Cardiac Reflexes Conducted by Vagal Afferents in Normotensive and Renal Hypertensive Dogs

1976 ◽  
Vol 51 (s3) ◽  
pp. 353s-355s ◽  
Author(s):  
P. Kezdi
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Pressure ◽  
Systemic Blood Pressure ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Balloon Occlusion ◽  
Ascending Aorta ◽  
Vagal Afferents ◽  
Vagus Nerves ◽  
Vagal Afferent

1. The renal sympathetic reflex responses to transient balloon occlusion of the descending aorta (systemic baroreceptor activation) and the ascending aorta (cardiac stretch-receptor activation) have been studied together with blood pressure increases after successive cutting of carotid sinus, aortic and vagus nerves in acute experiments in the dog. 2. Results from these experiments provide evidence for cardiac vagal afferent participation in the tonic regulation of systemic blood pressure. 3. In other experiments the reflex pressure-response curve of the isolated gracilis muscle at constant flow to transient ascending aorta occlusion was measured. This curve was moved to the right in renal hypertensive dogs as compared with normotensive dogs. The threshold response of left ventricular vagal afferent nerves was shifted to higher left ventricular pressure in the former. 3. These findings indicate resetting of ventricular receptors in hypertensive animals.

Apnea, tachypnea, and hypotension elicited by cardiac vagal afferents

1979 ◽  
Vol 47 (2) ◽  
pp. 312-318 ◽  
Author(s):  
D. R. Kostreva ◽  
F. A. Hopp ◽  
E. J. Zuperku ◽  
J. P. Kampine
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Initial Rate ◽  
Systemic Blood Pressure ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Systemic Hypotension ◽  
Stellate Ganglia ◽  
Conduction Velocities ◽  
The Right

The reflex effects of right and left ventricular distension, mediated by vagal afferents, were studied in mongrel dogs anesthetized with halothane or pentobarbital sodium on heart-lung bypass. Diaphragm electromyogram (D-EMG), systemic blood pressure, and left ventricular cardiogram were all measured during ventricular distension. After bilateral section of the stellate ganglia, distension of the left ventricle produced an apnea, or slowing of respiration and systemic hypotension, without a change in heart rate. A reflex decrease in the amplitude of the D-EMG occurred if the initial breathing rate was high; a decrease in frequency of the D-EMG bursts occurred if the initial rate was low. The left ventricular vagal afferents altering respiration had conduction velocities between 22 and 70 m/s, whereas those causing hypotension had conduction velocities less than 22 m/s. Distension of the right ventricle resulted in a significant tachypnea and systemic hypotension without a change in heart rate. The conduction velocities of the right ventricular vagal afferents causing both tachypnea and hypotension were less than 9 m/s. These reflex changes in respiration and blood pressure elicited by both right and left ventricular distension were eliminated with vagotomy.

Respiratory toxicity of direct lytic factor in the venom of the southern Chinese cobra (N. naja atra) in dogs

1996 ◽  
Vol 15 (8) ◽  
pp. 629-632 ◽  
Author(s):  
Shou-Jian Huang ◽  
Fu Jian ◽  
Jia-Jun Sun
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Pressure ◽  
Transpulmonary Pressure ◽  
Systemic Blood Pressure ◽  
Left Ventricular ◽  
Initial Manifestation ◽  
Early Effect ◽  
Southern Chinese ◽  
Direct Lytic Factor ◽  
Respiratory Toxicity

The effects of direct lytic factor (DLF) on respiratory ventilation, gas exchange as well as hemodynamics were studied in anesthetized dogs. After an intravenous DLF dose of 1 mg/kg, the initial manifestation of intoxication was observed as follows: (1) Increase in airway impedance characterized by slowed air flow rate and increased negative transpulmonary pressure. (2) Decrease in dy namic compliance. (3) Progressive increase in venoarter ial shunt (Qs/Qt) and decrease in PaO 2. (4) Elevation of pulmonary artery blood pressure and fall of mean systemic blood pressure and maximal left ventricular pressure. Above actions reached the peak values at 15 min and thereafter all respiratory functional parameters, except Qs/Qt and hypoxemia, returned gradually to approach the normal levels at 50 min. The tidal volume, PaCO2 and LVEDP remained unchanged until another DLF dose of 1.5 mg/kg was given. After a second dose of DLF (total 2.5 mg/kg), the respiratory functions and the cardiac performance deteriorated as follows: (1) Further increase in Qs/Qt and hypoxemia. (2) Appearance of hypercapnea and acidosis. (3) Fall of dP/dt max and elevation of LVEDP, widening of QRS complex of ECG. (4) Blood pressure run a downhill course. From above experimental evidence, we came to the conclusion that as well as the basic cardiotoxicity, respiratory toxicity of DLF must be considered as the primary, because of broad spectrum of action of DLF and early effect on respiratory function.

scholarly journals Possible mechanism of the cardio-renal protective effects of AVE-0991, a non-peptide Mas-receptor agonist, in diabetic rats

