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To determine if pancreatic sympathetic nerves can contribute to increased glucagon secretion during hypoglycemia, plasma glucagon and pancreatic glucagon secretion in situ were measured before and during insulin-induced hypoglycemia in three groups of halothane-anesthetized dogs. All dogs were bilaterally vagotomized to eliminate the input from pancreatic parasympathetic nerves. One group of dogs received only vagotomy (VAGX). A second group was vagotomized and adrenalectomized (VAGX + ADX). A third group received vagotomy, adrenalectomy, plus surgical denervation of the pancreas (VAGX + ADX + NERVX) to prevent activation of pancreatic sympathetic nerves. In dogs with VAGX only, hypoglycemia increased plasma epinephrine (Epi), pancreatic norepinephrine (NE) output (+320 +/- 140 pg/min, P < 0.05), arterial plasma glucagon (+28 +/- 12 pg/ml, P < 0.01), and pancreatic glucagon output (+1,470 +/- 370 pg/min, P < 0.01). The addition of ADX eliminated the increase of Epi but did not increase pancreatic NE output (+370 +/- 190 pg/min, P < 0.025), arterial plasma glucagon (+20 +/- 5 pg/ml, P < 0.01), or pancreatic glucagon output (+810 +/- 200 pg/min, P < 0.01). In contrast, the addition of pancreatic denervation eliminated the increase of pancreatic NE output (-20 +/- 40 pg/min, P < 0.05 vs. VAGX), the arterial glucagon (+1 +/- 2 pg/ml, P < 0.01 vs. VAGX), and pancreatic glucagon output responses (+210 +/- 280 pg/min, P < 0.025 vs. VAGX) to hypoglycemia. Thus activation of pancreatic sympathetic nerves can contribute to the increased glucagon secretion during severe insulin-induced hypoglycemia in dogs.

To determine whether norepinephrine (NE) and galanin are coreleased during reflex activation of the sympathetic nervous system by hypoglycemia, we administered insulin to halothane-anesthetized (0.8%) dogs and measured the spillover of NE and galanin-like immunoreactivity (GLIR) into pancreatic venous plasma. Insulin injection produced hypoglycemia [plasma glucose (PG) = 34 +/- 3 mg/dl] but did not activate pancreatic noradrenergic (delta pancreatic NE output = +20 +/- 130 pg/min) or galaninergic nerves (delta GLIR output = +40 +/- 50 fmol/min). To determine whether more severe hypoglycemia would activate these nerves, insulin was administered to dogs infused with somatostatin (SS; 2.5 micrograms/min) to block the counterregulatory increase of glucagon secretion. SS reduced the glucagon response to hypoglycemia by greater than 90%, which allowed PG to decrease to 14 +/- 1 mg/dl. Pancreatic NE output increased by 470 +/- 140 pg/min (P less than 0.005); however, pancreatic GLIR output did not increase significantly (delta = +70 +/- 50 fmol/min). When SS was discontinued, pancreatic NE output increased by 490 +/- 200 pg/min (P less than 0.025), and GLIR output increased by an additional +160 +/- 70 fmol/min (P less than 0.025; total delta from baseline = +230 +/- 90 fmol/min, P less than 0.025), suggesting that SS may restrain pancreatic NE and galanin release. Pancreatic NE and GLIR spillover were also increased during severe hypoglycemia when ganglionic neurotransmission was partially impaired with hexamethonium but not when the neural pathway was interrupted by spinal cord transection. We conclude that NE and galanin are coreleased from pancreatic sympathetic nerves when these nerves are centrally activated during severe hypoglycemia in halothane-anesthetized dogs.

