Effect of the intracranial hypertension on gastric compliance of anaesthetized rats: characterization of the phenomenology and neural mechanisms

Detalhes bibliográficos
Autor(a) principal: Gerardo Cristino Filho
Data de Publicação: 2004
Tipo de documento: Tese
Idioma: por
Título da fonte: Biblioteca Digital de Teses e Dissertações da UFC
Texto Completo: http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=410
Resumo: In humans, intracranial hypertension (ICH) disturbs cardiovascular function and also modifies gastrointestinal physiology as clinically manifested by nausea and vomiting symptoms. Since gastric compliance drives the gastric emptying of liquid which is inhibited by ICH, it was studied the ICH effect on gastric compliance behavior in anesthetized rats and the neuropathways possibly serving this phenomenon. Anesthetized male Wistar rats (N=65, 280-320g) received a carotid cannula to monitor arterial pressure (AP) and heart rate (HR). Under stereotactic guidance a cannula was positioned into each lateral ventricule: one for cerebrospinal fluid simile infusion and the other to record intracranial pressure (ICP in mmHg). All animals received a catheter balloon that was positioned in the proximal stomach and connected to a U shaped barostat filled with standard ionic solution set 4cm above the animals xyphoid appendix. Gastric volume changes transmitted to this communicant vessel system were sensed and recorded by a plethysmometer for 80min After a basal period of 20min the animals were randomly allocated to either experimental protocols: control or ICH. In controls the animals remained untouched while in ICH the ICP was increased from basal to 10, 20, 40, or 60 mmHg, for 30min. In crescent ICP, the pressure was increased in the same animal, at every 20min, from basal to 20, 40 and then 60 mmHg. Separate groups of animals also underwent neurotomy or respective sham operation: subdiafragmatic vagotomy, splancnotomy plus bilateral ganglionectomy and after the basal period were submitted to 10 mmHg of ICP. Brains from other animals (control ICP 10 and ICP 60 mmHg) were removed for histological studies. Data (mean  SEM) were compared to respective basal values after ANOVA and Bonferroniâs test. In controls, hemodynamic parameters and GV remained within stable levels. In ICP 10 mmHg, GV decreased (P<0.05) from basal levels (2.70Â0.12ml) to 2.30Â0.14ml at 30min to remain decreased afterwards, while at ICP 20, 40 and 60mmHg decreased early at 20min of ICH (2.36Â0.18 vs 2.03Â0.19, 2.69Â0.27 vs 2.03Â0.25 e 2.83Â0.12 vs 1.95Â0.11ml, respectively), remaining as such up to the end (P<0.05). In crescent ICP, GV decreased from basal levels (2.94Â0.04ml) at ICP 40mmHg to 2.70Â0.07ml as well as at ICP 60 mmHg to 2.67Â0.06ml (P<0.05). In all groups were observed arterial hypertension and bradycardia, typical findings of Cushingâs reflex. In animals without vagal connection, GV despite beginning from lower basal values (1.82Â0.18ml) decreased (P<0.05) at 30min to 1.69Â0.18ml. After sympathectomy, GV remained stable (P>0.05) throughout the experiment (2.29Â0.21ml vs 2.11Â0.23ml). Moderate meningeal edema-coroid plexus- was observed moreover at brains from ICP 60mmHg subset. In conclusion, experimental ICH besides inducing Cushingâs reflex (arterial hypertension and bradycardia) also decreases gastric compliance in anesthetized rats in an ICP dependent manner. Vagotomy had no effect and this phenomenon is likely to be mediated by sympathetic neuropathways.
