Role of Bradycardia and Cold per se in Increasing Mechanical Efficiency of Hypothermic Heart

1958 ◽  
Vol 192 (2) ◽  
pp. 331-334 ◽  
Author(s):  
Henry Badeer ◽  
Avedis Khachadurian
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
Arterial Pressure ◽  
Mechanical Efficiency ◽  
Metabolic Effect ◽  
Stroke Work ◽  
Per Se ◽  
Lung Preparation

The relative influence of bradycardia and of cold per se on the oxygen consumption and mechanical efficiency of the dog heart was investigated in the modified heart-lung preparation (11 experiments). Myocardial oxygen uptake was determined under constant arterial pressure and cardiac output in a) normothermia, b) normothermia with bradycardia induced by a cold thermode on the pacemaker, and c) hypothermia producing the same bradycardia as in ( b). At 36.8°C with a rate of 153 beats/min. the efficiency was 8.5% ± 0.3(S.E.), whereas with a rate of 110/min. efficiency was 9.1% ± 0.4(S.E.), a change that is statistically not significant. In hypothermia of 31.5°C with a rate of 110/min. the efficiency was 10.8% ± 0.3(S.E.), an increase that is statistically significant. Performing the same stroke work the hypothermic myocardium consumed less oxygen than the normothermic. It is concluded that the metabolic effect of cold per se is the chief factor responsible for increasing the mechanical efficiency of the hypothermic heart when pressure-volume work is kept constant.

Desflurane, Sevoflurane, and Isoflurane Impair Canine Left Ventricular-Arterial Coupling and Mechanical Efficiency

1996 ◽  
Vol 85 (2) ◽  
pp. 403-413 ◽  
Author(s):  
Douglas A. Hettrick ◽  
Paul S. Pagel ◽  
David C. Warltier
Keyword(s):  
Arterial Pressure ◽  
Myocardial Contractility ◽  
Minimum Alveolar Concentration ◽  
Systolic Pressure ◽  
Mechanical Efficiency ◽  
Left Ventricular ◽  
Stroke Work ◽  
Arterial Elastance ◽  
Ventricular Afterload ◽  
Left Ventricular Arterial Coupling

Background The effects of desflurane, sevoflurane, and isoflurane on left ventricular-arterial coupling and mechanical efficiency were examined and compared in acutely instrumented dogs. Methods Twenty-four open-chest, barbiturate-anesthetized dogs were instrumented for measurement of aortic and left ventricular (LV) pressure (micromanometer-tipped catheter), dP/dtmax, and LV volume (conductance catheter). Myocardial contractility was assessed with the end-systolic pressure-volume relation (Ees) and preload recruitable stroke work (Msw) generated from a series of LV pressure-volume diagrams. Left ventricular-arterial coupling and mechanical efficiency were determined by the ratio of Ees to effective arterial elastance (Ea; the ratio of end-systolic arterial pressure to stroke volume) and the ratio of stroke work (SW) to pressure-volume area (PVA), respectively. Results Desflurane, sevoflurane, and isoflurane reduced heart rate, mean arterial pressure, and left ventricular systolic pressure. All three anesthetics caused similar decreases in myocardial contractility and left ventricular afterload, as indicated by reductions in Ees, Msw, and dP/dtmax and Ea, respectively. Despite causing simultaneous declines in Ees and Ea, desflurane decreased Ees/Ea (1.02 +/- 0.16 during control to 0.62 +/- 0.14 at 1.2 minimum alveolar concentration) and SW/PVA (0.51 +/- 0.04 during control to 0.43 +/- 0.05 at 1.2 minimum alveolar concentration). Similar results were observed with sevoflurane and isoflurane. Conclusions The present findings indicate that volatile anesthetics preserve optimum left ventricular-arterial coupling and efficiency at low anesthetic concentrations (< 0.9 minimum alveolar concentration); however, mechanical matching of energy transfer from the left ventricle to the arterial circulation degenerates at higher end-tidal concentrations. These detrimental alterations in left ventricular-arterial coupling produced by desflurane, sevoflurane, and isoflurane contribute to reductions in overall cardiac performance observed with these agents in vivo.

