Cardiovascular changes in the unanaesthetized lingcod (Ophiodon elongatus) during short-term, progressive hypoxia and spontaneous activity

1982 ◽  
Vol 60 (5) ◽  
pp. 933-941 ◽  
Author(s):  
A. P. Farrell

Cardiac output [Formula: see text] and arterial blood pressures in the ventral and dorsal aortae (PVAnd PDA) were measured directly and simultaneously in the lingcod. The branchial and systemic conductances to blood flow (Gg and Gs) were calculated. During progressive hypoxia [Formula: see text], Gg, Gs, PVA, and PDA were all reduced when the water [Formula: see text] decreased below 45 mmHg (1 mmHg = 133.322 Pa). Spontaneous activity was characterized by an initial bradycardia and concurrent reduction in [Formula: see text], Gg, Gs, PVA, and PDA. Longer periods of activity were subsequently followed by a period of restitution where [Formula: see text], Gg, Gs, PVA, and PDA were all elevated.The beat by beat oscillations in flow were usually synchronized with, and in the same direction as, those in vascular conductance during both activity and hypoxia. This synchrony was most apparent between Gs and [Formula: see text] during the rapid cardiovascular adjustments occurring with activity. It is suggested that the observed relationship between flow and conductance changes was a result of passive changes in conductance when flow was altered, plus an active component which involved reflex vasoactivity.

1981 ◽  
Vol 91 (1) ◽  
pp. 293-305
Author(s):  
A. P. FARRELL

Adrenergic and cholinergic agonists were infused into the ventral aorta to evoke gill vasoactivity in the lingcod, Ophiodon elongatus. Arterial blood pressures were changed, and cardiac output and stroke volume were increased. As a consequence both the pressure and flow profiles across the gill were altered, and these changes should alter the pattern of lamellar perfusion. The changes in cardiac function were apparently reflexly mediated.


1999 ◽  
Vol 277 (2) ◽  
pp. H576-H583 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (V˙o 2 max) 4.7 ± 0.4 l/min (mean ± SE)] cycled for 30 min in the heat (35°C) in the upright and in the supine positions (V˙o 2 2.93 ± 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (Tes) was 37.8–38.0°C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (Tes = 38.7–38.8°C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 ± 6 ml, 3.0 ± 0.7 l/min, 6 ± 2 mmHg, 22 ± 8%, 14 ± 2 beats/min, and 50–96%, respectively; all P < 0.05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 ± 2 vs. 9 ± 1%) and the reductions in SV (13 ± 4 vs. 21 ± 3%) and cardiac output (8 ± 3 vs. 14 ± 3%) (all P< 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.


2003 ◽  
Vol 95 (3) ◽  
pp. 1159-1169 ◽  
Author(s):  
Joshua R. Rodman ◽  
Kathleen S. Henderson ◽  
Curtis A. Smith ◽  
Jerome A. Dempsey

In awake dogs, lactic acid was injected into the phrenic and deep circumflex iliac arteries to elicit the diaphragm and abdominal muscle metaboreflexes, respectively. At rest, injections into the phrenic or deep circumflex iliac arteries significantly increased mean arterial blood pressure 21 ± 7% and reduced cardiac output 6 ± 2% and blood flow to the hindlimbs 20 ± 9%. Simultaneously, total systemic, hindlimb, and abdominal expiratory muscle vascular conductances were reduced. These cardiovascular responses were not accompanied by significant changes in the amplitude or timing of the diaphragm electromyogram. During treadmill exercise that increased cardiac output, hindlimb blood flow, and vascular conductance 159 ± 106, 276 ± 309, and 299 ± 90% above resting values, lactic acid injected into the phrenic or deep circumflex iliac arteries also elicited pressor responses and reduced hindlimb blood flow and vascular conductance. Adrenergic receptor blockade at rest eliminated the cardiovascular effects of the respiratory muscle metaboreflex. We conclude that the cardiovascular effects of respiratory muscle metaboreflex activation are similar to those previously reported for limb muscles. When activated via metabolite production, the respiratory muscle metaboreflex may contribute to the increased sympathetic tone and redistribution of blood flow during exercise.


1988 ◽  
Vol 75 (2) ◽  
pp. 159-165 ◽  
Author(s):  
R. Hainsworth ◽  
Y. M. H. Al-Shamma

1. Carotid baroreceptors were stimulated by application of a subatmospheric pressure to a chamber fitted round the anterior and lateral aspects of the subject's neck (neck suction). Pulse interval and heart rate were determined from an electrocardiogram, cardiac output by a single-breath method and arterial blood pressure by an automatic sphygmomanometer. 2. The maximal prolongation of the pulse interval, determined during held expiration, occurred within 2–3 s from the onset of the neck suction. All the measured variables were in steady states between 2 and 3 min from the start of neck suction. 3. Neck suction at − 10 mmHg resulted only in an immediate change in pulse interval. All variables changed approximately linearly with the magnitude of the neck suction between − 10 and − 40 mmHg. 4. The reproducibilities of the responses to neck suction at − 30 mmHg, expressed as two standard deviations of the differences between responses on two occasions, were (mean responses in parentheses): immediate pulse interval, ± 32 (+ 236) ms; steady-state heart rate, ± 2.5 (− 6.5) beats/min; cardiac output ± 0.14 (− 0.59) 1/min; systolic and diastolic blood pressures, ± 10.0 (− 16.9) and ± 5.4 (− 10.1) mmHg, respectively. 5. Control values and responses to neck suction at − 30 mmHg were compared in subjects grouped in four age bands between 19 and 80 years. With increasing age, the control value of cardiac index (cardiac output divided by calculated body surface area) decreased, systolic and diastolic pressures increased, and the responses of all the measured variables to neck suction decreased. These results, obtained from a healthy population, provide reference values for comparison with those of individuals who may have abnormal baroreceptor reflexes.


