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.

Rho kinase and Ca2+ entry mediate increased pulmonary and systemic vascular resistance in l-NAME-treated rats

2007 ◽  
Vol 293 (5) ◽  
pp. L1306-L1313 ◽  
Author(s):  
Jasdeep S. Dhaliwal ◽  
David B. Casey ◽  
Anthony J. Greco ◽  
Adeleke M. Badejo ◽  
Thomas B. Gallen ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Systemic Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Rho Kinase ◽  
Systemic Arterial Pressure ◽  
Intravenous Injections ◽  
Pulmonary Arterial ◽  
Dose Dependent

The small GTP-binding protein and its downstream effector Rho kinase play an important role in the regulation of vasoconstrictor tone. Rho kinase activation maintains increased pulmonary vascular tone and mediates the vasoconstrictor response to nitric oxide (NO) synthesis inhibition in chronically hypoxic rats and in the ovine fetal lung. However, the role of Rho kinase in mediating pulmonary vasoconstriction after NO synthesis inhibition has not been examined in the intact rat. To address this question, cardiovascular responses to the Rho kinase inhibitor fasudil were studied at baseline and after administration of an NO synthesis inhibitor. In the intact rat, intravenous injections of fasudil cause dose-dependent decreases in systemic arterial pressure, small decreases in pulmonary arterial pressure, and increases in cardiac output. l-NAME caused a significant increase in pulmonary and systemic arterial pressures and a decrease in cardiac output. The intravenous injections of fasudil after l-NAME caused dose-dependent decreases in pulmonary and systemic arterial pressure and increases in cardiac output, and the percent decreases in pulmonary arterial pressure in response to the lower doses of fasudil were greater than decreases in systemic arterial pressure. The Ca++ entry blocker isradipine also decreased pulmonary and systemic arterial pressure in l-NAME-treated rats. Infusion of sodium nitroprusside restored pulmonary arterial pressure to baseline values after administration of l-NAME. These data provide evidence in support of the hypothesis that increases in pulmonary and systemic vascular resistance following l-NAME treatment are mediated by Rho kinase and Ca++ entry through L-type channels, and that responses to l-NAME can be reversed by an NO donor.

A canine model of neurogenic pulmonary edema

1985 ◽  
Vol 59 (3) ◽  
pp. 1019-1025 ◽  
Author(s):  
M. B. Maron
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Arterial Pressure ◽  
Canine Model ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Neurogenic Pulmonary Edema ◽  
Lung Water ◽  
Pulmonary Arterial ◽  
Alpha Chloralose

The purpose of this study was to evaluate the usefulness of the intracisternal administration of veratrine as a model of neurogenic pulmonary edema (NPE) in the alpha-chloralose-anesthetized dog. Veratrine (40–60 micrograms/kg) was injected into the cisterna magna of 17 animals, and systemic arterial, pulmonary arterial, and left ventricular end-diastolic (LVEDP) pressures were followed for 1 h. Eleven animals developed alveolar edema. In these animals, systemic arterial pressure increased to 273 +/- 9 (SE) Torr, pulmonary arterial pressure to 74.5 +/- 4.9 Torr, and LVEDP to 42.8 +/- 4.5 Torr, and large amounts of pink frothy fluid, with protein concentrations ranging from 48 to 93% of plasma, appeared in the airways. Postmortem extravascular lung water content (Qwl/dQl) averaged 7.30 +/- 0.46 g H2O/g dry lung wt. Six animals escaped developing this massive degree of edema after veratrine (Qwl/dQl = 4.45 +/- 0.24). These animals exhibited similar elevated systemic arterial pressures (268 +/- 15 Torr), but did not develop the degree of pulmonary hypertension (pulmonary arterial pressure = 52.5 +/- 6.7 Torr, LVEDP = 24.8 +/- 4.0 Torr) observed in the other group. These results suggest that both hemodynamic and permeability mechanisms may play a role in the development of this form of edema and that veratrine administration may provide a useful model of NPE.

Hemodynamic effects of arginine vasopressin in rats adapted to chronic hypoxia

1989 ◽  
Vol 66 (1) ◽  
pp. 151-160 ◽  
Author(s):  
H. K. Jin ◽  
R. H. Yang ◽  
Y. F. Chen ◽  
R. M. Thornton ◽  
R. M. Jackson ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Arginine Vasopressin ◽  
Pulmonary Arterial Pressure ◽  
Systemic Arterial Pressure ◽  
Systemic Hemodynamic ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
Air Control