scholarly journals Role of endothelial nitric oxide in control of peripheral vascular conductance during muscle metaboreflex activation

2017 ◽  
Vol 313 (1) ◽  
pp. R29-R34
Author(s):  
Danielle Senador ◽  
Jasdeep Kaur ◽  
Alberto Alvarez ◽  
Hanna W. Hanna ◽  
Abhinav C. Krishnan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Peripheral Vasodilation ◽  
Dependent Flow ◽  
Flow Mediated Vasodilation ◽  
The Relationship

The muscle metaboreflex is a powerful pressor reflex induced by the activation of chemically sensitive muscle afferents as a result of metabolite accumulation. During submaximal dynamic exercise, the rise in arterial pressure is primarily due to increases in cardiac output, since there is little systemic vasoconstriction. Indeed, in normal animals, we have often shown a small, but significant, peripheral vasodilation during metaboreflex activation, which is mediated, at least in part, by release of epinephrine and activation of vascular β2-receptors. We tested whether this vasodilation is in part due to increased release of nitric oxide caused by the rise in cardiac output eliciting endothelium-dependent flow-mediated vasodilation. The muscle metaboreflex was activated via graded reductions in hindlimb blood flow during mild exercise with and without nitric oxide synthesis blockade [ NG-nitro-l-arginine methyl ester (l-NAME); 5 mg/kg]. We assessed the role of increased cardiac output in mediating peripheral vasodilation via the slope of the relationship between the rise in nonischemic vascular conductance (conductance of all vascular beds excluding hindlimbs) vs. the rise in cardiac output. l-NAME increased mean arterial pressure at rest and during exercise. The metaboreflex-induced increases in mean arterial pressure were unaltered by l-NAME, whereas the increases in cardiac output and nonischemic vascular conductance were attenuated. However, the slope of the relationship between nonischemic vascular conductance and cardiac output was not affected by l-NAME, indicating that the rise in cardiac output did not elicit vasodilation via increased release of nitric oxide. Thus, although nitric oxide is intrinsic to the vascular tonus, endothelial-dependent flow-mediated vasodilation plays little role in the small peripheral vasodilation observed during muscle metaboreflex activation.

Hyperosmotic NaCl and severe hemorrhagic shock: role of the innervated lung

1981 ◽  
Vol 241 (6) ◽  
pp. H883-H890 ◽  
Author(s):  
O. U. Lopes ◽  
V. Pontieri ◽  
M. Rocha e Silva ◽  
I. T. Velasco
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Metabolic Response ◽  
Term Survival ◽  
Long Term Survival ◽  
Vagal Blockade ◽  
Intravenous Infusions ◽  
Acid Base Equilibrium

Infusions of hyperosmotic NaCl (2,400 mosmol/l; 4 ml/kg) were given to dogs in severe hemorrhagic hypotension by intravenous injection (72 expts) or intra-aortic injection (25 expts). In 46 experiments intravenous infusions were given during bilateral blockage of the cervical vagal trunks (local anesthesia or cooling). Intravenous infusions (without vagal blockade) restore arterial pressure, cardiac output, and acid-base equilibrium to normal and cause mesenteric flow to overshoot prehemorrhage levels by 50%. These effects are stable, and indefinite survival was observed in every case. Intra-aortic infusions of hyperosmotic NaCl produce only a transient recovery of arterial pressure and cardiac output but no long-term survival. Intravenous infusions with vagal blockage produce only a transient recovery of cardiac output, with non long-term survival. Measurement of pulmonary artery blood osmolarity during and after the infusions shows that a different pattern is observed in each of these three groups and strongly indicates that the first passage of hyperosmotic blood through the pulmonary circulation at a time when vagal conduction is unimpaired is essential for the production of the full hemodynamic-metabolic response, which is needed for indefinite survival.