2012 ◽  
Vol 13 (3) ◽  
pp. 334-340 ◽  
Author(s):  
Kulwinder Singh ◽  
Kuldeepak Sharma ◽  
Manjeet Singh ◽  
PL Sharma
Keyword(s):  
Blood Pressure ◽  
Receptor Agonist ◽  
Diastolic Pressure ◽  
Left Ventricular Pressure ◽  
Diabetic Rats ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Protective Effects ◽  
Mas Receptor ◽  
Arterial Blood

Hypothesis: This study was designed to investigate the cardio-renal protective effect of AVE-0991, a non-peptide Mas-receptor agonist, and A-779, a Mas-receptor antagonist, in diabetic rats. Materials and methods: Wistar rats treated with streptozotocin (50 mg/kg, i.p., once), developed diabetes mellitus after 1 week. After 8 weeks, myocardial functions were assessed by measuring left ventricular developed pressure (LVDP), rate of left ventricular pressure development (d p/d tmax), rate of left ventricular pressure decay (d p/d tmin) and left ventricular end diastolic pressure (LVEDP) on an isolated Langendorff’s heart preparation. Further, mean arterial blood pressure (MABP) was measured by using the tail-cuff method. Assessment of renal functions and lipid profile was carried out using a spectrophotometer. Results: The administration of streptozotocin to rats produced persistent hyperglycaemia, dyslipidaemia and hypertension which consequently produced cardiac and renal dysfunction in 8 weeks. AVE0991 treatment produced cardio-renal protective effects, as evidenced by a significant increase in LVDP, d p/d tmax, d p/d tmin and a significant decrease in LVEDP, BUN, and protein urea. Further, AVE-0991 treatment for the first time has been shown to reduce dyslipidaemia and produced antihyperglycaemic activity in streptozotocin-treated rats. However, MABP and creatinine clearance remained unaffected with AVE-0991 treatment. Conclusions: AVE-0991 produced cardio-renal protection possibly by improving glucose and lipid metabolism in diabetic rats, independent of its blood pressure lowering action.

scholarly journals Influence of dual ETA/ETB-receptor blockade on coronary responses to treadmill exercise in dogs

2000 ◽  
Vol 89 (5) ◽  
pp. 2041-2048 ◽  
Author(s):  
Masayuki Takamura ◽  
Robert Parent ◽  
Peter Cernacek ◽  
Michel Lavallée
Keyword(s):  
Coronary Sinus ◽  
Adrenergic Receptor ◽  
Left Ventricular Pressure ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Receptor Blockade ◽  
Etb Receptor ◽  
Dual Blockade ◽  
The Relationship

We hypothesized that endothelin (ET) release during exercise may be triggered by α-adrenergic-receptor activation and thereby influence coronary hemodynamics and O2 metabolism in dogs. Exercise resulted in coronary blood flow increases (to 1.88 ± 0.26 from 1.10 ± 0.12 ml · min−1 · g−1) and in a fall ( P < 0.01) in coronary sinus O2saturation (17.4 ± 1.5 to 9.6 ± 0.7 vol%), whereas myocardial O2 consumption (MV˙o 2) increased (109 ± 13% from 145 ± 16 μl O2 · min−1 · g−1). Tezosentan, a dual ETA/ETB-receptor blocker, slightly reduced mean arterial pressure (MAP) and increased heart rate throughout exercise. The relationship between coronary sinus O2 saturation and MV˙o 2 was shifted upward ( P < 0.05) after tezosentan administration; i.e., as MV˙o 2 increased during exercise, coronary sinus O2 saturation was disproportionately higher after ET-receptor blockade. After propranolol, tezosentan resulted in significant decreases ( P < 0.05) in left ventricular pressure, the first derivative of left ventricular pressure over time, and MAP during exercise. As MV˙o 2 increased during exercise, coronary sinus O2 saturation levels after tezosentan became superimposable over those observed before ET-receptor blockade. Thus dual blockade of ETA/ETBreceptors alters coronary hemodynamics and O2 metabolism during exercise, but ET activity failed to increase beyond baseline levels.

Reflex cardiovascular changes with veratridine in the conscious dog

1982 ◽  
Vol 242 (5) ◽  
pp. H810-H817 ◽  
Author(s):  
K. W. Barron ◽  
V. S. Bishop
Keyword(s):  
Blood Flow ◽  
Vascular Resistance ◽  
Left Ventricular Pressure ◽  
Peripheral Circulation ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Inotropic Response ◽  
Inotropic Effects ◽  
Conscious Dog ◽  
Renal Vascular