To address the hypothesis that the neutropeptide, galanin, functions as a sympathetic neurotransmitter in the endocrine pancreas, we sought to determine if galanin is released from pancreatic sympathetic nerves during their direct electrical stimulation in halothane-anesthetized dogs. During bilateral thoracic splanchnic nerve stimulation (BTSNS), both peripheral arterial and pancreatic venous levels of galanin-like immunoreactivity (GLIR) increased (delta at 10 min = +92 +/- 31 and +88 +/- 25 fmol/ml, respectively). Systemic infusions of synthetic galanin demonstrated that 1) the increment of arterial GLIR observed during BTSNS was sufficient to modestly restrain basal insulin secretion and 2) only 25% of any given increment of arterial GLIR appears in the pancreatic vein, suggesting that the pancreas extracts galanin, as it does other neurotransmitters. By use of 75% for pancreatic extraction of circulating galanin, it was calculated that pancreatic galanin spillover (output) increased by 410 +/- 110 fmol/min during BTSNS. To reinforce the conclusion that pancreatic sympathetic nerves release galanin, GLIR spillover was next measured during direct local stimulation of the pancreatic sympathetic input produced by electrical stimulation of the mixed autonomic pancreatic nerves (MPNS) in the presence of the ganglionic blocker, hexamethonium. During this local pancreatic sympathetic nerve stimulation, arterial GLIR remained unchanged, but pancreatic venous GLIR increased by 123 +/- 34 fmol/ml. Thus pancreatic GLIR spillover increased by 420 +/- 110 fmol/min during MPNS in the presence of hexamethonium. We conclude that galanin is released from both pancreatic and extrapancreatic sources during sympathetic neural activation in dogs.

Determines the role of glucagon in hepatic glutamine (Gln) metabolism during exercise in dogs. Implantation of sampling and infusion catheters and flow probes; Infusion of somatostatin throughout the study; Simulation of exercise-induced insulin decrement through the reduction of insulin infusion; Increase of hepatic Gln uptake and fractional extraction.

Studies the relative contribution of phasic and tonic excitatory synaptic drives to the augmenting discharge patterns of inspiratory (I) neurons within the ventral respiratory group (VRG) in dogs. Responses of I neurons to GABAergic and glutamatergic antagonists; Effects of strychnine.

Examines the presence of clathrin in mitotic spindles. Role of clathrin in the regulation of receptor-mediated endocytosis; Immunostaining of subconfluent cultures of Madin-Darby canine kidney and CV-1 cells with monoclonal antibodies against clathrin heavy chain; Colocalization of clathrin with microtubular arrays in the spindle.

Shows that the inducible isoform of nitric oxide synthase (iNOS) is present in freshly dispersed vascular smooth muscle cells (VSMC) from canine femoral artery. Absence of relationship between iNOS expression in cultured VSMC; Failure of insulin to acutely affect iNOS activity in VSMC; Augmentation of cyclic guanosine monophosphate production.

Studies the relationship between autonomic activity to the pancreas and insulin secretion in chronically catheterized dogs when food was shown. Pancreatic polypeptide output, pancreatic norepinephrine spillover and arterial epinephrine (Epi); Mediation of the insulin response by the beta2-adrinergic effect of Epi.

To determine the suitability of halothane anesthesia for studies of parasympathetic control of the endocrine pancreas in dogs, we assessed the effect of halothane on reflex, direct neural, and direct chemical activation of the parasympathetic input to the islet. Levels or output of pancreatic polypeptide (PP), an islet hormone under predominant cholinergic influence, were used as an indicator of the degree of parasympathetic activation and its potential suppression by anesthesia. Reflex stimulation of the parasympathetic nervous system by 2-deoxy-D-glucose (2-DG) in dogs anesthetized with halothane (0.8%) caused a fourfold increase in plasma PP levels, equivalent to the response in conscious dogs. In contrast, 2-DG at this dose and at a threefold higher dose did not alter PP levels in dogs anesthetized with pentobarbital (30 mg/kg iv), suggesting that halothane at this dose is not suppressive and that pentobarbital is very suppressive on reflex activation of the parasympathetic nerves to the pancreas. Bilateral electrical stimulation of the cervical vagi in halothane-anesthetized dogs elicited a sixfold increase in the pancreatic output of PP. The same stimulation caused only a twofold increase of PP output in pentobarbital-anesthetized dogs. These data suggests that halothane is also less inhibitory than pentobarbital on either peripheral neurotransmission or pancreatic F-cell responsiveness. The effect of direct activation of the F-cell by bethanechol did not differ between the two anesthesias. Therefore, the attenuated PP response to vagal stimulation in pentobarbital-anesthetized dogs is probably due to an action of pentobarbital on peripheral neurotransmission, perhaps at the intrapancreatic parasympathetic ganglia.(ABSTRACT TRUNCATED AT 250 WORDS)

