BACKGROUND: Epidural block is known to block sympathetic efferent nerve fiber, resulting in the decrease of catecholamine. We examined the effects of thoracic epidural block on DFT, neuroendocrine responses and hemodynamic changes in dogs. METHODS: Twenty one dogs were divided into three groups. The control group (N = 7) was anesthesized with only alpha-chloralose for general anesthesia, and a high thoracic epidural (T; N = 7) while the thoracolumbar epidural groups (TL; N = 7) were put under general anesthesia with high thoracic or thoracolumbar epidural blocks, respectively. The DFT was determined at 30 mins after surgical manipulation in the control group and at 10 mins after the epidural blocks in the two epidural groups. Four hemodynamic variables, catecholamine, cAMP and lactate were measured at 30 mins after the surgical manipulation (resting period), at 10 mins after epidural blocks and after defibrillation. RESULTS: 1) The DFT levels were significantly higher in the T (6.4 +/- 2.2 J) and TL groups (11.2 +/- 9.3 J) than in the control group (3.2 +/- 1.6 J)(P < 0.05). In the TL group, epinephrine-induced second DFT was lower (3.0 +/- 1.5 J) than the first DFT (11.2 +/- 9.3 J)(P < 0.05). 2) Catecholamine levels and hemodynamic variables including heart rate, mean arterial pressure, and cardiac output significantly decreased in the TL group compared with the control group after epidural block and defibrillation (P < 0.05). The DFT showed a significant correlation with plasma epinephrine levels after the epidural block (r = 0.56, P < 0.05). CONCLUSIONS: Our results show, an increase in transmyocardial DFT by the epidural block which may be caused by a decrease in catecholamine, especially epinephrine.
Anesthesia, General ; Animals ; Arterial Pressure ; Cardiac Output ; Chloralose ; Dogs* ; Epinephrine ; Heart Rate ; Hemodynamics ; Lactic Acid ; Nerve Fibers ; Plasma

The purpose of this study was to investigate the influence of NK1 receptor antagonists on the pulpal blood flow (PBF) when applied iontophoretically through the dentinal cavity of the teeth in order to understand whether iontophoretically applied NK1 receptor antagonists can control the pulpal inflammation. Eleven cats were anesthetized with alpha-chloralose and urethane, and substance P (SP) was administered to the dental pulp through the catheterized lingual artery in doses that caused PBF change without the influence of systemic blood pressure. NK1 receptor antagonists were applied iontophoretically to the prepared dentinal cavity of ipsilateral canine teeth of the drug administration, and PBF was monitored. Data were analyzed statistically with paired t-test. PBF increase after iontophoretic application of the NK1 receptor antagonists followed by the intra-arterial administration of SP was significantly less than PBF increase after iontophoretic application of the 0.9% saline followed by the intra-arterial administration of SP as a control (p < 0.05). Iontophoretic application of the NK1 receptor antagonists (0.2~3.4 mM) following the intra-arterial administration of SP resulted in less increase of PBF than the iontophoretic application of the 0.9% saline following the intra-arterial administration of SP as a control (p < 0.05). Therefore, the results of the present study provide evidences that the iontophoretic application is an effective method to deliver drugs to the dental pulp, and that iontophoretically applied NK1 receptor antagonists block SP-induced vasodilation effectively. The above results show the possibility that the iontophoretical application of NK1 receptor antagonists can control the neurogenic inflammation in the dental pulp.
