Cardiovascular events associated with air breathing in two teleosts, Hoplerythrinus unitaeniatus and Arapaima gigas

1978 ◽  
Vol 56 (4) ◽  
pp. 953-958 ◽  
Author(s):  
A. P. Farrell

Cardiovascular events associated with air breathing were investigated in two teleosts, Hoplerythrinus unitaeniatus and Arapaima gigas, in which the air-breathing organs are modified swim bladders. These fish are bimodal breathers whilst in water; they maintain gill ventilation and take periodic air breaths. Cardiac output, blood flow to the air bladder, dorsal aortic blood pressure, and air bladder gas pressure were measured directly in A. unitaeniatus. Dorsal aortic blood pressure and air bladder gas pressure were measured in A. gigas. Both fish were subject to air exposure by draining water from the holding tank. Hoplerythrinus unitaeniatus increased air bladder perfusion following an air breath by redistributing blood flow. There was also a tachycardia after an air breath, but cardiac output did not change significantly at or between air breaths. Preferential perfusion of gill arches 3 and 4 and increased general systemic resistance both probably contribute to produce blood redistribution. During air exposure, H. unitaeniatus demonstrated hyperventilation and heart rate was elevated. In A. gigas in water the mean dorsal aortic blood pressure and heart rate remained constant, which is atypical in comparison with other air-breathing fish.

1964 ◽  
Vol 207 (6) ◽  
pp. 1325-1329 ◽  
Author(s):  
David E. Donald ◽  
John T. Shepherd

In three normal dogs and in six dogs with cardiac denervation, there was a rapid increase in cardiac output (electromagnetic flowmeter) from the start of exercise. The denervated group showed an average delay of 25 sec in reaching plateau values of cardiac output and a deficit of 18% in the accumulated flow over the first minute of running; augmentation of output was due principally to a rapid increase in stroke volume since acceleration of heart rate was slow. In normal dogs, the augmentation of output came from a rapid increase in heart rate. The steady-state values for cardiac output and oxygen consumption were similar in the two groups as was the pattern of oxygen consumption in the first minutes of exercise and the manner in which the oxygen debt was repaid. This suggested that the denervated dogs extracted more oxygen from the circulating blood in the first moments of running. The changes with exercise in aortic blood pressure were similar in the two groups.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Bernard I. Levy ◽  
Jean-Guillaume Dillinger ◽  
Patrick Henry ◽  
Damien Logeart ◽  
Stephane Manzo Silberman ◽  
...  

Background: Treatment of hypertensive patients with beta-blockers reduces heart rate (HR) and increases central blood pressure, implying that the decrease in HR could explain reported increases in cardiovascular risk with beta-blocker. This analysis from a randomized, double-blind study explores whether HR reduction with the I f inhibitor ivabradine had an impact on central blood pressure and coronary perfusion. Methods and results: We included 12 normotensive patients with stable CAD, HR ≥70 bpm (sinus rhythm), and stable background beta-blocker therapy. Patients received ivabradine 7.5 mg bid or matched placebo for two 3-week periods with a crossover design and evaluation by aplanation tonometry. Treatment with ivabradine was associated with a significant reduction in resting HR after 3 weeks versus no change with placebo (-15.8±7.7 versus +0.3±5.8 bpm, p=0.0010). There was no relevant between-group difference in change in central aortic SBP (-4.0±9.6 versus +2.4±12.0 mm Hg, p=0.13) or augmentation index (-0.8±10.0% versus +0.3±7.6%, p=0.87). Treatment with ivabradine was associated with prolongation of diastolic perfusion time by 41% from baseline to 3 weeks (+215.6±105.3 versus -3.0±55.8 ms with placebo, p=0.0005) (Figure) and with a pronounced increase in an index of myocardial viability (Buckberg index, +39.3±27.6% versus -2.5±13.5% with placebo, p=0.0015). There were no safety issues during the study. Conclusion: Heart rate reduction with ivabradine does not modify central aortic blood pressure and is associated with a marked prolongation of diastolic perfusion time and an improvement in myocardial perfusion.


1967 ◽  
Vol 24 (8) ◽  
pp. 1775-1790 ◽  
Author(s):  
L. S. Smith ◽  
J. R. Brett ◽  
J. C. Davis

Dorsal aortic blood pressure, heart rate, and oral water pressure were recorded in adult sockeye salmon (Oncorhynchus nerka) while they were resting in darkened aquaria or swimming in an illuminated tunnel-respirometer. Pressures were recorded on an oscillograph attached to pressure transducers connected with cannulae in the dorsal aorta and oral cavity. The velocity of the water in the swimming chamber was increased in stepwise fashion every 30 min until the fish stopped swimming and were swept against an electrified grid. At the cessation of swimming, which was considered as the onset of fatigue, water velocity was decreased to a minimum which permitted the fish to rest and dorsal aortic blood pressure, heart rate, and oral water pressure were recorded for about 1 hr as they returned toward resting levels. Resting values were 44/38 mm Hg (systolic/diastolic) and 49 heartbeats/min. At maximal swimming speed dorsal aortic blood pressure was 55/49 mm Hg and heart rate was 83 beats/min. No abrupt changes in cardiovascular function occurred at the onset of fatigue.A number of morphological (length and weights of the body and ventricle) and cardiovascular (pressures, rates) variables were measured in six adult sockeye salmon. A significant correlation was found between hematocrit, ventricle weight, and heart rate; a change in one apparently caused adjustments in the other two in order to maintain a constant supply of oxygen to the tissues during subfatigue levels of activity.The effects of removal and replacement of blood or isotanic saline in the dorsal aorta were observed in three adult sockeye salmon. Removal of blood produced a proportionate decrease in blood pressure and an increase in heart rate. Neither dilution of the blood by replacement with saline nor increase in blood volume from addition of saline had any significant effect on heart rate and blood pressure.