To determine the suitability of halothane anesthesia for studies of sympathetic control of the endocrine pancreas in dogs, we assessed the effect of halothane anesthesia (0.8% inspired concentration) on the sympathetic response to central neuroglucopenia. In dogs anesthetized with halothane, intravenous administration of the neuroglucopenic agent, 2-deoxy-D-glucose (2-DG; 100 mg/kg), produced increases of both systemic plasma epinephrine (EPI; delta = 269 +/- 86 pg/ml, P less than 0.025) and norepinephrine (NE; delta = 157 +/- 55 pg/ml, P less than 0.025) equivalent to those previously observed in conscious dogs. Measurement of plasma NE kinetics revealed that the plasma NE response to 2-DG during halothane was due to an increase in the rate of NE appearance that was identical to that of conscious dogs, rather than to an impairment of NE clearance. In contrast, 2-DG at this dose did not increase plasma EPI or NE levels in dogs anesthetized with pentobarbital sodium (30 mg/kg). Plasma glucose increased modestly after 2-DG (100 mg/kg) in both conscious and halothane-anesthetized dogs but not in the pentobarbital-anesthetized dogs. Although 2-DG at a threefold higher dose (300 mg/kg) caused plasma EPI, NE, and glucose (delta = 12 +/- 3 mg/dl, P less than 0.001) to increase in pentobarbital-anesthetized dogs, the responses to this higher dose of 2-DG were all significantly larger in halothane-anesthetized dogs (delta of plasma glucose = 30 +/- 8 mg/dl, P less than 0.005; P less than 0.0025 vs. pentobarbital).(ABSTRACT TRUNCATED AT 250 WORDS)

Provides information on a study which estimated regional left ventricular wall stresses in intact canine hearts. Theoretical background; Materials and methods; Results and discussion.

Presents a study which examined the effects prokinetic drugs in regional gastrointestinal transit in the dog using scintigraphic measurement. Materials and methods; Results and discussion.

Presents a study investigating the mutual information discloses relationship between hemodynamic variables in artificial heart-implanted dogs. Methodology used to conduct the study; Recording of nerve activity; Information on the power spectrum analysis of heart rate (HR) or arterial blood pressure (BP); Findings of the study.

Focuses on a study which examined six dogs in saline infusion, sufentanil infusion, after endotoxin injection and during combined endotoxin injection, to determine the effects of sufentanil on the inflammatory, neuroendocrine, and metabolic responses to endotoxin. Evaluation of whether exogenous opiates modulated the inflammatory, endocrine and metabolic responses; Method used to prepare the dogs; Results of the clinical parameters.

Presents a study which was conducted to determine the role of the posterior atrial ganglionated plexus (PAGP) in the control of the canine heart rate (HR) response. Materials and methods used to conduct the study; Reference to the importance of the physiological importance of autonomic neurons located on the heart; Results and discussion of the study.

Focuses on a study which tested the theory that acute hyperglycemia abolishes ischemic preconditioning-induced myocardial protection, and increases myocardial infarct size in a dose-related fashion in barbiturate-anesthetized dogs. Methods used to conduct the study; Information on the possible role of ischemic preconditioning to reduce the extent of myocardial infarction in patients with a history of angina; Discussion on the study.

Presents a study which examined the effects of angiotensin-converting enzyme (ACE) inhibitors on cardiomyocyte apoptosis in dogs with heart failure. Methods used to conduct the study; Reduction of mortality after long-term therapy with ACE; What causes modern heart failure in dogs; Results and discussion on the study.

Presents a study which examined the delayed rectifier K+ current of dog bronchial myocytes, while focusing on the effectiveness of the pollen sensitization and protein kinase C (PKC) activation. Excision of canine lungs; Dissection of bronchial trees; What the dysfunctional control of smooth muscle tone contributes to; Importance of the level of resting membrane potential.

Presents a study which focused on the autonomic nervous control relating to the venous pressure (Phv) and secretion in submandibular gland of the anesthetized dogs. What the parasympathetic nerve stimulation causes; Dependency of the fluid movement across the capillary walls; Relation of the sympathetic inhibition of parasympathetic salivation to prevention of an increased Phv.