Animals ; Arteries ; Blood Pressure ; Catheters ; Cats* ; Chloralose ; Cuspid ; Dental Pulp ; Dentin ; Inflammation ; Iontophoresis ; Neurogenic Inflammation ; Substance P ; Tooth ; Urethane ; Vasodilation

BACKGROUND AND OBJECTIVES: The ventricular pacing electrodes are customarily placed into the right ventricular muscle because there is easily accessible. However detailed physiologic studies have shown that the single stimulation of right ventricular sites causes dysynchronous ventricular contraction due to early depolarization of the right ventricle and delayed depolarization of the left ventricle. In contrast, normal human ventricular activation, which is conducted by the Purkinje system, spreads transmurally from the endocardium to multiple paraseptal epicardial regions and results in more synchronous contraction of the ventricle. Therefore, the hypothesis that producing biventricular activation by simultaneously pacing ventricles across the septum might confer hemodynamic benefits over those of conventional right ventricular pacing. The purpose of this study was to evaluate the acute hemodynamic changes of different pacing modes (right ventricular : RV, biventricular : BV, atrio-right ventricular : A-RV, and atrio-biventricular : A-BV pacing). MATERIALS AND METHOD: In 9 open chest dogs anesthetized with alpha-chloralose, sinus node crushing was done, and then hemodynamic data (QRS width, femoral arterial pressure : FAP, pulmonary arterial pressure : PAP, and Cardiac output : CO) were acquired after 5 minutes of pacing at a fixed rate during each pacing mode. RESULTS: Results were as follow : 1. BV pacing significantly increased cardiac output compared with RV pacing (P<0.01). BV pacing significantly shortened QRS width compared with RV pacing (P<0.01). 2. A-BV pacing significantly increased cardiac output compared with A-RV pacing (P<0.01). A-BV pacing significantly shortened QRS width compared with A-RV pacing (P<0.01). 3. A-RV pacing significantly increased systolic pulmonary arterial pressure and cardiac output compared with BV pacing (P<0.01). CONCULSION: These results support the use of atrio-biventricular pacing to improve acute hemodynamic performance.
Animals ; Arterial Pressure ; Cardiac Output ; Cardiac Resynchronization Therapy* ; Chloralose ; Dogs* ; Electrodes ; Endocardium ; Heart Ventricles ; Hemodynamics* ; Humans ; Sinoatrial Node ; Thorax*

The medullospinal tract cells are known to play an important role in the control of the cardiovascular activities. To clarify the modes of action of the neurotransmitters on these cells, glutamate, GABA (gamma-aminobutyric acid) and bicuculline were applicated iontophoretically into the rostral ventrolateral medulla in adult cats anesthetised with alpha-chloralose. Followings are the results obtained : 1. The spontaneous activities of the cardiac-related neurons in rostral ventrolateral medulla (RVLM) were increased by the glutamate and decreased by the GABA. 2. Bicuculline, an antagonist of GABA, alone didn't increase the frequency of the action potentials, but could reverse the cellular response to the GABA, simultaneously applicated. 3. GABA seemed to decrease the peak as well as the basal discharge of the neurons in RVLM, but hardly changed their periodicities. 4. The cellular responses of RVLM evoked by the peripheral nerve stimulation could be inhibited by the iontophoretically released GABA. In conclusion, GABA seemed to act as an inhibitory neurotransmitter on the cardiac-related neurons in RVLM of the cats anesthetized with alpha-chloralose. But the maintenance of the periodicities of these cells after the application of bicuculline suggested that the afferent activity of the baroreceptor didn't play a key role in the spontaneous activities of the RVLM neurons.