1987 ◽  
Vol 253 (5) ◽  
pp. R779-R785
Author(s):  
B. T. Engel ◽  
M. I. Talan

Heart rate, stroke volume, and intra-arterial blood pressures were monitored continuously in each of four monkeys for 18 consecutive hours, 5 days/wk, for several weeks. Mean heart rate, stroke volume, cardiac output, systolic and diastolic pressure, and total peripheral resistance were calculated each minute, and these averages were analyzed further to yield hourly means and intercorrelations. The main findings from the analyses of mean levels were that cardiac output fell throughout the night and that peripheral resistance rose during the same interval so that arterial pressure fell only slightly; the highest levels of peripheral resistance and lowest levels of cardiac output were recorded between 0500 and 0700. Furthermore, the levels of these responses during the remainder of the morning were higher (peripheral resistance) and lower (cardiac output) than those recorded in the evening.


1991 ◽  
Vol 69 (7) ◽  
pp. 1985-1992 ◽  
Author(s):  
Malcolm E. Forster ◽  
Michael Axelsson ◽  
Anthony P. Farrell ◽  
Stefan Nilsson

The hagfish circulation contains a high volume of blood (180 mL∙kg−1) and is remarkable for the number of accessory pumps. Cardiac output from the branchial heart of hagfishes is comparable to that of elasmobranch and most teleost fishes, but blood pressures are considerably lower than in any other vertebrate group. Cardiac output is extremely sensitive to both venous return and ventral aortic pressure (afterload). Owing to the low arterial blood pressures, myocardial power output is lower than for any other vertebrate heart. The concomitant low energy requirement of the myocardium allows ATP generated anaerobically through glycolysis to maintain cardiac output during severe hypoxia. In vivo and in vitro administration of adrenergic agonists and antagonists increase and decrease cardiac performance, respectively. This suggests that the catecholamines that are stored beneath the endothelium of the branchial and portal hearts are involved in the tonic control of cardiac function.


2008 ◽  
Vol 105 (6) ◽  
pp. 1837-1844 ◽  
Author(s):  
Brett J. Wong ◽  
Don D. Sheriff

The “push-pull” effect denotes the reduced tolerance to +Gz (hypergravity) when +Gz stress is preceded by exposure to hypogravity, i.e., fractional, zero, or negative Gz. The purpose of this study was to test the hypothesis that an exaggerated, myogenically mediated rise in leg vascular conductance contributes to the push-pull effect, using heart level arterial blood pressure as a measure of G tolerance. The approach was to impose control (30 s of 30° head-up tilt) and push-pull (30 s of 30° head-up tilt immediately preceded by 10 s of −15° head-down tilt) gravitational stress after administration of hexamethonium (5 mg/kg) to inhibit autonomic ganglionic neurotransmission in seven dogs. Cardiac output or thigh level arterial pressure (myogenic stimulus) was maintained constant by computer-controlled ventricular pacing. The animals were sedated with acepromazine and lightly restrained in lateral recumbency on a tilt table. Following the onset of head-up tilt, the magnitude of the fall in heart level arterial pressure from baseline was −11.6 ± 2.9 and −17.1 ± 2.2 mmHg for the control and push-pull trials, respectively ( P < 0.05), when cardiac output was maintained constant. Over 40% of the exaggerated fall in heart level arterial pressure was attributable to an exaggerated rise in hindlimb vascular conductance ( P < 0.05). Maintaining thigh level arterial pressure constant abolished the exaggerated rise in hindlimb blood flow. Thus a push-pull effect largely attributable to a myogenically induced rise in leg vascular conductance occurs when autonomic function is inhibited.