1997 ◽  
Vol 272 (2) ◽  
pp. R607-R614 ◽  
Author(s):  
E. C. Bowman ◽  
G. P. Roderick ◽  
S. R. Bloom ◽  
A. V. Edwards

Ingestion of milk during suckling causes hypertension and tachycardia in young, unweaned animals of many species, but these responses are most pronounced in the calf. The present study was undertaken to assess the extent to which this phenomenon depends on activation of adrenoceptors in these animals. Mean basal heart rate was 100 +/- 8 beats/min and mean basal aortic blood pressure was 92 +/- 5 mmHg. The rise in heart rate during feeding was almost completely suppressed after propranolol (2-4 mg/kg iv), which also significantly reduced the rise in blood pressure from 67 +/- 4 to 44 +/- 3 mmHg (P < 0.005). Additional pretreatment with phentolamine (1.0 mg/kg and < or =0.1 mg x min(-1) x kg(-1) iv) virtually eliminated the rise in blood pressure during feeding; it rose by only 8 +/- 4 mmHg (P < 0.001). Section of both splanchnic nerves also significantly reduced the rise in blood pressure during feeding, especially after pretreatment with propranolol. Neither section of the splanchnic nerves nor the administration of the blocking agents significantly affected the rises in plasma insulin and pancreatic polypeptide that occurred after feeding. There was no detectable rise in plasma neuropeptide Y concentration in response to feeding. The hypertensive response to direct electrical stimulation of the peripheral end of a splanchnic nerve and to intra-arterial injections of norepinephrine were completely abolished after combined pretreatment with atropine, propranolol, and phentolamine after the ipsilateral adrenal vein had been tied off. It is concluded that the cardiovascular changes that occur during feeding in these animals are attributable very largely, if not entirely, to activation of adrenoceptors.


2003 ◽  
Vol 95 (2) ◽  
pp. 751-757 ◽  
Author(s):  
A. S. Thakor ◽  
C. N. Brown ◽  
A. V. Edwards

Submandibular vascular and secretory responses to parasympathetic chorda-lingual (C-L) stimulation were investigated in anesthetized sheep before, during, and after an intracarotid (ic) infusion of endothelin-1 (ET-1). Stimulation of the peripheral end of the C-L nerve at 4 and 8 Hz produced a frequency-dependent reduction in submandibular vascular resistance (SVR) associated with a frequency-dependent increase in submandibular blood flow, salivary flow, and Na+, K+, and protein output from the gland. During stimulation at 4 Hz, ic ET-1 significantly increased SVR ( P < 0.01), without significantly affecting either the aortic blood pressure or heart rate. Submandibular blood flow (SBF) was reduced by 48 ± 4% and the flow of saliva by 50 ± 1%. The effect on blood and salivary flow persisted for at least 30 min after the infusion of ET-1. The reduction in SBF was associated with a diminution in the output of Na+,K+, and protein in the saliva ( P < 0.01). These effects persisted for 30 min after the infusion of ET-1 had been discontinued and were linearly related to the flow of plasma throughout.


1994 ◽  
Vol 190 (1) ◽  
pp. 265-279 ◽  
Author(s):  
M Axelsson ◽  
B Davison ◽  
M Forster ◽  
S Nilsson

The mechanisms of cardiovascular control in the Antarctic fish Pagothenia borchgrevinki were investigated during rest and swimming exercise using pharmacological tools to reveal the nature of the control systems involved. Simultaneous and continuous recordings of ventral and dorsal aortic blood pressure, heart rate and ventral aortic blood flow (cardiac output) were made using standard cannulation procedures and a single-crystal Doppler flowmeter. Exercise produced a clear and consistent decrease in dorsal aortic blood pressure caused by a decrease in systemic vascular resistance. At the same time, ventral aortic blood pressure increased owing to the combined effects of a markedly increased cardiac output (by about 80 %) and branchial vasoconstriction. Judged from the effects of the alpha-adrenoceptor antagonist prazosin, control of the branchial vasculature involves an alpha-adrenoceptor-mediated vasoconstriction, in addition to more traditional cholinergic vasoconstrictor and ss-adrenoceptor-mediated dilatory mechanisms. The range of heart rates is large, from 3-4 beats min-1 in individual fish during hypertensive bradycardia to about 28 beats min-1 after atropine treatment. Both chronotropic and inotropic effects are responsible for a marked increase in cardiac output during exercise. The increase in blood pressure caused by adrenaline injection was due largely to an increase in cardiac output, while direct effects on the systemic vasculature were small and transient. The increase in cardiac output, in turn, was due solely to an adrenergic stimulation of stroke volume. A barostatic bradycardia, often seen in other vertebrates in response to adrenaline injection, was absent and it is possible that a decrease in heart rate was offset by direct adrenergic stimulation of the heart. Angiotensin II (Ang II) produced consistent hypertension by systemic vasoconstriction. In contrast to the effects of adrenaline injection, the hypertension caused by Ang II was accompanied by a marked bradycardia. This could be abolished by atropine, suggesting a cholinergic vagal reflex of the type found in other vertebrates. Angiotensin I also caused an elevated blood pressure, and this effect was abolished by the angiotensin converting enzyme inhibitor enalapril, demonstrating elements of an angiotensin-related cardiovascular control system.


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