Effect of hemorrhagic hypotension on oxygen consumption of dogs

1964 ◽  
Vol 207 (3) ◽  
pp. 647-649 ◽  
Author(s):  
Elvin E. Smith ◽  
Jack W. Crowell
Keyword(s):  
Blood Flow ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
Arterial Pressure ◽  
Flow Rate ◽  
Blood Oxygen ◽  
Oxygen Utilization ◽  
Epinephrine Administration ◽  
Utilization Coefficient ◽  
Subsequent Rise

The effects of hematocrit, Dibenzyline, and epinephrine on oxygen consumption were studied in 220 dogs whose arterial pressure was lowered to and maintained at 30 mm Hg. Oxygen consumption was recorded previous to and during the period of hypotension. The average oxygen consumption was 7.20 ml/kg min prior to hemorrhage. Ten minutes after hemorrhage the oxygen consumption was 3.58 ml/kg min (50% of control). After 30 min of hypotension the oxygen consumption was 4.70 ml/kg min (65% of control), and the oxygen consumption increased to 5.33 ml/kg min (74% of control) after 1 hr. Pretreatment with Dibenzyline increased the oxygen consumption during the early stages of hypotension but had little effect in the latter stages. Epinephrine administration decreased the oxygen consumption during the entire hypotensive period. Previous studies have shown that the oxygen utilization coefficient approaches its maximal value during the hypotensive period; therefore, oxygen uptake becomes limited by the blood flow and the changes in oxygen consumption indicate changes in flow rate to active tissue. Simultaneous studies showed that the hematocrit influenced oxygen transport by effects on both the blood oxygen content and the blood flow. The results illustrate that animals with hematocrits of 35–39 are able to transport more oxygen than animals with other hematocrits. Evidence is presented to show that the initial fall and the subsequent rise in oxygen consumption during hypotension may be a local autoregulation of blood flow.

Mechanism of decreased cardiac output during ANP infusion in conscious anephric dogs

1992 ◽  
Vol 262 (1) ◽  
pp. R120-R125
Author(s):  
H. L. Mizelle ◽  
C. A. Gaillard ◽  
R. D. Manning ◽  
J. E. Hall
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Atrial Natriuretic Peptide ◽  
Blood Cells ◽  
Venous Return ◽  
Control Period ◽  
Peripheral Resistance ◽  
Circulating Blood Volume

Atrial natriuretic peptide (ANP) may decrease cardiac output (CO) by lowering circulating blood volume (BV) or by altering the vasculature in a manner that would decrease venous return. The purpose of this study was to determine the role of decreased BV in mediating the decrease in CO during acute infusion of ANP. BV was measured by dilution of 51Cr-labeled red blood cells in seven trained conscious splenectomized dogs studied after unilateral (UNX) and total (TNX) nephrectomy. BV, hematocrit (Hct), CO, mean arterial pressure (MAP), and total peripheral resistance (TPR) were determined during a 90-min control period and 270 min of infusion of ANP (20 ng.kg-1.min-1 iv). In UNX dogs, ANP decreased BV from 60.9 +/- 1.4 to 58.6 +/- 1.4 ml/kg and increased Hct from 39.3 +/- 1.8% to 41.1 +/- 1.8% (P less than 0.05). MAP was not changed and CO fell to a low that was 86 +/- 2% of control (P less than 0.05) 240 min after starting ANP. TPR increased significantly during ANP infusion. All variables returned to control after ANP was stopped. In the same dogs studied 24 h after TNX, MAP averaged 111 +/- 5 mmHg during control and did not change during ANP infusion. CO fell to a low of 82 +/- 3% of control (P less than 0.05) after 120 min of infusion and remained reduced until after the ANP was stopped.(ABSTRACT TRUNCATED AT 250 WORDS)

