RESUMO
OBJECTIVE: To compare the survival rate and alveolar bone levels at implants installed in healed sites and functionally loaded within 1 h from installation or after 3 months. MATERIAL AND METHODS: A total of 30 patients (17 male and 13 female) were recruited and 71 implants with a SLA(®) surface, 4.1 mm in diameter and 8-12 mm long, were installed in a fully healed alveolar ridge, 36 as test and 35 as control implants. The test implants were immediately loaded with a temporary reconstruction in proper occlusion, while the randomly selected control sites received the final reconstruction after 3 months. Radiographic bone levels were determined after implant installation, prosthesis delivery, and at annual intervals thereafter. RESULTS: One patient of the control and one patient of the test were excluded from evaluation. No further losses of implants or patients were seen up to the 3-year follow-up. Hence, data from 28 patients were accounted for. A total of 37 and 36 metal-ceramic crowns were provided at the test and control sites, respectively. No biological and technical complications were observed during the 3-year follow-up. Bone levels at the time of implant installation were at 1.6 ± 0.8 and 1.7 ± 0.9 mm from the implant shoulder at the test and control sites, respectively. At prosthesis delivery, the bone levels were located at 2.4 ± 0.7 mm at the control sites 3 months after implant placement. After 1 year of function, similar bone levels were observed at both sites, displaying 2.4 ± 1.0 and 2.5 ± 0.8 mm at the test and control sites, respectively. No differences were found in the subsequent observation periods. CONCLUSION: Survival rates and radiographic bone levels after 1, 2, and 3 years of observation did not differ between conventionally installed implants loaded immediately or delayed (after 3 months). Moreover, insertion torque values did not affect osseointegration.
Assuntos
Perda do Osso Alveolar/diagnóstico por imagem , Implantação Dentária Endóssea , Prótese Dentária Fixada por Implante , Prótese Parcial Fixa , Carga Imediata em Implante Dentário , Perda do Osso Alveolar/etiologia , Implantação Dentária Endóssea/efeitos adversos , Prótese Dentária Fixada por Implante/efeitos adversos , Prótese Parcial Fixa/efeitos adversos , Feminino , Seguimentos , Humanos , Masculino , Maxila/diagnóstico por imagem , Maxila/cirurgia , Estudos Prospectivos , Alvéolo Dental/diagnóstico por imagem , Alvéolo Dental/cirurgiaRESUMO
The existence of neural connections between the medial preoptic area (MPOA) and the salivary glands and the increase in salivation by thermal or electrical stimulation of the MPOA have suggested an important role of MPOA in the control of salivary gland function. Although direct cholinergic activation of the salivary glands induces salivation, recent studies have suggested that salivation produced by i.p. pilocarpine may also depend on the activation of central mechanisms. Therefore, in the present study, we investigated the effects of bilateral electrolytic lesions of the MPOA on the salivation induced by i.p. pilocarpine. Adult male Holtzman rats (n = 11-12/group) with bilateral sham or electrolytic lesions of the MPOA were used. One, five, and fifteen days after the brain surgery, under ketamine anesthesia, the salivation was induced by i.p. pilocarpine (1 mg/kg of body weight), and saliva was collected using pre-weighed small cotton balls inserted into the animal's mouth. Pilocarpine-induced salivation was reduced 1 and 5 days after MPOA lesion (341 +/- 41 and 310 +/- 35 mg/7 min, respectively, vs. sham lesions: 428 +/- 32 and 495 +/- 36 mg/7 min, respectively), but it was fully recovered at the 15th day post-lesion (561 +/- 49 vs. sham lesion: 618 +/- 27 mg/7 min). Lesions of the MPOA did not affect baseline non-stimulated salivary secretion. The results confirm the importance of MPOA in the control of salivation and suggest that its integrity is necessary for the full sialogogue effect of pilocarpine. However, alternative mechanisms probably involving other central nuclei can replace MPOA function in chronically lesioned rats allowing the complete recovery of the effects of pilocarpine.
