The evaluation of pituitary damage associated with cardiac arrest: An experimental rodent model

Abstract The pituitary gland plays an important endocrinal role, however its damage after cardiac arrest (CA) has not been well elucidated. The aim of this study was to determine a pituitary gland damage induced by CA. Rats were subjected to 10-min asphyxia and cardiopulmonary resuscitation (CPR). I...

Full description

Bibliographic Details
Main Authors: Yu Okuma, Tomoaki Aoki, Santiago J. Miyara, Kei Hayashida, Mitsuaki Nishikimi, Ryosuke Takegawa, Tai Yin, Junhwan Kim, Lance B. Becker, Koichiro Shinozaki
Format: Article
Language:English
Published: Nature Portfolio 2021-01-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-020-79780-3
_version_ 1818346211547021312
author Yu Okuma
Tomoaki Aoki
Santiago J. Miyara
Kei Hayashida
Mitsuaki Nishikimi
Ryosuke Takegawa
Tai Yin
Junhwan Kim
Lance B. Becker
Koichiro Shinozaki
author_facet Yu Okuma
Tomoaki Aoki
Santiago J. Miyara
Kei Hayashida
Mitsuaki Nishikimi
Ryosuke Takegawa
Tai Yin
Junhwan Kim
Lance B. Becker
Koichiro Shinozaki
author_sort Yu Okuma
collection DOAJ
description Abstract The pituitary gland plays an important endocrinal role, however its damage after cardiac arrest (CA) has not been well elucidated. The aim of this study was to determine a pituitary gland damage induced by CA. Rats were subjected to 10-min asphyxia and cardiopulmonary resuscitation (CPR). Immunohistochemistry and ELISA assays were used to evaluate the pituitary damage and endocrine function. Samples were collected at pre-CA, and 30 and 120 min after cardio pulmonary resuscitation. Triphenyltetrazolium chloride (TTC) staining demonstrated the expansion of the pituitary damage over time. There was phenotypic validity between the pars distalis and nervosa. Both CT-proAVP (pars nervosa hormone) and GH/IGF-1 (pars distalis hormone) decreased over time, and a different expression pattern corresponding to the damaged areas was noted (CT-proAVP, 30.2 ± 6.2, 31.5 ± 5.9, and 16.3 ± 7.6 pg/mg protein, p < 0.01; GH/IGF-1, 2.63 ± 0.61, 0.62 ± 0.36, and 2.01 ± 0.41 ng/mg protein, p < 0.01 respectively). Similarly, the expression pattern between these hormones in the end-organ systems showed phenotypic validity. Plasma CT-proAVP (r = 0.771, p = 0.025) and IGF-1 (r = −0.775, p = 0.024) demonstrated a strong correlation with TTC staining area. Our data suggested that CA induces pathological and functional damage to the pituitary gland.
first_indexed 2024-12-13T17:14:40Z
format Article
id doaj.art-7fc1625c4de34b6c93af84813e35c18c
institution Directory Open Access Journal
issn 2045-2322
language English
last_indexed 2024-12-13T17:14:40Z
publishDate 2021-01-01
publisher Nature Portfolio
record_format Article
series Scientific Reports
spelling doaj.art-7fc1625c4de34b6c93af84813e35c18c2022-12-21T23:37:27ZengNature PortfolioScientific Reports2045-23222021-01-0111111210.1038/s41598-020-79780-3The evaluation of pituitary damage associated with cardiac arrest: An experimental rodent modelYu Okuma0Tomoaki Aoki1Santiago J. Miyara2Kei Hayashida3Mitsuaki Nishikimi4Ryosuke Takegawa5Tai Yin6Junhwan Kim7Lance B. Becker8Koichiro Shinozaki9The Feinstein Institutes for Medical Research, Northwell HealthThe Feinstein Institutes for Medical Research, Northwell HealthThe Feinstein Institutes for Medical Research, Northwell HealthThe Feinstein Institutes for Medical Research, Northwell HealthThe Feinstein Institutes for Medical Research, Northwell HealthThe Feinstein Institutes for Medical Research, Northwell HealthThe Feinstein Institutes for Medical Research, Northwell HealthThe Feinstein Institutes for Medical Research, Northwell HealthThe Feinstein Institutes for Medical Research, Northwell HealthThe Feinstein Institutes for Medical Research, Northwell HealthAbstract The pituitary gland plays an important endocrinal role, however its damage after cardiac arrest (CA) has not been well elucidated. The aim of this study was to determine a pituitary gland damage induced by CA. Rats were subjected to 10-min asphyxia and cardiopulmonary resuscitation (CPR). Immunohistochemistry and ELISA assays were used to evaluate the pituitary damage and endocrine function. Samples were collected at pre-CA, and 30 and 120 min after cardio pulmonary resuscitation. Triphenyltetrazolium chloride (TTC) staining demonstrated the expansion of the pituitary damage over time. There was phenotypic validity between the pars distalis and nervosa. Both CT-proAVP (pars nervosa hormone) and GH/IGF-1 (pars distalis hormone) decreased over time, and a different expression pattern corresponding to the damaged areas was noted (CT-proAVP, 30.2 ± 6.2, 31.5 ± 5.9, and 16.3 ± 7.6 pg/mg protein, p < 0.01; GH/IGF-1, 2.63 ± 0.61, 0.62 ± 0.36, and 2.01 ± 0.41 ng/mg protein, p < 0.01 respectively). Similarly, the expression pattern between these hormones in the end-organ systems showed phenotypic validity. Plasma CT-proAVP (r = 0.771, p = 0.025) and IGF-1 (r = −0.775, p = 0.024) demonstrated a strong correlation with TTC staining area. Our data suggested that CA induces pathological and functional damage to the pituitary gland.https://doi.org/10.1038/s41598-020-79780-3
spellingShingle Yu Okuma
Tomoaki Aoki
Santiago J. Miyara
Kei Hayashida
Mitsuaki Nishikimi
Ryosuke Takegawa
Tai Yin
Junhwan Kim
Lance B. Becker
Koichiro Shinozaki
The evaluation of pituitary damage associated with cardiac arrest: An experimental rodent model
Scientific Reports
title The evaluation of pituitary damage associated with cardiac arrest: An experimental rodent model
title_full The evaluation of pituitary damage associated with cardiac arrest: An experimental rodent model
title_fullStr The evaluation of pituitary damage associated with cardiac arrest: An experimental rodent model
title_full_unstemmed The evaluation of pituitary damage associated with cardiac arrest: An experimental rodent model
title_short The evaluation of pituitary damage associated with cardiac arrest: An experimental rodent model
title_sort evaluation of pituitary damage associated with cardiac arrest an experimental rodent model
url https://doi.org/10.1038/s41598-020-79780-3
work_keys_str_mv AT yuokuma theevaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT tomoakiaoki theevaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT santiagojmiyara theevaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT keihayashida theevaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT mitsuakinishikimi theevaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT ryosuketakegawa theevaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT taiyin theevaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT junhwankim theevaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT lancebbecker theevaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT koichiroshinozaki theevaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT yuokuma evaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT tomoakiaoki evaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT santiagojmiyara evaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT keihayashida evaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT mitsuakinishikimi evaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT ryosuketakegawa evaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT taiyin evaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT junhwankim evaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT lancebbecker evaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel
AT koichiroshinozaki evaluationofpituitarydamageassociatedwithcardiacarrestanexperimentalrodentmodel