Action Potentials ; Adult ; Animals ; Bicuculline ; Cats ; Chloralose ; gamma-Aminobutyric Acid ; Glutamic Acid ; Humans ; Iontophoresis ; Neurons ; Neurotransmitter Agents* ; Periodicity ; Peripheral Nerves ; Pressoreceptors

BACKGROUND: The hemodynamic effects of an episode of ventricular tachycardia (VT) may vary from mild decrease in blood pressure to sustained hypotension, collapse, and death. Little is known about the factors responsible for these diverse effects. Ventricular function, vasomotor tone, and tachycardia cycle length could be major determinants of variable hemodynamic responses to VT. The site of origin was found to be a factor affecting pulse pressure even in an isolated ventricular premature contraction. However, the role of origin site in hemodynamics of VT is not yet elucidated. The purposes of this study were to evaluate the effects of VT origin site and VT cycle length to their hemodynamic changes. And we also have assessed the role of cardiac autonomic receptor activation in hemodynamic recovery during and immediate after VT. METHODS: In 18 open chest dogs anesthetized with chloralose, bipolar ventricular pacing (VP) was performed using sutured epicardial electrodes at 3 different sites ; left ventricular apex (LVA), right ventricular outflow tract (RVOT), and right ventricular apex (RVA). At each site, VP was repeated for 60 seconds at 3 different rates; 1.75X, 2X, and 2.25X of baseline heart rate (BHR). Mean arterial pressure (MAP), mean left atrial pressure (MLAP) and mean pulmonary artery pressure (MPAP) were monitored during VP. deltaMAP was defined as the difference between the baseline MAP and lowest MAP during VP. deltaMLAP was defined as the difference between highest MLAP during VP and baseline MLAP. Cardiac vagal and beta-adrenoreceptor blockades were achieved by intravenous bolus administration of propranolol (1 mg/kg and then 1 mg/kg/hr) and atropine (0.5 mg/kg and then 0.5 mg/kg/hr). After cardiac autonomic blockade, VP was repeated at 2X of baseline heart rate for 60 seconds at each site. RESULTS: Baseline MAP, MLAP, and MPAP were 101+/-8.1 mmHg, 0.3+/-0.41 mmHg, and 10+/-2.4 mmHg, respectively. At the same pacing site of VP, MAP was decreased significantly with VP and deltaMAP was increased significantly as VP cycle length shortened (all P<0.001). At the same pacing cycle length of VP, deltaMAP was significantly greater at RVA or RVOT than LVA: LVA vs RVOT ; all P<0.001 at 3 different rates, LVA vs RVA ; P<0.05 (1.75X & 2X of BHR), P<0.001 (2.25X of BHR). But there was no significant difference in deltaMAP between RVA and RVOT. At the same pacing site of VP, MLAP and deltaMLAP were increased significantly as VP cycle length shortened (all P<0.01), but at the same cycle length of VP, there was no significant differences in deltaMLAP at 3 different VP sites. Ventricular pacing after autonomic blockade induced a greater increase in deltaMAP and deltaMLAP compared to controls (all P<0.01 at 3 pacing sites). And cardiac autonomic blockade also resulted in significant blunting of recovery of MAP during VP compared to controls. CONCLUSION: Above results showed that pacing cycle length plays a major role in determining the hemodynamic outcomes during ventricular pacing, and that the site of origin could be an independent factor of ventricular tachycardia hemodynamics. And also modulation of tone of the adrenergic nervous system is essentially required for the hemodynamic recovery during ventricular tachycardia.
Animals ; Arterial Pressure ; Atrial Pressure ; Atropine ; Blood Pressure ; Chloralose ; Dogs* ; Electrodes ; Heart Rate ; Hemodynamics* ; Hypotension ; Nervous System ; Propranolol ; Pulmonary Artery ; Tachycardia ; Tachycardia, Ventricular ; Thorax ; Ventricular Function

BACKGROUND: Patients with obstructive sleep apnea syndrome are known to have high long-term mortality compared to healthy subjects because of their cardiovascular dysfunction. The observation of hemodynamic changes by obstructive apneas is helpful to understand when attempting to understand the pathophysiological mechanism of the development of cardiovascular dysfunction in those patients. Therefore, we studied the changes of in cardiovascular function with the an animal model and tried to obtain the basic data for an ideal experimental model (this phrase is unclear), which is required a requirement for the a more advanced study. METHODS: In 16 Sixteen anesthetized dogs with alpha-chloralose, experimental subjects (delete) were divided into two groups : 8 dogs of room air breathing group and 8 dogs of oxygen breathing group. We measured PaO2, PaCO2, heart rate, cardiac output, mean femoral artery pressure, and mean pulmonary artery pressure at specified times during the apnea-breathing cycle : before endotracheal tube occlusion (baseline), 25 seconds after endotracheal tube occlusion (apneic period), 10 seconds (early phase of postapneic period, EPA) and 25 seconds (late phase of postapneic period, LPA) after spontaneous breathing. RESULTS: In room air breathing group, the heart rate significantly decreased significantly decreased at during the apneic period compared to that at baseline (P<0.01) and increased at EPA and LPA compared to that during the apneic period (P<0.01). But, the heart rate showed no significant changes during apneic and postapneic periods in the oxygen breathing group. Cardiac output tended to decrease at during apneic period compared to that at baseline, but did not show statistical significance was statistically significant. Cardiac output significantly decreased at LPA compared to at baseline (P<0.01). Mean femoral artery pressure was significantly decreased at during apneic period compared to that at baseline (P<0.05). CONCLUSION: Through this experiment, we were partially able to understand the changes of cardiovascular function indirectly, but it is suggested that the (delete) new experimental animal model displaying physiological mechanism close to sleep in nature might natural sleep should be established (,)and the advanced study of in the changes of cardiovascular function and its cause their causes should be continued.