Assuntos
Agonistas Muscarínicos/farmacologia , Pilocarpina/farmacologia , Área Pré-Óptica/fisiopatologia , Salivação/efeitos dos fármacos , Animais , Traumatismos por Eletricidade/fisiopatologia , Masculino , Área Pré-Óptica/lesões , Ratos , Ratos Sprague-Dawley , Fatores de TempoRESUMO
The cholinergic agonist pilocarpine injected intraperitoneally (ip) increases mean arterial pressure (MAP) and superior mesenteric (SM) vascular resistance and reduces submandibular/sublingual gland (SSG) vascular resistance. In the present study, we investigated the effects of electrolytic lesions of the anteroventral third ventricle (AV3V) region on the changes in MAP, SM, and SSG vascular resistances induced by ip pilocarpine. Male Holtzman rats anesthetized with urethane (1.0 g/kg) and chloralose (60 mg/kg) were submitted to sham or electrolytic AV3V lesions and had pulsed Doppler flow probes implanted around the arteries. Contrary to sham rats, in 1-h and 2-day AV3V-lesioned rats, pilocarpine (4 micromol/kg) ip decreased MAP (-41 +/- 4 and -26 +/- 4 mm Hg, respectively, vs. sham: 19 +/- 4 mm Hg) and SM (-48 +/- 11 and -45 +/- 10%, respectively, vs. sham: 41 +/- 10%) and hindlimb vascular resistances (-65 +/- 32 and -113 +/- 29%, respectively, vs. sham: 19 +/- 29%). In 7-day AV3V-lesioned rats, pilocarpine produced no changes on MAP and SM and hindlimb vascular resistances. Similar to sham rats, pilocarpine reduced SSG vascular resistance 1 h after AV3V lesions (-46 +/- 6%, vs. sham: -40 +/- 6%), but it produced no effect 2 days after AV3V lesions and increased SSG vascular resistance (37 +/- 6%) in 7-day AV3V-lesioned rats. The responses to ip pilocarpine were similar in 15-day sham and AV3V-lesioned rats. The cholinergic antagonist atropine methyl bromide (10 nmol) iv slightly increased the pressor response to ip pilocarpine in sham rats and abolished for 40 min the fall in MAP induced by ip pilocarpine in 1-h AV3V-lesioned rats. The results suggest that central mechanisms dependent on the AV3V region are involved in the pressor responses to ip pilocarpine. Although it was impaired 2 and 7 days after AV3V lesions, pilocarpine-induced salivary gland vasodilation was not altered 1 h after AV3V lesions which suggests that this vasodilation is not directly dependent on the AV3V region.
Assuntos
Pressão Sanguínea/efeitos dos fármacos , Agonistas Muscarínicos/farmacologia , Pilocarpina/farmacologia , Glândulas Salivares/efeitos dos fármacos , Terceiro Ventrículo/efeitos dos fármacos , Vasodilatação/efeitos dos fármacos , Análise de Variância , Animais , Atropina/farmacologia , Interações Medicamentosas , Eletrólise/efeitos adversos , Frequência Cardíaca/efeitos dos fármacos , Injeções Intraventriculares , Fluxometria por Laser-Doppler/métodos , Masculino , Antagonistas Muscarínicos/farmacologia , Ratos , Glândulas Salivares/fisiologia , Terceiro Ventrículo/lesões , Fatores de TempoRESUMO
Peripheral treatment with the cholinergic agonist pilocarpine induces intense salivation that is inhibited by central injections of the alpha2-adrenergic/imidazoline receptor agonist moxonidine. Salivary gland blood flow controlled by sympathetic and parasympathetic systems may affect salivation. We investigated the changes in mean arterial pressure (MAP) and in the vascular resistance in the submandibular/sublingual gland (SSG) artery, superior mesenteric (SM) artery and low abdominal aorta (hindlimb) in rats treated with intraperitoneal (i.p.) pilocarpine alone or combined with intracerebroventricular (i.c.v.) moxonidine. Male Holtzman rats with stainless steel cannula implanted into lateral ventricle (LV) and anesthetized with urethane were used. Pilocarpine (4 micromol/kg of body weight) i.p. reduced SSG vascular resistance (-50+/-13% vs. vehicle: 5+/-3%). Pilocarpine i.p. also increased mesenteric vascular resistance (15+/-5% vs. vehicle: 2+/-3%) and MAP (16+/-3 mmHg, vs. vehicle: 2+/-3 mmHg). Moxonidine (20 nmol) i.c.v. increased SSG vascular resistance (88+/-12% vs. vehicle: 7+/-4%). When injected 15 min following i.c.v. moxonidine, pilocarpine i.p. produced no change on SSG vascular resistance. Pilocarpine-induced pressor responses and increase in mesenteric vascular resistance were not modified by i.c.v. moxonidine. The treatments produced no change in heart rate (HR) and hindlimb vascular resistance. The results show that (1) i.p. pilocarpine increases mesenteric vascular resistance and MAP and reduces salivary gland vascular resistance and (2) central moxonidine increases salivary gland vascular resistance and impairs pilocarpine-induced salivary gland vasodilatation. Therefore, the increase in salivary gland vascular resistance may play a role in the anti-salivatory response to central moxonidine.