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spelling info:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/doctoralThesisEffect of the intracranial hypertension on gastric compliance of anaesthetized rats: characterization of the phenomenology and neural mechanismsEfeito da HipertensÃo Intracraniana sobre a complacÃncia GÃstrica de ratos Anestesiados: CauterizaÃÃo do FenÃmeno e dos Mecanismos Neurais2004-12-03ArmÃnio Aguiar dos Santos21268789372http://lattes.cnpq.br/6367176618425888 Paulo Roberto LeitÃo de Vasconcelos11852844353http://buscatextual.cnpq.br/buscatextual/servletrecuperafoto?id=K4787736J6Josà Renan de Cunha Melo80412903131http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4787682P0Fernando Menezes Braga0284676849http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4787072J5Ricardo Brandt de Oliveira23267488834http://lattes.cnpq.br/052005332707497016416678349http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4781139Z6Gerardo Cristino FilhoUniversidade Federal do CearÃPrograma de PÃs-GraduaÃÃo em CirurgiaUFCBRHipertensÃo intracraniana Motilidade gastrointestinal Traumatismos cerebraisGastrointestinal motilityBrain injury Brain injuryIntracranial hypertension CIRURGIAIn humans, intracranial hypertension (ICH) disturbs cardiovascular function and also modifies gastrointestinal physiology as clinically manifested by nausea and vomiting symptoms. Since gastric compliance drives the gastric emptying of liquid which is inhibited by ICH, it was studied the ICH effect on gastric compliance behavior in anesthetized rats and the neuropathways possibly serving this phenomenon. Anesthetized male Wistar rats (N=65, 280-320g) received a carotid cannula to monitor arterial pressure (AP) and heart rate (HR). Under stereotactic guidance a cannula was positioned into each lateral ventricule: one for cerebrospinal fluid simile infusion and the other to record intracranial pressure (ICP in mmHg). All animals received a catheter balloon that was positioned in the proximal stomach and connected to a U shaped barostat filled with standard ionic solution set 4cm above the animals xyphoid appendix. Gastric volume changes transmitted to this communicant vessel system were sensed and recorded by a plethysmometer for 80min After a basal period of 20min the animals were randomly allocated to either experimental protocols: control or ICH. In controls the animals remained untouched while in ICH the ICP was increased from basal to 10, 20, 40, or 60 mmHg, for 30min. In crescent ICP, the pressure was increased in the same animal, at every 20min, from basal to 20, 40 and then 60 mmHg. Separate groups of animals also underwent neurotomy or respective sham operation: subdiafragmatic vagotomy, splancnotomy plus bilateral ganglionectomy and after the basal period were submitted to 10 mmHg of ICP. Brains from other animals (control ICP 10 and ICP 60 mmHg) were removed for histological studies. Data (mean  SEM) were compared to respective basal values after ANOVA and Bonferroniâs test. In controls, hemodynamic parameters and GV remained within stable levels. In ICP 10 mmHg, GV decreased (P<0.05) from basal levels (2.70Â0.12ml) to 2.30Â0.14ml at 30min to remain decreased afterwards, while at ICP 20, 40 and 60mmHg decreased early at 20min of ICH (2.36Â0.18 vs 2.03Â0.19, 2.69Â0.27 vs 2.03Â0.25 e 2.83Â0.12 vs 1.95Â0.11ml, respectively), remaining as such up to the end (P<0.05). In crescent ICP, GV decreased from basal levels (2.94Â0.04ml) at ICP 40mmHg to 2.70Â0.07ml as well as at ICP 60 mmHg to 2.67Â0.06ml (P<0.05). In all groups were observed arterial hypertension and