Presents information on the secretory effects of adenosine triphosphate (ATP) on nontransformed dog pancreatic duct epithelial cells. How the effects of ATP are mediated; Impact of short-circuiting of spontaneous potential differences.

Focuses on the stimulation of ion transport by histamine, in connection with the dog pancreatic duct epithelial cells through H1 receptors. Effects of histamine on pancreatic secretion; Characteristics of histamine; Consistency of pancreatic exocrine function.

Provides information on a study investigating renal effects of physiological amounts of vasopressin natriuresis in conscious dogs during servocontrolled overhyration. Methodology and materials used to conduct the study; State of water diuresis; Analysis of vasopressin natruiresis; Findings of the study.

Investigates the role of potassium channels in secretion of adrenal catecholamine in response to splanchnic nerve stimulation, while highlighting studies conducted on anesthetized dogs. Conditions under which experiments were conducted; What findings of studies indicate; Methodology of studies.

Analyses R-R intervals with approximate entropy and entropy of symbolic dynamics to assess the effects of reducing system complexity, while highlighting studies conducted on the heart rate of conscious dogs. Factors which attribute to changes in the heart rate; Conditions under which studies were conducted.

Examines how the ventricular stretch affects the contractile strength, calcium transient, adenosine 3', 5'-cyclic monophosphate (cAMP) in intact canine hearts. How were the isovolumic contractions imposed; Circumstances surrounding the stretching of the myocardium; Information on the measurement of the regional blood flow (RBF).

Discusses the left ventricular diastolic function of remodeled myocardium in dogs with pacing-induced heart failure. Information on the biological status of patients with heart failure; How elastic properties of the myocardium were determined; Characterization of the elastic recoil.

Examines how the ischemic preconditioning on contractile and metabolic function can effects the hypoperfusion in dogs. Information regarding the left anterior descending coronary artery (LAD); Description of most ischemia; Suggestions of results; How regional myocardinal blood flow was determined; Circumstances surrounding the ascertaining of the baseline measurements.

Focuses on a study of the hemodilution and hyperoxia locally change distribution of regional pulmonary perfusion in dogs. Monitoring of normovolemic hemodilution (ANH); Spatial correlation of rPBF in the whole lung; Methodology used in the study; Details on the experimental design; Measurement of the blood volume; Performance of statistical analyses; Results of the study.

Studies load-sensitive diastolic relaxation in hypertrophied left ventricles in sixteen dogs. Effects of enalaprilat and L-158,809, and angiotensin II type-1receptor antagonist; Purpose of the study; Methods and materials used in the study; Assessment of left ventricular relaxation rate; Provision of statistical analysis; Detailed information on the results; Conclusion reached based on the results.

Focuses on a study of the selective large coronary endothelial dysfunction in conscious dogs with chronic coronary pressure overload. Investigation of coronary vascular responses to acetylcholine, nitroglycerin, and a 20-s coronary artery occlusion; Amount of dogs who participated in the study; Details on the methods used; Results of the study; Conclusion reached based on the results.

Discusses the lack of beneficial effects of growth hormone treatment in conscious dogs during development of heart failure. Information on the study of fourteen conscious dogs; Significant increase of both body weight and plasma insulin-like growth factor; Reference to the results of the conducted study.

Looks at how insulin acutely suppresses glucose production by both peripheral and hepatic effects in normal dogs. Determination of predominant effect of insulin in supressing tracer-determined glucose production; Details on the experimental procedure used to prepare animals; Examination of the plasma insulin and C-peptide levels; Result obtained from high-rate insulin fusion study.

Presents a study which indicates that the early hypotension and cardiac dysfunction in dogs was not associated with an increase in plasma nitric oxide (NOx) production. Effects of endotoxin in late cardiovascular dysfunction in dogs; Cardiac and vascular dysfunction after lipopolysaccharide (LPS); Methodology used to carry out the study; Results of the study.

Presents a study where epicardial lymph pressure generation was studied in a region of left ventricular myocardium during normal contraction and while contraction in that region was impaired with lidocaine in anesthetized dogs. Methodology used to conduct the study; What epicardial lymph pressure measurements can provide; Results of the study.