Assuntos
Pressão Sanguínea/efeitos dos fármacos , Frequência Cardíaca/efeitos dos fármacos , Imidazóis/administração & dosagem , Pilocarpina/farmacologia , Glândulas Salivares/efeitos dos fármacos , Animais , Pressão Sanguínea/fisiologia , Combinação de Medicamentos , Frequência Cardíaca/fisiologia , Membro Posterior/irrigação sanguínea , Membro Posterior/efeitos dos fármacos , Membro Posterior/fisiologia , Injeções Intraventriculares , Masculino , Artéria Mesentérica Superior/efeitos dos fármacos , Artéria Mesentérica Superior/fisiologia , Ratos , Ratos Sprague-Dawley , Glândulas Salivares/irrigação sanguínea , Glândulas Salivares/fisiologia , Resistência Vascular/efeitos dos fármacos , Resistência Vascular/fisiologiaRESUMO
Salivation induced by intraperitoneal (i.p.) injections of pilocarpine (cholinergic agonist) is reduced by intracerebroventricular (i.c.v.) injections of moxonidine (alpha(2) adrenergic and imidazoline receptor agonist). In the present study, we investigated the involvement of central alpha(2) adrenergic receptors in the inhibitory effect of i.c.v. moxonidine on i.p. pilocarpine-induced salivation. Male Holtzman rats with stainless steel cannula implanted into the lateral ventricle (LV) were used. Saliva was collected using pre-weighted small cotton balls inserted into the animal's mouth under ketamine (100 mg x kg(-1)) anesthesia. Salivation was induced by i.p. injection of pilocarpine (4 micromol x kg(-1)). Pilocarpine-induced salivation was reduced by i.c.v. injection of moxonidine (10 nmol) and enhanced by i.c.v. injections of either RX 821002 (160 nmol) or yohimbine (320 nmol). The inhibitory effect of i.c.v. moxonidine on pilocarpine-induced salivation was abolished by prior i.c.v. injections of the alpha(2) adrenergic receptor antagonists, RX 821002 (160 nmol) or yohimbine (160 and 320 nmol). The alpha(1) adrenergic receptor antagonist prazosin (320 nmol) injected i.c.v. did not change the effect of moxonidine on pilocarpine-induced salivation. The results suggest that moxonidine acts on central alpha(2) adrenergic receptors to inhibit pilocarpine-induced salivation, and that this salivation is tonically inhibited by central alpha(2) adrenergic receptors.