bradycardia, typical findings of Cushingâs reflex. In animals without vagal connection, GV despite beginning from lower basal values (1.82Â0.18ml) decreased (P<0.05) at 30min to 1.69Â0.18ml. After sympathectomy, GV remained stable (P>0.05) throughout the experiment (2.29Â0.21ml vs 2.11Â0.23ml). Moderate meningeal edema-coroid plexus- was observed moreover at brains from ICP 60mmHg subset. In conclusion, experimental ICH besides inducing Cushingâs reflex (arterial hypertension and bradycardia) also decreases gastric compliance in anesthetized rats in an ICP dependent manner. Vagotomy had no effect and this phenomenon is likely to be mediated by sympathetic neuropathways.Em humanos, a hipertensÃo intracraniana (HIC) alÃm de promover distÃrbios hemodinÃmicos, tambÃm provoca alteraÃÃes na funÃÃo gastrintestinal, apresentadas clinicamente com nÃuseas e vÃmitos. Como a HIC em ratos acordados inibe o esvaziamento gÃstrico de lÃquido e este à influenciado pela complacÃncia gÃstrica (CG), estudou-se o efeito da HIC sobre a CG e os mecanismos neurais envolvidos no fenÃmeno. Ratos Wistar (N=65, 280-320g) anestesiados com uretana tiveram a artÃria carÃtida canulada para registro hemodinÃmico. Mediante estereotaxia, cÃnulas-guias foram implantadas bilateralmente nos ventrÃculos laterais, para registro simultÃneo da PIC e compressÃo do sistema ventricular por infusÃo de lÃquido cefalorraquidiano-sÃmile (LCR-sÃmile). Um catÃter com um balÃo na extremidade foi posicionado no estÃmago proximal e conectado a um sistema de vasos comunicantes com barostato. VariaÃÃes do volume do balÃo gÃstrico (VG) transmitidas ao barostato foram detectadas por um sensor eletrÃnico de volume e registradas continuamente por 80min num pletismÃmetro. ApÃs um perÃodo basal de 20min, os ratos foram aleatoriamente submetidos Ãs seguintes condiÃÃes: Controle (PIC espontÃnea), PIC 10mmHg, PIC 20mmHg, PIC 40mmHg, PIC 60mmHg e PIC Crescente. ApÃs a compressÃo ventricular, os animais foram monitorados por mais 30min. Para o estudo dos mecanismos neurais, grupos de ratos, previamente submetidos a laparotomia seguida ou nÃo (falsa cirurgia) de vagotomia subdiafragmÃtica ou esplancnicectomia+gangliectomia celÃaca bilaterais, foram estudados sob PIC de 10mmHg. Um grupo à parte de animais (n=9) PIC controle, PIC 10mmHg e PIC 60mmHg tiveram seus encÃfalos retirados para avaliaÃÃo histolÃgica. Os dados foram expressos em mÃdiaÂEPM e analisados pela ANOVA seguido pelo teste de Bonferroni. No grupo controle, os parÃmetros hemodinÃmicos e de VG se mantiveram constantes. No grupo PIC 10mmHg, em relaÃÃo ao perÃodo basal (2.70Â0.12ml), o VG diminuiu para 2.30Â0.14ml aos 30min de HIC, assim permanecendo por todo o experimento (P<0.05). Jà nos grupos PIC 20mmHg, PIC 40mmHg e PIC 60mmHg, o VG diminuiu em relaÃÃo ao perÃodo basal aos 20min de HIC (2.36Â0.18 vs 2.03Â0.19, 2.69Â0.27 vs 2.03Â0.25 e 2.83Â0.12 vs 1.95Â0.11ml, respectivamente), assim permanecendo atà o final (P<0.05). No grupo PIC crescente, em relaÃÃo ao perÃodo basal (2.94Â0.04ml), o VG diminuiu para 2.70Â0.07ml com PIC 40 mmHg e para 2.67Â0.06ml com PIC 60mmHg (P<0.05). Em todos os grupos observou-se hipertensÃo arterial e bradicardia, efeitos tÃpicos do reflexo de Cushing. Nos animais sem conexÃo vagal, o VG embora partindo de nÃveis basais menores (1.82Â0.18ml) diminuiu (P<0.05) aos 30min para 1.69Â0.18ml. Nos animais submetidos a esplacnicectomia, em relaÃÃo ao perÃodo basal (2.29Â0.21ml), o VG permaneceu inalterado (P>0.05) durante (2.11Â0.23ml) e apÃs a compressÃo ventricular. Nas lÃminas analisadas identificou-se edema parenquimatoso e congestÃes menÃngea, do plexo corÃide e parenquimatosa de graus leve a moderado, principalmente nos animais submetidos a PIC de 60 mmHg. A HIC diminui a CG de ratos anestesiados, sendo o fenÃmeno PIC dependente e possivelmente mediado por via esplÃncnicaCoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superiorhttp://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=410application/pdfinfo:eu-repo/semantics/openAccessporreponame:Biblioteca Digital de Teses e Dissertações da UFCinstname:Universidade Federal do Cearáinstacron:UFC2019-01-21T11:13:31Zmail@mail.com -