Low exercise pulmonary resistance is not dependent on vasodilator prostaglandins

1983 ◽  
Vol 55 (2) ◽  
pp. 558-561 ◽  
Author(s):  
J. Lindenfeld ◽  
J. T. Reeves ◽  
L. D. Horwitz
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Cyclooxygenase Inhibitors ◽  
Pulmonary Resistance ◽  
Before And After ◽  
Pulmonary Arterial

In resting conscious dogs, administration of cyclooxygenase inhibitors results in modest increases in pulmonary arterial pressure and pulmonary vascular resistance, suggesting that vasodilator prostaglandins play a role in maintaining the low vascular resistance in the pulmonary bed. To assess the role of these vasodilator prostaglandins on pulmonary vascular resistance during exercise, we studied seven mongrel dogs at rest and during exercise before and after intravenous meclofenamate (5 mg/kg). Following meclofenamate, pulmonary vascular resistance rose both at rest (250 24 vs. 300 +/- 27 dyn . s . cm-5, P less than 0.01) and with exercise (190 +/- 9 vs. 210 +/- 12 dyn . s . cm-5, P less than 0.05). Systemic vascular resistance rose slightly following meclofenamate both at rest and during exercise. There were no changes in cardiac output. The effects of cyclooxygenase inhibition, although significant, were less during exercise than at rest. This suggests that the normal fall in pulmonary vascular resistance during exercise depends largely on factors other than vasodilator prostaglandins.

Effects of arteriovenous fistula on systemic and pulmonary circulations

1964 ◽  
Vol 207 (6) ◽  
pp. 1319-1324 ◽  
Author(s):  
Jiro Nakano ◽  
Christian De Schryver
Keyword(s):  
Cardiac Output ◽  
Blood Transfusion ◽  
Arterial Pressure ◽  
Left Atrial ◽  
Pulmonary Arterial Pressure ◽  
Peripheral Resistance ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Pulmonary Arterial

The effects of arteriovenous fistulas of different magnitudes on cardiovascular dynamics were studied in anesthetized dogs. It was found that A-V fistula decreases mean systemic arterial pressure, effective systemic blood flow, total and pulmonary peripheral resistances, whereas it increases heart rate, total cardiac output, stroke volume, left atrial pressure, pulmonary arterial pressure, and systemic peripheral resistance. The magnitude of the above hemodynamic changes was essentially proportional to the size of the fistula. At equivalent increments in total cardiac output produced by A-V fistula and blood transfusion, the former condition causes a greater increase in pulmonary arterial pressure than the latter, although both conditions decrease the pulmonary peripheral resistance by the same degree. It was also found that, at equivalent left atrial pressures, left ventricular stroke work with A-V fistula was greater than that with blood transfusion.

Altered hemodynamic responses to acute hypoxemia in spontaneously hypertensive rats

1978 ◽  
Vol 234 (3) ◽  
pp. H275-H279 ◽  
Author(s):  
G. M. Walsh ◽  
M. Tsuchiya ◽  
A. C. Cox ◽  
A. J. Tobia ◽  
E. D. Frohlich
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Arterial Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Early Stage ◽  
Peripheral Resistance ◽  
Oxygen Availability ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Total Body Oxygen

Conscious spontaneously hypertensive rats (SHR), 5--7 wk old, were studied hemodynamically by the direct Fick procedure to determine whether high total peripheral resistance (TPR) coexisted with increased oxygen consumption (QO2) at an early stage of hypertension development. Since under resting conditions cardiac output in SHR was not significantly different from normotensive controls, the elevated arterial pressure and QO2 were associated with increased TPR. Arterial hypoxemia was induced to reduce oxygen availability and to assess whether increased TPR in SHR could be reversed by this procedure. During hypoxemia, normotensive controls (WKY) responded with increased cardiac output and decreased arterial pressure and TPR. In contrast, arterial pressure and cardiac output fell in SHR; and the increased TPR persisted. QO2 fell in hypoxemic SHR demonstrating that the relationship between total body oxygen consumption and cardiac output was abnormal in young SHR, and that increased TPR in SHR was not dependent on resting levels of QO2 or oxygen availability. Although QO2 was elevated in SHR compared to age-matched WKY, this condition was not essential for maintained elevated vascular resistance.