Assuntos
Encéfalo/metabolismo , Salivação/efeitos dos fármacos , Antagonistas Adrenérgicos alfa/administração & dosagem , Antagonistas Adrenérgicos alfa/farmacologia , Animais , Idazoxano/administração & dosagem , Idazoxano/análogos & derivados , Idazoxano/farmacologia , Imidazóis/administração & dosagem , Imidazóis/farmacologia , Injeções Intraperitoneais , Injeções Intraventriculares , Masculino , Agonistas Muscarínicos/administração & dosagem , Agonistas Muscarínicos/farmacologia , Pilocarpina/administração & dosagem , Pilocarpina/farmacologia , Prazosina/administração & dosagem , Prazosina/farmacologia , Ratos , Receptores Adrenérgicos alfa 2/metabolismo , Salivação/fisiologia , Simpatolíticos/administração & dosagem , Simpatolíticos/farmacologia , Ioimbina/administração & dosagem , Ioimbina/farmacologiaRESUMO
Peripheral treatment with cholinergic or adrenergic agonists results in salivation and the possibility of synergy between cholinergic and adrenergic efferent mechanisms in the control of salivation has been proposed. Central injections of the cholinergic agonist pilocarpine also induce salivation, while the effects of central injections of noradrenaline (norepinephrine) are not known. Here (a) the effects of intracerebroventricular (i.c.v.) injection of noradrenaline on the salivation induced by i.c.v. or intraperitoneal (i.p.) injection of pilocarpine and (b) the receptors involved in the effects of central noradrenaline on pilocarpine-induced salivation were investigated. Male Holtzman rats with a stainless-steel guide cannula implanted into the lateral ventricle were used. Rats were anaesthetized with tribromoethanol (200mg/kg body weight) and saliva was collected on small, preweighed cotton balls inserted into the animal's mouth. Noradrenaline (40, 80 and 160 nmol/1 microl) injected i.c.v. reduced the salivary secretion induced by pilocarpine (0.5 micro mol/1 microl) injected i.c.v.. Noradrenaline (80 and 160 nmol/1 microl) injected i.c.v. also reduced the salivation induced by pilocarpine (4 micromol/kg) injected i.p. Previous treatment with the alpha(2)-adrenergic receptor antagonists RX 821002 (40, 80 and 160 nmol/1 microl) or yohimbine (160 and 320 nmol/1 microl) abolished the inhibitory effect produced by i.c.v. injection of noradrenaline on pilocarpine-induced salivation in rats. Prazosin (alpha(1)-adrenergic receptor antagonist) injected icv did not change the effect of noradrenaline on pilocarpine-induced salivation. Prior icv injection of only RX 821002 (80 or 160 nmol/1 microl) or yohimbine (320 nmol/1 microl) increased pilocarpine-induced salivation. The results show that (1) contrary to its peripheral effects, noradrenaline acting centrally inhibits cholinergic-induced salivation in rats; (2) central mechanisms involving alpha(2)-adrenergic receptors inhibit pilocarpine-induced salivation.
Assuntos
Agonistas alfa-Adrenérgicos/farmacologia , Idazoxano/análogos & derivados , Agonistas Muscarínicos/metabolismo , Norepinefrina/farmacologia , Pilocarpina/antagonistas & inibidores , Salivação/efeitos dos fármacos , Antagonistas de Receptores Adrenérgicos alfa 1 , Antagonistas de Receptores Adrenérgicos alfa 2 , Agonistas alfa-Adrenérgicos/administração & dosagem , Antagonistas Adrenérgicos alfa/farmacologia , Análise de Variância , Animais , Idazoxano/farmacologia , Injeções Intraperitoneais , Injeções Intraventriculares , Masculino , Agonistas Muscarínicos/administração & dosagem , Norepinefrina/administração & dosagem , Pilocarpina/administração & dosagem , Prazosina/farmacologia , Ratos , Ratos Sprague-Dawley , Saliva/efeitos dos fármacos , Saliva/metabolismo , Estatística como Assunto , Ioimbina/farmacologiaRESUMO
O efeito da noradrenalina, isoproterenol, fentolamina e propanolol, injetados no núcleo basolateral da amigdala, sobre a ingestäo de água, foi investigado em ratos Holtzman. A injeçäo de noradrenalina (40nmol) no complexo amigdalóide (CA) de ratos saciados näo produziu nenhuma mudança na ingestäo de água em ratos saciados (1,93 ñ 0,23 ml/lh). A noradrenalina injetada no CA produziu uma diminuiçäo na ingestäo de água de ratos privados (0,40 ñ 0,19 ml/lh). A injeçäo de isoproterenol no CA de ratos privados näo produziu nenhuma mudança na ingestäo de água em comparaçäo aos controles (11,65 ñ 1,02 e 10,92 ñ 0,88 ml/lh, respectivamente). Quando comparado com valores controles, a fentolamina injetada prévia à noradrenalina bloqueou o efeito inibitório da noradrenalina sobre a ingestäo de água em ratos privados 10,40 ñ 1,31 ml/lh). O propanolol bloqueou o efeito do isorpoterenol em ratos saciados (0,85 ñ 0,49 ml/lh) e também bloqueou a ingestäo água induzida por privaçäo (0,53 ñ 0,38 ml/lh). Tanto em animais saciados quanto em privados, a injeçäo de fentolamina, antes da administraçäo de hexametônio, bloqueou o efeito inibitório do hexametônio na ingestäo de água. Em animais saciados, quando o hexametônio foi injetado sozinho, a ingestäo de água foi de 0,39 ñ 0,25 ml/lh; quando acompanhado de fentolamina, a ingestäo de água foi de 1,04 ñ 0,3 ml/lh. Em ratos privados, o hexametônio sozinho bloqueou a ingestäo de água (0,40 ñ 0,17 ml/lh) e quando injetado com fentolamina produziu uma ingestäo de 9,7 ñ 1,8 ml/lh. Este resultados demonstram claramente a participaçäo de receptores catecolaminérgicos do CA na regulaçäo da ingestäo de água.