Animals ; Apnea* ; Cardiac Output ; Chloralose* ; Dogs* ; Femoral Artery ; Heart Rate ; Hemodynamics ; Humans ; Models, Animal ; Models, Theoretical ; Mortality ; Oxygen ; Pulmonary Artery ; Respiration ; Sleep Apnea Syndromes ; Sleep Apnea, Obstructive

Noxious peripheral nerve stimulation causes changes of arterial blood pressure by way of somatosympathetic reflex, and may play an important role in determining the periodicity of respiratory neurons at the same time. However, little has been known about how noxious stimulation does mediate respiratory control. In the present study, the respiratory neurons of the ventrolateral medulla were identified and characterized, and the responses of these neurons to noxious stimulation were observed, to investigate the role of noxious stimulation in determining respiratory rhythm. Cats were anesthetized with alpha-chloralose and mechanically ventilated after muscle relaxation. Occipital craniectomy was performed and the floor of the fourth ventricle was exposed. Single cell activities of the ventrolateral medulla were recorded using carbon-filament microelectrodes. Neurons related with respiratory rhythm were identified and the responses to vagal and sciatic nerve stimulation were observed. The following results were obtained. 1) A total of 46 neurons related with mechanical ventilatory cycle was identified, including 13 expiratory augmenting neurons, 11 inspiratory decrementing neurons, and 9 unclassified neurons. 2) The activity of inspiratory augmenting neurons was increased by A-delta intensity stimulation of the vagal and sciatic nerves, and inhibited by C-intensity stimulation of the sciatic nerve. 3) The inspiratory decrementing neurons did not show a significant response to vagal nerve stimulation, but the cell activity was inhibited by A-delta and C-intensity stimulation of the sciatic nerve. 4) The expiratory neuron did not show a significant response to peripheral nerve stimulation. 5) 27 neurons had slower rhythmic activity than mechanical ventilation. Sciatic nerve stimulation increased frequency of rhythmic discharges in these cells. 6) Most of the neurons with slower rhythmic activity during spontaneous respiration followed faster rhythm of mechanical ventilation after muscle relaxation. From these results, it is concluded that the activities of the respiratory neurons, especially inspiratory ones, in ventrolateral medulla are under influence of noxious peripheral stimulation, and they are dependent on the state of the experimental animal.
Animals ; Arterial Pressure ; Cats* ; Chloralose ; Fourth Ventricle ; Microelectrodes ; Muscle Relaxation ; Neurons* ; Periodicity ; Peripheral Nerves* ; Reflex ; Respiration ; Respiration, Artificial ; Sciatic Nerve ; Vagus Nerve ; Vagus Nerve Stimulation

BACKGROUND: Recent findings suggest that a coupling between the somatic and sympathetic nervous system is critical not only for the development but also for the maintenance of pain behavioral changes. However, studies on the effect of sympathetic efferent system on sensory receptors in the visceral organ that is more dependent on the autonomic nervous system are lacking. This study examined whether norepinephrine (NE) had an influence on the mechanoreceptors in the feline urinary bladder. METHODS: Ten adult male cats were used and anesthetized with alpha-chloralose and artificially ventilated. A cannula with the pressure transducer was inserted through the urethra to apply mechanical stimuli and monitor the pressure of bladder. A tiny cannula inserted into the bilateral side branches of vesical arteries were used as a route for a NE (10A.M 9:40 01-10-08 bilaterally) injection. Nerve fiber recordings were obtained from the distal stump of the pelvic nerve. RESULTS: After the NE injection, the response of mechanoreceptors (n = 13) to the isotonic pressure stimulus (50 - 60 mmHg) decreased significantly (p < 0.05) in terms of sensitivity (i.e., ratio of nerve activity change to urinary bladder pressure change). The responses to pressure stimuli after an injection of an alpha1 adrenoceptor blocker (terazosin) reversed the effect of NE. The responses of mechanoreceptors to isotonic pressure stimulus were not affected significantly by NE with preinjection of an alpha2 adrenoceptor blocker (yohimbine). CONCLUSIONS: These results suggest that NE may have influence on the sensitivity of mechanoreceptors in the normal feline urinary bladder via an alpha1 adrenoceptor.
