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1.
J Appl Physiol (1985) ; 87(2): 722-31, 1999 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-10444633

RESUMO

Glucose utilization increases markedly in the normal dog during stress induced by the intracerebroventricular (ICV) injection of carbachol. To determine the extent to which insulin, glucagon, and selective (alpha/beta)-adrenergic activation mediate the increment in glucose metabolic clearance rate (MCR) and glucose production (R(a)), we used five groups of normal mongrel dogs: 1) pancreatic clamp (PC; n = 7) with peripheral somatostatin (0.8 microg x kg(-1) x min(-1)) and intraportal replacement of insulin (1,482 +/- 84 pmol x kg(-1) x min(-1)) and glucagon (0.65 ng x kg(-1) x min(-1)) infusions; 2) PC plus combined alpha (phentolamine)- and beta (propranolol)-blockade (7 and 5 microg x kg(-1) x min(-1), respectively; alpha+beta; n = 5); 3) PC plus alpha-blockade (alpha; n = 6); 4) PC plus beta-blockade (beta; n = 5); and 5) a carbachol control group without PC (Con; n = 10). During ICV carbachol stress (0-120 min), catecholamines, ACTH, and cortisol increased in all groups. Baseline insulin and glucagon levels were maintained in all groups except Con, where glucagon rose 33%, and alpha, where insulin increased slightly but significantly. Stress increased (P < 0.05) plasma glucose in Con, PC, and alpha but decreased it in beta and alpha+beta. The MCR increment was greater (P < 0.05) in beta and alpha+beta than in Con, PC, and alpha. R(a) increased (P < 0.05) in all groups but was attenuated in alpha+beta. Stress-induced lipolysis was abolished in beta (P < 0.05). The marked rise in lactate in Con, PC, and alpha was abolished in alpha+beta and beta. We conclude that the stress-induced increase in MCR is largely independent of changes in insulin, markedly augmented by beta-blockade, and related, at least in part, to inhibition of lipolysis and glycogenolysis, and that R(a) is augmented by glucagon and alpha- and beta-catecholamine effects.


Assuntos
Glucose/metabolismo , Insulina/metabolismo , Estresse Fisiológico/metabolismo , Adrenérgicos/farmacologia , Animais , Glicemia/metabolismo , Carbacol , Catecolaminas/sangue , Ventrículos Cerebrais , Cães , Ácidos Graxos/sangue , Glucagon/sangue , Hemodinâmica/efeitos dos fármacos , Ácido Láctico/sangue , Ligadura , Masculino , Taxa de Depuração Metabólica , Pâncreas/metabolismo , Fentolamina/farmacologia , Estresse Fisiológico/induzido quimicamente
2.
Diabetes Metab ; 22(2): 111-21, 1996 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-8792091

RESUMO

Hyperglycaemia in diabetes results from a combination of increased hepatic glucose production and decreased metabolic clearance of glucose. Our report summarizes recent work conducted in our laboratory to investigate the regulatory factors involved in the control of glucose turnover in diabetes. The action of insulin, both directly and indirectly, in regulating glucose turnover in diabetic dogs is considered. 1) In the depancreatized diabetic dog, peripheral rather than portal insulin levels determine the suppression of hepatic glucose production via indirect mechanisms such as limiting, precursors for gluconeogenesis and/or inhibiting glucagon secretion. 2) The differential effects of insulin and insulin-like growth factor I on glucose turnover may be dependent on a decline in glycaemia since previously observed differential effects on glucose turnover were masked under conditions of clamped hyperglycaemia in the depancreatized dog. 3) In a paradoxical dichotomous fashion, hyperglycaemia both contributes to, and compensates for, defective glucose clearance in diabetes. Acute restoration of euglycaemia significantly improves glucose clearance at rest and normalizes the exercise-induced increment in clearance in alloxan-diabetic dogs. 4) Our model of centrally-induced stress also shows that an increase in glucose utilization and clearance is largely independent of changes in insulin and that the combined effects of catecholamines and glucagon are responsible for increasing glucose production.


Assuntos
Diabetes Mellitus Experimental/metabolismo , Diabetes Mellitus Experimental/fisiopatologia , Glucose/metabolismo , Insulina/fisiologia , Animais , Glicemia/metabolismo , Carbacol/farmacologia , Ventrículos Cerebrais/efeitos dos fármacos , Ventrículos Cerebrais/fisiologia , Ventrículos Cerebrais/fisiopatologia , Cães , Homeostase , Hiperglicemia/metabolismo , Hiperglicemia/fisiopatologia , Insulina/farmacologia , Fator de Crescimento Insulin-Like I/fisiologia , Fígado/metabolismo , Agonistas Muscarínicos/farmacologia , Pancreatectomia , Esforço Físico , Receptor IGF Tipo 1/fisiologia , Receptores Adrenérgicos/fisiologia , Estresse Fisiológico
3.
Health Care Strateg Manage ; 2(10): 14-6, 1984 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-10268565

RESUMO

There are a variety of marketing approaches available to hospitals to help maintain and/or increase their influence in the competitive health care system. This article will focus on one important but relatively ignored aspect tha must be an integral part of any successful hospital marketing program. Referring physicians and the network this group forms around a hospital through the different referral patterns is of primary influence on the hospital's future. This article supports the thesis that the hospital's eventual survival or demise is directly linked to this often unconscious referral network.


Assuntos
Hospitais/estatística & dados numéricos , Marketing de Serviços de Saúde , Encaminhamento e Consulta , Médicos , Estados Unidos
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