Non-invasive Measurement of Cardiac Output and Ventricular Ejection Fractions in Chronic Cardiac Failure: Relationship to Impaired Exercise Tolerance

1997 ◽  
Vol 93 (3) ◽  
pp. 195-203 ◽  
Author(s):  
Ian C. Steele ◽  
ANN Moore ◽  
Anne-Marie Nugent ◽  
Marshall S. Riley ◽  
Norman P. S. Campbell ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Oxygen Consumption ◽  
Oxygen Uptake ◽  
Cardiac Failure ◽  
Exercise Tolerance ◽  
Perceived Exertion ◽  
Lactate Concentration ◽  
Submaximal Exercise ◽  
Chronic Cardiac Failure ◽  
And Control

1. The role of cardiac output limitation in the pathophysiology of exercise in patients with chronic failure remains undefined. During steady-state submaximal exercise, oxygen uptake is similar in patients and control subjects, but it is not known if cardiac output is also similar. We wished to determine if the reduced exercise tolerance of patients with chronic cardiac failure during such exercise is related to reduced cardiac output, or to peripheral factors. 2. Ten male patients with stable chronic failure and ten age-matched male normal controls were studied at rest and during exercise. Each subject performed a familiarization exercise test, a symptom-limited maximal exercise test and two submaximal exercise tests. Cardiac output was measured by a carbon dioxide rebreathing method. We also measured oxygen consumption, ventilation, Borg score of perceived exertion and venous lactate concentration, and ejection fractions. 3. As expected, patients had lower peak oxygen consumption [median (range) 1.18 (0.98–1.76) versus 1.935 (1.53–2.31) 1/min; P < 0.001], lower peak venous lactate concentration but a similar overall level of perceived exertion. At the same submaximal workload, patients and control subjects had similar oxygen consumption [0.67 (0.59–0.80) versus 0.62 (0.52–0.82) 1/min] and cardiac output [6.92 (5.79–9.76) versus 7.3 (5.99–10.38) 1/min] but the patients had a greater perceived level of exertion [Borg score: 4 (1–6) versus 3 (1–5); P < 0.005], higher venous lactate concentration [1.6 (1–3.3) versus 1.14 (0.7–1.7) mmol/l; P < 0.05] and higher heart rate [106 (89–135) versus 87 (69–112) beats/min;P < 0.005]. 4. During submaximal exercise at a similar absolute workload, patients with cardiac failure have a similar oxygen uptake and cardiac output but greater anaerobiosis and increased fatigue when compared with normal subjects. These findings appear to relate predominantly to changes that occur in the periphery rather than abnormalities of central cardiac function.

Cardiac output of the hypothermic rat

1959 ◽  
Vol 196 (2) ◽  
pp. 415-419 ◽  
Author(s):  
Robert W. Bullard
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Total Resistance ◽  
Vascular Geometry ◽  
Per Se ◽  
Colonic Temperature

As the colonic temperature of the rat was lowered the heart rate and cardiac output fell linearly with the temperature. The arterial pressure did not fall linearly indicating an increase of total peripheral resistance. The increase of hematocrit ratio and the effect of cold on blood per se combined to increase the in vitro viscosity threefold as the colonic temperature approached 15°C. It appears from these data that the increase in viscosity of the blood is the important factor in the increase in total resistance to flow and that little change in total or average vascular geometry took place. However, comparison of the local clearances of 1131 from specific extravascular areas shows that individual vascular geometries may be changing but in such a fashion as to balance out each other.

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