2011 ◽  
Vol 301 (5) ◽  
pp. H2102-H2112 ◽  
Author(s):  
Michael E. Tschakovsky ◽  
Kristine Matusiak ◽  
Catherine Vipond ◽  
Lisa McVicar

The cause(s) of initial orthostatic hypotension (transient fall in blood pressure within 15 s upon active rising) have not been established. We tested the hypothesis that this hypotension is due to local vascular phenomena in contracting leg muscles from the brief effort of standing up. Seventeen young healthy subjects (2 male and 15 female, 22.5 ± 1.0 years) performed an active rise from resting squat after a 10-s squat, a 1-min squat, or a 5-min squat. Beat-by-beat arterial blood pressure, cardiac output, heart rate, and stroke volume (Finometer finger photoplethysmography) and right common femoral artery blood flow (Doppler and Echo ultrasound) were recorded. Data are means ± SE. Quiet standing before squat represented baseline. Peak increases in lower limb and total vascular conductance (ml·min−1·mmHg−1) upon standing were not different within squat conditions (10-s squat, 50.0 ± 12.4 vs. 44.3 ± 5.0; 1-min squat, 54.7 ± 9.2 vs. 50.5 ± 4.5; 5-min squat, 67.4 ± 13.7 vs. 58.8 ± 3.9; all P > 0.574). Mean arterial blood pressure (in mmHg) fell to a nadir well below standing baseline in all conditions despite increases in cardiac output. The hypotension predicted by the increase in leg vascular conductance accounted for this hypotension [observed vs. predicted (in mmHg): 10-s squat, −17.1 ± 2.1 vs. −18.3 ± 5.5; 1-min squat, −22.0 ± 3.8 vs. −25.3 ± 4.9; 5-min squat, −28.3 ± 4.0 vs. −29.2 ± 6.7]. We conclude that rapid contraction induced dilation in leg muscles with the effort of standing, along with a minor potential contribution of elevated lower limb arterio-venous pressure gradient, outstrips compensatory cardiac output responses and is the cause of initial orthostatic hypotension upon standing from squat.


1990 ◽  
Vol 69 (5) ◽  
pp. 1792-1798 ◽  
Author(s):  
L. Makrides ◽  
G. J. Heigenhauser ◽  
N. L. Jones

Factors contributing to maximal incremental and short-term exercise capacity were measured before and after 12 wk of high-intensity endurance training in 12 old (60-70 yr) and 10 young (20-30 yr) sedentary healthy males. Peak O2 uptake in incremental cycle ergometer exercise increased from 1.60 +/- 0.073 to 2.21 +/- 0.073 (SE) l/min (38% increase) in the old subjects and from 2.54 +/- 0.141 to 3.26 +/- 0.181 l/min (29%) in the young subjects. Peak cardiac output, estimated by extrapolation from a series of submaximal measurements by the CO2 rebreathing method, increased by 30% (from 12.7 to 16.5 l/min) in the old subjects, associated with a 6% increase (from 126 to 135 ml/l) in arteriovenous O2 difference; in the young subjects there were equal 14% increases in both variables (18.0 to 20.5 l/min and 140 to 159 ml/l, respectively). Submaximal mean arterial pressure and cardiac output were lower posttraining in the old subjects; total vascular conductance and cardiac stroke volume increased. Although peak power at the start of a short-term maximal isokinetic test did not change, total work accomplished in 30 s at a pedaling frequency of 110 revolutions/min increased in both groups, from 11.2 to 12.6 kJ and from 15.7 to 16.9 kJ in the old and young, respectively; fatigue during the 30-s test was less, and postexercise plasma lactate concentrations were lower. In older subjects, increases in aerobic power after high-intensity endurance training are at least as large as in younger subjects and are associated with increases in vascular conductance, maximal cardiac output, and stroke volume.


2007 ◽  
Vol 103 (5) ◽  
pp. 1496-1505 ◽  
Author(s):  
Connie C. W. Hsia ◽  
Robert L. Johnson ◽  
D. Merrill Dane ◽  
Eugene Y. Wu ◽  
Aaron S. Estrera ◽  
...  

In athletic animals the spleen induces acute polycythemia by dynamic contraction that releases red blood cells into the circulation in response to increased O2 demand and metabolic stress; when energy demand is relieved, the polycythemia is rapidly reversed by splenic relaxation. We have shown in adult foxhounds that splenectomy eliminates exercise-induced polycythemia, thereby reducing peak O2 uptake and lung diffusing capacity for carbon monoxide (DLCO) as well as exaggerating preexisting DLCO impairment imposed by pneumonectomy (Dane DM, Hsia CC, Wu EY, Hogg RT, Hogg DC, Estrera AS, Johnson RL Jr. J Appl Physiol 101: 289–297, 2006). To examine whether the postsplenectomy reduction in DLCO leads to abnormalities in O2 diffusion, ventilation-perfusion inequality, or hemodynamic function, we studied these animals via the multiple inert gas elimination technique at rest and during exercise at a constant workload equivalent to 50% or 80% of peak O2 uptake while breathing 21% and 14% O2 in balanced order. From rest to exercise after splenectomy, minute ventilation was significantly elevated with respect to O2 uptake compared with exercise before splenectomy; cardiac output, O2 delivery, and mean pulmonary and systemic arterial blood pressures were 10–20% lower, while O2 extraction was elevated with respect to O2 uptake. Ventilation-perfusion inequality was unchanged, but O2 diffusing capacities of lung (DLO2) and peripheral tissue during exercise were lower with respect to cardiac output postsplenectomy by 32% and 25%, respectively. The relationship between DLO2 and DLCO was unchanged by splenectomy. We conclude that the canine spleen regulates both convective and diffusive O2 transport during exercise to increase maximal O2 uptake.


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