dc.title.en.fl_str_mv Effect of the intracranial hypertension on gastric compliance of anaesthetized rats: characterization of the phenomenology and neural mechanisms
dc.title.alternative.pt.fl_str_mv Efeito da HipertensÃo Intracraniana sobre a complacÃncia GÃstrica de ratos Anestesiados: CauterizaÃÃo do FenÃmeno e dos Mecanismos Neurais
title Effect of the intracranial hypertension on gastric compliance of anaesthetized rats: characterization of the phenomenology and neural mechanisms
spellingShingle Effect of the intracranial hypertension on gastric compliance of anaesthetized rats: characterization of the phenomenology and neural mechanisms
Gerardo Cristino Filho
HipertensÃo intracraniana
Motilidade gastrointestinal
Traumatismos cerebrais
Gastrointestinal motility
Brain injury
Brain injury
Intracranial hypertension
CIRURGIA
title_short Effect of the intracranial hypertension on gastric compliance of anaesthetized rats: characterization of the phenomenology and neural mechanisms
title_full Effect of the intracranial hypertension on gastric compliance of anaesthetized rats: characterization of the phenomenology and neural mechanisms
title_fullStr Effect of the intracranial hypertension on gastric compliance of anaesthetized rats: characterization of the phenomenology and neural mechanisms
title_full_unstemmed Effect of the intracranial hypertension on gastric compliance of anaesthetized rats: characterization of the phenomenology and neural mechanisms
title_sort Effect of the intracranial hypertension on gastric compliance of anaesthetized rats: characterization of the phenomenology and neural mechanisms
author Gerardo Cristino Filho
author_facet Gerardo Cristino Filho
author_role author
dc.contributor.advisor1.fl_str_mv ArmÃnio Aguiar dos Santos
dc.contributor.advisor1ID.fl_str_mv 21268789372
dc.contributor.advisor1Lattes.fl_str_mv http://lattes.cnpq.br/6367176618425888
dc.contributor.referee1.fl_str_mv Paulo Roberto LeitÃo de Vasconcelos
dc.contributor.referee1ID.fl_str_mv 11852844353
dc.contributor.referee1Lattes.fl_str_mv http://buscatextual.cnpq.br/buscatextual/servletrecuperafoto?id=K4787736J6
dc.contributor.referee2.fl_str_mv Josà Renan de Cunha Melo
dc.contributor.referee2ID.fl_str_mv 80412903131
dc.contributor.referee2Lattes.fl_str_mv http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4787682P0
dc.contributor.referee3.fl_str_mv Fernando Menezes Braga
dc.contributor.referee3ID.fl_str_mv 0284676849
dc.contributor.referee3Lattes.fl_str_mv http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4787072J5
dc.contributor.referee4.fl_str_mv Ricardo Brandt de Oliveira
dc.contributor.referee4ID.fl_str_mv 23267488834
dc.contributor.referee4Lattes.fl_str_mv http://lattes.cnpq.br/0520053327074970
dc.contributor.authorID.fl_str_mv 16416678349
dc.contributor.authorLattes.fl_str_mv http://buscatextual.cnpq.br/buscatextual/visualizacv.jsp?id=K4781139Z6
dc.contributor.author.fl_str_mv Gerardo Cristino Filho
contributor_str_mv ArmÃnio Aguiar dos Santos
Paulo Roberto LeitÃo de Vasconcelos
Josà Renan de Cunha Melo
Fernando Menezes Braga
Ricardo Brandt de Oliveira