The present study was undertaken to examine the reflex responses of activation of cardiac sensory receptors in the conscious dog. Intracoronary (left circumflex coronary artery) injection of veratridine (0.10 micrograms/kg) reduced mean arterial pressure (-40 mmHg, P less than 0.05), heart rate (-34 beats/min, P less than 0.05), and maximum rate of rise of left ventricular pressure (LV dP/dtmax) (-419 mmHg/s, P less than 0.05). Bilateral cervical vagal cold block (BVB) eliminated the depressor and bradycardic responses of veratridine. BVB not only eliminated the negative inotropic response to veratridine but reversed it to a positive inotropic response (LV dP/dtmax increased 313 +/- 76 mmHg/s). Ganglionic blockade abolished all effects of veratridine. The bradycardia and negative inotropic effects caused by veratridine were attenuated by either atropine or metoprolol and completely eliminated by the combination of the two antagonists. Veratridine also produced a decrease in renal artery blood flow but had no effect on renal vascular resistance. In contrast, iliac blood flow was increased with veratridine, and this, combined with the depressor effect, resulted in a decrease in iliac vascular resistance (-37%), P less than 0.05). BVB abolished the changes in renal and iliac blood flow or resistance caused by veratridine. The results indicate that activation of cardiac receptors in the conscious dog elicits inhibitory reflexes to the heart and peripheral circulation that are mediated by vagal afferents. After vagotomy, veratridine elicited a reflex positive inotropic response, which may have resulted from activation of cardiac sympathetic afferent fibers.

Stability of cardiodynamic and some blood parameters in the baboon following intravenous anaesthesia with ketamine and diazepam

1998 ◽  
Vol 69 (1) ◽  
Author(s):  
W.J. Du Plooy ◽  
P.J. Schutte ◽  
J. Still ◽  
L. Hay ◽  
C.P. Kahler
Keyword(s):  
Blood Pressure ◽  
Continuous Infusion ◽  
Total Duration ◽  
Systolic Pressure ◽  
Left Ventricular Pressure ◽  
Blood Parameters ◽  
Left Ventricular ◽  
Ventricular Pressure ◽  
Pressure Curve ◽  
Arterial Blood

The stability of cardiodynamic and some blood parameters during a slow, continuous infusion of a combination of ketamine and diazepam is reported. Contractility (dP/dt), myocardial relaxation (Tln), left ventricular end-diastolic pressure (LVEDP), left ventricular systolic pressure (LVSP), arterial blood pressure and certain blood parameters were assessed in 3 male and 3 female juvenile baboons (Papio ursinus). Anaesthesia was induced with 15 mg/kg ketamine IM and maintained with a continuous IV infusion (40-60 mℓ/h) of ketamine and diazepam. The mixture consisted of 2 mℓ ketamine (100 mg/mℓ), 2 mℓ diazepam (5 mg/mℓ) and 50 mℓ saline. A period of 75 + 10 min was allowed for preparation of the animals, after which lead II of the ECG, femoral artery blood pressure and left ventricular pressure were recorded at 15-min intervals for a period of 2 h: the total duration of anaesthesia was 195 min. Arterial blood samples were analysed at 30-min intervals for blood gases, electrolytes, glucose and insulin. Left ventricular parameters were derived from the left ventricular pressure curve. Tln, LVSP and LVEDP showed small fluctuations. Contractility decreased (p < 0.037) at the 195-min interval. No arrhythmias or ECG changes were seen, while blood pressure decreased gradually. Serum calcium concentration decreased and blood glucose levels increased gradually over time. Anaesthesia and analgesia were sufficient and no other drugs were necessary. The animals appeared sedated and dazed 60-80 min after the procedure. A continuous infusion of a combination of ketamine and diazepam for a duration of 150 min can provide stable anaesthesia for cardiodynamic measurements.

scholarly journals Merit of Anisodamine Combined with Opioidδ-Receptor Activation in the Protection against Myocardial Injury during Cardiopulmonary Bypass

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Xuan Hong ◽  
Huimin Fan ◽  
Rong Lu ◽  
Paul Chan ◽  
Zhongmin Liu
Keyword(s):  
Cardiopulmonary Bypass ◽  
Troponin T ◽  
Ischemia Reperfusion ◽  
Combined Treatment ◽  
Left Ventricular Pressure ◽  
Receptor Activation ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Control Group ◽  
Myocardial Ischemia Reperfusion

Myocardial ischemia/reperfusion (MIR) injury easily occurrs during cardiopulmonary bypass surgery in elderly patients. In an attempt to develop an effective strategy, we employed a pig model of MIR injury to investigate the maximum rate of change of left ventricular pressure, left ventricular enddiastolic pressure, and left intraventricular pressure. Coronary sinus cardiac troponin T (TnT) and adenosine-triphosphate (ATP) content in myocardium were measured. The ultrastructures for MIR injury were visualized by transmission electron microscopy (TEM). The role ofδ-opioid receptor activation using D-Ala2, D-Leu5-enkephalin (DADLE) in both early (D1) and late (D2) phases of cardioprotection was identified. Also, the merit of cardioprotection by DADLE in combination with anisodamine, the muscarinic receptor antagonist (D+M), was evaluated. Glibenclamide was employed at the dose sufficient to block ATP-sensitive potassium channels. Significant higher cardiac indicators, reduced TnT and increased ATP contents, were observed in D1, D2, and D+M groups compared with the control group. DADLE induced protection was better in later phase of ischemia that was attenuated by glibenclamide. DADLE after the ischemia showed no benefit, but combined treatment with anisodamine showed a marked postischemic cardioprotection. Thus, anisodamine is helpful in combination with DADLE for postischemic cardioprotection.

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