, is a proton-activated chloride channel.
    Science (New York, N.Y.), 2019, 04-26, Volume: 364, Issue:6438

    Topics: Animals; Calcium; Cell Death; Chloride Channels; Chlorides; Conserved Sequence; Evolution, Molecular

2019
Autophagy Mediates Astrocyte Death During Zinc-Potentiated Ischemia--Reperfusion Injury.
    Biological trace element research, 2015, Volume: 166, Issue:1

    Topics: Animals; Astrocytes; Autophagy; Blotting, Western; Cell Culture Techniques; Cell Hypoxia; Cell Line;

2015
A rabbit model of cerebral microembolic signals for translational research: preclinical validation for aspirin and clopidogrel.
    Journal of thrombosis and haemostasis : JTH, 2016, Volume: 14, Issue:9

    Topics: Animals; Aspirin; Carotid Artery Thrombosis; Chlorides; Clopidogrel; Disease Models, Animal; Drug Ev

2016
Salt deficiency states in tropical climates.
    Journal of the Royal Naval Medical Service, 1945, Volume: 31

    Topics: Chlorides; Heat Stroke; Hot Temperature; Humans; Hygiene; Sodium; Sodium Chloride; Stroke; Tropical

1945
Electrolyte changes in stroke.
    Mymensingh medical journal : MMJ, 2012, Volume: 21, Issue:4

    Topics: Adult; Aged; Cerebral Hemorrhage; Cerebral Infarction; Chlorides; Electrolytes; Female; Humans; Male

2012
Calcium influx constitutes the ionic basis for the maintenance of glutamate-induced extended neuronal depolarization associated with hippocampal neuronal death.
    Cell calcium, 2003, Volume: 33, Issue:2

    Topics: Animals; Animals, Newborn; Brain Injuries; Calcium; Calcium Channel Blockers; Calcium Signaling; Cel

2003
Testing of potassium, sodium and chlorine in liquor at the patients with diabetes mellitus.
    Medicinski arhiv, 2004, Volume: 58, Issue:6

    Topics: Blood-Brain Barrier; Chlorides; Diabetes Mellitus; Humans; Potassium; Sodium; Stroke

2004
Chloride-dominant salt sensitivity in the stroke-prone spontaneously hypertensive rat.
    Hypertension (Dallas, Tex. : 1979), 2005, Volume: 45, Issue:5

    Topics: Animals; Bicarbonates; Blood Pressure; Body Weight; Chlorides; Creatinine; Drug Combinations; Electr

2005
Acute vascular events and electrolytes variations in elderly patients.
    Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme, 2006, Volume: 38, Issue:3

    Topics: Aged; Aging; Calcium; Chlorides; Electrolytes; Female; Glucose Intolerance; Glucose Tolerance Test;

2006
Activation of a novel injury-induced calcium-permeable channel that plays a key role in causing extended neuronal depolarization and initiating neuronal death in excitotoxic neuronal injury.
    The Journal of pharmacology and experimental therapeutics, 2007, Volume: 322, Issue:2

    Topics: 6-Cyano-7-nitroquinoxaline-2,3-dione; Animals; Animals, Newborn; Apoptosis; Calcium; Calcium Channel

2007
Acetazolamide and enalapril combination offers complete protection from nitric oxide-deficient stroke in stroke-prone spontaneously hypertensive rats.
    Pharmacological research, 2000, Volume: 41, Issue:6

    Topics: Acetazolamide; Angiotensin-Converting Enzyme Inhibitors; Animals; Barium Compounds; Blood Pressure;

2000
Chloride-sensitive renal microangiopathy in the stroke-prone spontaneously hypertensive rat.
    Kidney international, 2001, Volume: 59, Issue:3

    Topics: Animals; Bicarbonates; Blood Pressure; Chlorides; Creatinine; Disease Susceptibility; Hypertension;

2001