dc.subject.por.fl_str_mv HipertensÃo intracraniana
Motilidade gastrointestinal
Traumatismos cerebrais
Gastrointestinal motility
Brain injury
Brain injury
topic HipertensÃo intracraniana
Motilidade gastrointestinal
Traumatismos cerebrais
Gastrointestinal motility
Brain injury
Brain injury
Intracranial hypertension
CIRURGIA
dc.subject.eng.fl_str_mv Intracranial hypertension
dc.subject.cnpq.fl_str_mv CIRURGIA
dc.description.sponsorship.fl_txt_mv CoordenaÃÃo de AperfeiÃoamento de Pessoal de NÃvel Superior
dc.description.abstract.por.fl_txt_mv In humans, intracranial hypertension (ICH) disturbs cardiovascular function and also modifies gastrointestinal physiology as clinically manifested by nausea and vomiting symptoms. Since gastric compliance drives the gastric emptying of liquid which is inhibited by ICH, it was studied the ICH effect on gastric compliance behavior in anesthetized rats and the neuropathways possibly serving this phenomenon. Anesthetized male Wistar rats (N=65, 280-320g) received a carotid cannula to monitor arterial pressure (AP) and heart rate (HR). Under stereotactic guidance a cannula was positioned into each lateral ventricule: one for cerebrospinal fluid simile infusion and the other to record intracranial pressure (ICP in mmHg). All animals received a catheter balloon that was positioned in the proximal stomach and connected to a U shaped barostat filled with standard ionic solution set 4cm above the animals xyphoid appendix. Gastric volume changes transmitted to this communicant vessel system were sensed and recorded by a plethysmometer for 80min After a basal period of 20min the animals were randomly allocated to either experimental protocols: control or ICH. In controls the animals remained untouched while in ICH the ICP was increased from basal to 10, 20, 40, or 60 mmHg, for 30min. In crescent ICP, the pressure was increased in the same animal, at every 20min, from basal to 20, 40 and then 60 mmHg. Separate groups of animals also underwent neurotomy or respective sham operation: subdiafragmatic vagotomy, splancnotomy plus bilateral ganglionectomy and after the basal period were submitted to 10 mmHg of ICP. Brains from other animals (control ICP 10 and ICP 60 mmHg) were removed for histological studies. Data (mean  SEM) were compared to respective basal values after ANOVA and Bonferroniâs test. In controls, hemodynamic parameters and GV remained within stable levels. In ICP 10 mmHg, GV decreased (P<0.05) from basal levels (2.70Â0.12ml) to 2.30Â0.14ml at 30min to remain decreased afterwards, while at ICP 20, 40 and 60mmHg decreased early at 20min of ICH (2.36Â0.18 vs 2.03Â0.19, 2.69Â0.27 vs 2.03Â0.25 e 2.83Â0.12 vs 1.95Â0.11ml, respectively), remaining as such up to the end (P<0.05). In crescent ICP, GV decreased from basal levels (2.94Â0.04ml) at ICP 40mmHg to 2.70Â0.07ml as well as at ICP 60 mmHg to 2.67Â0.06ml (P<0.05). In all groups were observed arterial hypertension and bradycardia, typical findings of Cushingâs reflex. In animals without vagal connection, GV despite beginning from lower basal values (1.82Â0.18ml) decreased (P<0.05) at 30min to 1.69Â0.18ml. After sympathectomy, GV remained stable (P>0.05) throughout the experiment (2.29Â0.21ml vs 2.11Â0.23ml). Moderate meningeal edema-coroid plexus- was observed moreover at brains from ICP 60mmHg subset. In conclusion, experimental ICH besides inducing Cushingâs reflex (arterial hypertension and bradycardia) also decreases gastric compliance in anesthetized rats in an ICP dependent manner. Vagotomy had no effect and this phenomenon is likely to be mediated by sympathetic neuropathways.
