Myocardial work load is a major determinant of norepinephrine-induced left ventricular dysfunction.
Anesthesia; Animals; Blood Pressure/*drug effects; Cardiovascular; Consciousness; Diastole/drug effects; Dose-Response Relationship; Drug; General; Heart Rate/*drug effects; Heart/drug effects/*physiology; Left/drug effects/*physiology; Models; Norepinephrine/*pharmacology; Pentobarbital; Rabbits; Systole/drug effects; Time Factors; Ventricular Function
This study was conducted to determine whether increased myocardial energy demand plays a role in norepinephrine (NE)-induced left ventricular (LV) dysfunction. A range of arterial pressure-heart rate (P-R) products (myocardial energy demand) was produced in both conscious and pentobarbital sodium-anesthetized rabbits with the same dose of NE (10 micrograms priming bolus plus 2.5 micrograms.kg-1 x min-1 for 2.5 h). After NE treatment, LV function was evaluated in vitro and found to be markedly diminished in the rabbits that had an elevated P-R product. In contrast, LV function was not significantly affected when the P-R product was maintained near control levels during NE treatment. In separate experiments, rabbit hearts were isolated and exposed to NE (10,000 or 50,000 pg/ml) for 2.5 h under low P-R product conditions. These hearts exhibited a dose-dependent decrease in LV function that was modest compared with that observed in rabbits that had elevated P-R products during in vivo NE treatment. Our results suggest that high concentrations of NE may cause modest degrees of LV dysfunction independently of increases in myocardial energy demand, but the LV dysfunction is exacerbated when myocardial energy demand is elevated.
Bosso F J; Allman F D; Pilati C F
The American journal of physiology
1994
1994-02
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1152/ajpheart.1994.266.2.H531" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1994.266.2.H531</a>
Enhanced cardiopulmonary reflex inhibition of heart rate during exercise.
Animals; Rats; Analysis of Variance; Physical Stimulation; Blood Pressure/drug effects/physiology; Rest; Biguanides/pharmacology; Blood Volume; Bradycardia/physiopathology; Heart Rate/drug effects/*physiology; Heart/drug effects/*physiology; Hypoglycemic Agents/pharmacology; Lung/drug effects/*physiology; Physical Exertion/*physiology; Reflex/drug effects/*physiology; Sympathetic Nervous System/drug effects/physiology; Vagotomy; Vagus Nerve/drug effects/physiology; Neurons; Chemical; Stimulation; Afferent/drug effects/physiology
We tested the hypothesis that the reflex inhibition of heart rate (HR) during mechanical (acute bolus injection of 0.5% and 2% of estimated blood volume) and chemical (phenylbiguanide, PBG, 2.5 and 5 micrograms.kg-1) stimulation of cardiopulmonary receptors would be enhanced during exercise. Rats were instrumented with arterial and venous catheters. The reflex response to mechanical (N = 7) and chemical (N = 8) stimulation of cardiopulmonary receptors was examined at rest and during exercise (6 m.min-1, 10% grade). A two-way analysis of covariance (ANCOVA) with repeated measures was used to test for differences in the reflex regulation of HR at rest vs exercise. HR was used as the covariate because exercise significantly increased baseline HR. There was no significant treatment effect (rest vs exercise) for the reflex inhibition of HR during mechanical stimulation. However, the two-way ANCOVA revealed a significant treatment effect (rest vs exercise) for the reflex inhibition of HR during chemical stimulation. The reflex decreases in HR were enhanced (-delta 23 +/- 8 vs -delta 133 +/- 47 and -delta 208 +/- 40 vs -delta 374 +/- 10 bpm at 2.5 and 5 micrograms.kg-1, respectively). These data suggest that factors associated with exercise enhanced the cardiopulmonary reflex inhibition of heart rate during chemical stimulation.
Chen C Y; DiCarlo S E; Collins H L
Medicine and science in sports and exercise
1995
1995-10
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1249/00005768-199510000-00008" target="_blank" rel="noreferrer noopener">10.1249/00005768-199510000-00008</a>