Assuntos
Animais , Masculino , Ratos , Tonsila do Cerebelo/efeitos dos fármacos , Relação Dose-Resposta a Droga , Ingestão de Líquidos , Isoproterenol/farmacologia , Norepinefrina/farmacologia , Fentolamina/farmacologia , Propranolol/farmacologia , Hexametônio/administração & dosagem , Ratos Endogâmicos , Ratos Sprague-Dawley , Receptores Adrenérgicos alfaRESUMO
No presente trabalho foi estudado o efeito da estimulaçäo e nicotínica do complexo amigdalóide (CA) sobre a ingestäo de sódio e água em ratos saciados e privados de água. A nicotina näo produziu nenhuma alteraçäo no apetite ao sódio e água em ratos saciados. Em ratos privados, a nicotina injetada no núcleo basolateral somente bloqueou a ingestäo de cloreto de sódio. Nós demonstramos previamente que o carbacol, injetado no CA, inibiu a ingestäo de água e cloreto de sódio em ratos saciados e privados de água. A injeçäo de hexametônio no CA bloqueou totalmente a ingestäo de água em ratos saciados e privados de água. A administraçäo de hexametônio no CA, antes da injeçäo de nicotina,näo produziu alteraçäo na ingestäo de sódio. Assim, estes resultados sugerem que a populaçäo de neurônios colinoceptivos específicos do CA medeiam a ingestäo de água e cloreto de sódio
Assuntos
Animais , Ratos , Tonsila do Cerebelo/efeitos dos fármacos , Compostos de Hexametônio/farmacologia , Ingestão de Líquidos , Nicotina/farmacologia , Cloreto de Sódio , Privação de ÁguaRESUMO
Injetaram-se, intraperitonealmente, soluçäo fisiológica ou 50 µg/kg/dia de cloridrato de cocaína em camundongos albinos com 23 dias de idade. O volume nuclear das células acinares e ductulares foi determinado morfometricamente. Foi observada uma reduçäo estatisticamente significativa na média dos volumes nucleares das células dos ductos granulosos e nas acinares de glândulas submandibulares provenientes de animais tratados com cocaína quando comparados com o controle. Estas alteraçöes induzidas pela cocaína podem ser devidas ao bloqueio da captaçäo neuronal induzido pela droga ou a interferência da droga com a atividade das gonadas ou outras glândulas endócrinas
Assuntos
Animais , Masculino , Camundongos , Cocaína/farmacologia , Glândula Submandibular/anatomia & histologia , CariometriaRESUMO
Foram estudados os efeitos sobre a pressäo arterial sistêmica após a administraçäo de noradrenalina e de dois antagonistas de alfa-adrenoceptores no hipotálamo médio de ratos normotensos. Tanto o prazosin quanto a ioimbina antagonizaram a açäo do agonista misto de alfa1/alfa2-adrenoceptores, a noradrenalina ; entretanto a administraçäo prévia de prazosin mostrou uma maior interaçäo da noradrenalina pelos adrenoceptores alfa1. Estes resultados sugerem que os adrenoceptores alfa1 do hipotálamo médio exerceriam uma maior influência que os adrenoceptores alfa2 no controle de pressäo arterial sistêmica