Em humanos, a hipertensÃo intracraniana (HIC) alÃm de promover distÃrbios hemodinÃmicos, tambÃm provoca alteraÃÃes na funÃÃo gastrintestinal, apresentadas clinicamente com nÃuseas e vÃmitos. Como a HIC em ratos acordados inibe o esvaziamento gÃstrico de lÃquido e este à influenciado pela complacÃncia gÃstrica (CG), estudou-se o efeito da HIC sobre a CG e os mecanismos neurais envolvidos no fenÃmeno. Ratos Wistar (N=65, 280-320g) anestesiados com uretana tiveram a artÃria carÃtida canulada para registro hemodinÃmico. Mediante estereotaxia, cÃnulas-guias foram implantadas bilateralmente nos ventrÃculos laterais, para registro simultÃneo da PIC e compressÃo do sistema ventricular por infusÃo de lÃquido cefalorraquidiano-sÃmile (LCR-sÃmile). Um catÃter com um balÃo na extremidade foi posicionado no estÃmago proximal e conectado a um sistema de vasos comunicantes com barostato. VariaÃÃes do volume do balÃo gÃstrico (VG) transmitidas ao barostato foram detectadas por um sensor eletrÃnico de volume e registradas continuamente por 80min num pletismÃmetro. ApÃs um perÃodo basal de 20min, os ratos foram aleatoriamente submetidos Ãs seguintes condiÃÃes: Controle (PIC espontÃnea), PIC 10mmHg, PIC 20mmHg, PIC 40mmHg, PIC 60mmHg e PIC Crescente. ApÃs a compressÃo ventricular, os animais foram monitorados por mais 30min. Para o estudo dos mecanismos neurais, grupos de ratos, previamente submetidos a laparotomia seguida ou nÃo (falsa cirurgia) de vagotomia subdiafragmÃtica ou esplancnicectomia+gangliectomia celÃaca bilaterais, foram estudados sob PIC de 10mmHg. Um grupo à parte de animais (n=9) PIC controle, PIC 10mmHg e PIC 60mmHg tiveram seus encÃfalos retirados para avaliaÃÃo histolÃgica. Os dados foram expressos em mÃdiaÂEPM e analisados pela ANOVA seguido pelo teste de Bonferroni. No grupo controle, os parÃmetros hemodinÃmicos e de VG se mantiveram constantes. No grupo PIC 10mmHg, em relaÃÃo ao perÃodo basal (2.70Â0.12ml), o VG diminuiu para 2.30Â0.14ml aos 30min de HIC, assim permanecendo por todo o experimento (P<0.05). Jà nos grupos PIC 20mmHg, PIC 40mmHg e PIC 60mmHg, o VG diminuiu em relaÃÃo ao perÃodo basal aos 20min de HIC (2.36Â0.18 vs 2.03Â0.19, 2.69Â0.27 vs 2.03Â0.25 e 2.83Â0.12 vs 1.95Â0.11ml, respectivamente), assim permanecendo atà o final (P<0.05). No grupo PIC crescente, em relaÃÃo ao perÃodo basal (2.94Â0.04ml), o VG diminuiu para 2.70Â0.07ml com PIC 40 mmHg e para 2.67Â0.06ml com PIC 60mmHg (P<0.05). Em todos os grupos observou-se hipertensÃo arterial e bradicardia, efeitos tÃpicos do reflexo de Cushing. Nos animais sem conexÃo vagal, o VG embora partindo de nÃveis basais menores (1.82Â0.18ml) diminuiu (P<0.05) aos 30min para 1.69Â0.18ml. Nos animais submetidos a esplacnicectomia, em relaÃÃo ao perÃodo basal (2.29Â0.21ml), o VG permaneceu inalterado (P>0.05) durante (2.11Â0.23ml) e apÃs a compressÃo ventricular. Nas lÃminas analisadas identificou-se edema parenquimatoso e congestÃes menÃngea, do plexo corÃide e parenquimatosa de graus leve a moderado, principalmente nos animais submetidos a PIC de 60 mmHg. A HIC diminui a CG de ratos anestesiados, sendo o fenÃmeno PIC dependente e possivelmente mediado por via esplÃncnica