Presents a study which relates to the central gain involved with the cardiac sympathetic afferent reflex in dogs with heart failure. Information on the reflex activities of fifteen dogs during an experiment; Identification of left stellate ganglion; Details on the significance of the reflex renal sympathetic nerve activity responses to stimulation of the cardiac sympathetic nerves; Suggestion of data.

Focuses on a study which looked at whether canine hepatic galanin is localized in the sympathetic nerves, using dog livers. Indepth look at the parallel decrease of galanin-like immuno-reactivity (GALIR); Methodology used to conduct the study; Results of the study.

Investigates whether the dihydropyridine-sensitive L-type Ca2+ channel is operative in adrenal catecholamine (CA) secretion induced by a novel neuropeptide, pituitary adenylate cyclase-activating polypeptide (PACAP), in anesthetized dogs. Methodology used in study; Amplitude of epinephrine response to PACAP-27; Indications on both PACAP-27 and PACAP-38; Suggestions about the dihydropyridine-sensitive L-type Ca2+ channel.

Investigates whether cervical nerve stimulation after AV conduction-related para-sympathetic nerves (AVCRPN) denervation also prolonged the AV conduction time shortened by sympathetic interventions as does cervical vagus stimulation on sinus rate in anesthetized dogs. Methodology used in study; Impact of vagus stimulation on A-H interval; What results suggested about regional vagus inputs during sympathetic activation.

Investigates the role of ...- and ...-adrenoceptors in the total vascular capacitance responses to changing pressure in vascularly isolated carotid sinuses of anesthetized and atropinized dogs. Methodology used in study; Result of changes recorded in carotid sinus pressure; Suggestions drawn from results of study.

Examines the study of the K+-C1- cotransport and regulatory volume decrease in dog red blood cells with high K+, low Na+ and high glutathione (GSH) content. Materials and methods of used in the study; Results of the study.

Studies the left venticular spherical dilation and regional contractile dysfunction in dogs with heart failure. Methodology of study; Results of the study; Discussion on the study.

Presents information on a study which examined the blood flow versus blood pressure in the control of renin release in conscious dogs. Materials and methods used in testing; How shear stress was measured; Results of experiments conducted.

Gives detailed information pertaining to the study which states that volume-overload cardiac hypertrophy is unaffected by ACE inhibitor treatment in dogs. Methodology used to conduct the study; Observations made in the study.

Examines the activity and expression of sarcoplasmic reticulum (SR) Ca2+-ATPase in left ventricular (LV) myocardium of dogs with chronic heart failure (HF). Details on the process of LV dysfunction; Study methodology; Materials used; Results indicating that SR Ca2+-ATPase activity and expression are reduced in the LV myocardium of dogs with chronic HF.

Presents information from a study of direct quantification of norepinephrine spillover and hormone output from the pancreas of the conscious dog. Methodology necessary to conduct study; What was chronically cannulated; Details on the study; Materials used to conduct study; Results of study; Conclusions of study.

Compares the frequency of gastric pacesetter potential (PP) while isolating the volume distension to either the stomach or the small bowel during the course of gastric emptying in dogs. Techniques used in experiment; Findings; References.

Tests various hypotheses on the canine intrinsic cardiac nervous system. Association of the specific marker for nitric oxide production with canine intrinsic cardiac neurons; Alternation of the transmembrane properties of these neurons by nitric oxide donors; Sensitivity to nitric oxide neurons of in situ neurons; Neuronal involvement in cardiac regulation.

Examines the impact of an acute decrease in glucagon to nonseptic levels on gluconeogenesis in an infected dog. Effect of sepsis basal parameters; Hormone levels, hepatic blood flows and glucose metabolism; Hepatic gluconeogenesis; Hepatic glycogen.

Investigates the effects of captopril on the autonomic control of the circulation in conscious dogs and in dynamic conditions. Link between Sympathetic activation and systolic arterial pressure variabilities; Subjecting dogs to bilateral carotid artery occlusion, transient myocardial ischemia and treadmill exercise.

Investigates the beta-adrenergic receptor signaling mechanisms in mediating physiological responses to sympathomimetic amines after reperfusion. Infusion of isoproterenol or forskolin in dogs; Myocardial blood flow; Beta-adrenergic receptor agonist binding; Adenylyl cyclase activity and G proteins; Measurement of catecholamine levels.