Adrenergic alpha-1 Receptor Antagonists ; Adult ; Animals ; Arteries ; Autonomic Nervous System ; Catheters ; Cats* ; Chloralose ; Humans ; Male ; Mechanoreceptors* ; Nerve Fibers ; Norepinephrine* ; Sensory Receptor Cells ; Sympathetic Nervous System ; Transducers, Pressure ; Urethra ; Urinary Bladder*

BACKGROUND: Atrial fibrillation (Af) after open heart surgery may result in hypotension, heart failure, embolic complication and prolongation in length of hospital stay. Several studies have investigated the efficacy of pharmacological prophylaxis in reducing the incidence of Af after cardiac surgery. The pericardial sac represents a natural physical barrier and provides a drug receptacle to restrict drug delivery to the heart. The overall objective of this study was to determine whether the pericardial sac could function as a delivery chamber for antiarrhythmic drugs. We investigated whether quinidine delivered into the pericardial sac exerted an effect on atrial and ventricular refractoriness, impulse generation, and conduction. METHODS: All animals were anesthetized with alpha-chloralose. After a sternotomy, the pericardium was opened and cradled to produce a "container" of approximately 30 ml. Experimental animals received quinidine, 3.33 mg/ml, dissolved in Krebs-Henseleit solution instilled into their pericardial sacs for 30 minutes. Baseline and 5, 10 and 30 minutes postinstillation electrophysiologic studies were performed. Plasma quinidine levels were measured at each of the time intervals in three different sites i.e., right ventricle (RV), aortic root and femoral vein (FV). RESULTS: Baseline systolic (SAP) and diastolic aortic pressure (DAP) were 148+/-16.8 mmHg, and 111+/-23.9 mmHg, respectively. Both SAP and DAP were significantly decreased at 5, 10 and 30 minutes after instillation of quinidine solution into pericardial sac. In electrocardiographic parameters, the increase in sinus cycle length and corrected QT interval were significantly greater compared with baseline at each of the time intervals after instillation of quinidine solution into pericardial sac. All electrophysiologic parameters including 1:? AV conduction, effective refractory period (ERP) of RA and RV were significantly increased compared with baseline at three time points. Quinidine concentrations in RV and aorta were significantly higher than in FV at three time points. In RV and aorta, quinidine concentrations at 30 min were significantly lower than those at 5 and 10 min postinstillation periods. There were significant correlations between plasma quinidine levels and corrected QT interval or RAERP. CONCLUSION: Above results showed that quinidine instilled into the pericardial sac migrates transmurally and produces significant prolongation of effective refractory period and may appear to prevent various arrhythmias including atrial fibrillation after cardiac surgery.
Animals ; Anti-Arrhythmia Agents ; Aorta ; Arrhythmias, Cardiac ; Arterial Pressure ; Atrial Fibrillation ; Chloralose ; Electrocardiography ; Electrophysiology ; Femoral Vein ; Heart ; Heart Failure ; Heart Ventricles ; Hypotension ; Incidence ; Length of Stay ; Pericardium ; Plasma ; Quinidine* ; Sternotomy ; Thoracic Surgery