description In humans, intracranial hypertension (ICH) disturbs cardiovascular function and also modifies gastrointestinal physiology as clinically manifested by nausea and vomiting symptoms. Since gastric compliance drives the gastric emptying of liquid which is inhibited by ICH, it was studied the ICH effect on gastric compliance behavior in anesthetized rats and the neuropathways possibly serving this phenomenon. Anesthetized male Wistar rats (N=65, 280-320g) received a carotid cannula to monitor arterial pressure (AP) and heart rate (HR). Under stereotactic guidance a cannula was positioned into each lateral ventricule: one for cerebrospinal fluid simile infusion and the other to record intracranial pressure (ICP in mmHg). All animals received a catheter balloon that was positioned in the proximal stomach and connected to a U shaped barostat filled with standard ionic solution set 4cm above the animals xyphoid appendix. Gastric volume changes transmitted to this communicant vessel system were sensed and recorded by a plethysmometer for 80min After a basal period of 20min the animals were randomly allocated to either experimental protocols: control or ICH. In controls the animals remained untouched while in ICH the ICP was increased from basal to 10, 20, 40, or 60 mmHg, for 30min. In crescent ICP, the pressure was increased in the same animal, at every 20min, from basal to 20, 40 and then 60 mmHg. Separate groups of animals also underwent neurotomy or respective sham operation: subdiafragmatic vagotomy, splancnotomy plus bilateral ganglionectomy and after the basal period were submitted to 10 mmHg of ICP. Brains from other animals (control ICP 10 and ICP 60 mmHg) were removed for histological studies. Data (mean  SEM) were compared to respective basal values after ANOVA and Bonferroniâs test. In controls, hemodynamic parameters and GV remained within stable levels. In ICP 10 mmHg, GV decreased (P<0.05) from basal levels (2.70Â0.12ml) to 2.30Â0.14ml at 30min to remain decreased afterwards, while at ICP 20, 40 and 60mmHg decreased early at 20min of ICH (2.36Â0.18 vs 2.03Â0.19, 2.69Â0.27 vs 2.03Â0.25 e 2.83Â0.12 vs 1.95Â0.11ml, respectively), remaining as such up to the end (P<0.05). In crescent ICP, GV decreased from basal levels (2.94Â0.04ml) at ICP 40mmHg to 2.70Â0.07ml as well as at ICP 60 mmHg to 2.67Â0.06ml (P<0.05). In all groups were observed arterial hypertension and bradycardia, typical findings of Cushingâs reflex. In animals without vagal connection, GV despite beginning from lower basal values (1.82Â0.18ml) decreased (P<0.05) at 30min to 1.69Â0.18ml. After sympathectomy, GV remained stable (P>0.05) throughout the experiment (2.29Â0.21ml vs 2.11Â0.23ml). Moderate meningeal edema-coroid plexus- was observed moreover at brains from ICP 60mmHg subset. In conclusion, experimental ICH besides inducing Cushingâs reflex (arterial hypertension and bradycardia) also decreases gastric compliance in anesthetized rats in an ICP dependent manner. Vagotomy had no effect and this phenomenon is likely to be mediated by sympathetic neuropathways.
publishDate 2004
dc.date.issued.fl_str_mv 2004-12-03
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dc.publisher.country.fl_str_mv BR
publisher.none.fl_str_mv Universidade Federal do CearÃ
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