Acute and chronic pulmonary and systemic hemodynamic responses to arginine vasopressin (AVP) were examined in 4-wk hypoxia-adapted and air control rats. AVP, administered intravenously as bolus injections or sustained infusions, produced major dose-dependent V1-receptor-mediated reductions in mean pulmonary arterial pressure in hypoxia-adapted rats. These effects were comparable in pentobarbital-anesthetized, thoracotomized animals and in conscious, intact rats. Chronic infusions of AVP induced a sustained reduction in mean pulmonary arterial pressure and partially prevented the development of pulmonary hypertension without changing systemic arterial pressure. AVP induced significant decreases in cardiac output in both groups; the cardiac output response was not significantly different in hypoxia-adapted and air control animals. AVP induced almost no change in MPAP in air control rats. Furthermore the systemic pressor effects of AVP were significantly blunted in hypoxia-adapted rats compared with air controls. We conclude that the pulmonary depressor and blunted systemic pressor effects of AVP observed in hypoxia-adapted rats may be related to release of a vasodilator, such as endothelium-derived relaxing factor, vasodilator prostaglandins, or atrial natriuretic peptides. Further study is needed to elucidate these mechanisms and assess the usefulness of AVP and/or its analogues in the treatment and prevention of hypoxia-induced pulmonary hypertension.

Cardiorespiratory Disturbances Associated with Infective Fever in Man: Studies of Ethiopian Louse-Borne Relapsing Fever

1970 ◽  
Vol 39 (1) ◽  
pp. 123-145 ◽  
Author(s):  
D. A. Warrell ◽  
Helen M. Pope ◽  
E. H. O. Parry ◽  
P. L. Perine ◽  
A.D.M. Bryceson
Keyword(s):  
Cardiac Output ◽  
Body Temperature ◽  
Arterial Pressure ◽  
Metabolic Rate ◽  
Vascular Resistance ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Ventilation ◽  
Systemic Arterial Pressure ◽  
Relapsing Fever ◽  
Pulmonary Arterial

1. Nineteen patients with louse-borne relapsing fever were studied in Addis Abeba (altitude 2285 m). 2. Following treatment with tetracycline a febrile Jarisch—Herxheimer-like reaction developed which showed the phases described in artificially-induced endotoxin fever. 3. During the chill phase body temperature, metabolic rate and pulmonary ventilation increased. Despite alveolar hyperventilation pulmonary venous admixture was high. Cardiac output, heart rate and systemic arterial pressure increased but pulmonary arterial pressure decreased. 4. During the flush phase systemic arterial pressure fell and remained low for many hours due to reduced vascular resistance, but pulmonary arterial pressure and inflow resistance increased. Small increases in glucose, lactate, and pyruvate concentrations were prevented by inhaling oxygen. 5. Stimulation of metabolic rate, ventilation and cardiac output during the reaction was not due simply to increased body temperature, hypoxia, or acidosis but was probably attributable to spirochaetal endotoxin. 6. Limitation of pulmonary oxygen diffusion may have been responsible for the impaired pulmonary oxygen uptake in these patients. 7. During the prolonged flush phase a greatly increased cardiac output is necessary to maintain systemic arterial pressure because of the very low vascular resistance. Prevention of extracellular fluid volume depletion, early detection and prompt treatment of cardiac failure and oxygen therapy may reduce fatalities during this critical period but hydrocortisone in large doses failed to reduce the severity of the reaction.

Hemodynamic responses to acute carboxyhemoglobinemia in the rat

1983 ◽  
Vol 244 (3) ◽  
pp. H320-H327 ◽  
Author(s):  
W. E. Kanten ◽  
D. G. Penney ◽  
K. Francisco ◽  
J. E. Thill
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Cardiac Index ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Peripheral Resistance ◽  
Systolic Pressure ◽  
Left Ventricular ◽  
Stroke Work

The effects of carbon monoxide on the hemodynamics of the adult rat were investigated. A number of parameters were measured using an open-chest, chloralose-urethan anesthetized preparation. Our experiments showed this anesthetic agent to have several advantages over pentobarbital sodium. One group inhaled 150 ppm CO for 0.5-2 h, carboxyhemoglobin (HbCO) reaching 16%. Heart rate, cardiac output, cardiac index, dF/dtmax (aortic), and stroke volume rose significantly; mean arterial pressure, total peripheral resistance, and left ventricular systolic pressure fell, whereas stroke work, left ventricular dP/dtmax, and stroke power changed little. These effects were evident at a HbCO saturation as low as 7.5% (0.5 h). A second group inhaled 500 ppm CO for 5-48 h, HbCO reaching 35-38%. The same parameters changed in the same direction as in the first group, with mean arterial pressure and peripheral resistance remaining depressed, while heart rate, cardiac output, cardiac index, and stroke volume remained elevated. Heart rate and arterial systolic pressure were also monitored in conscious rats; rats in one group inhaled 500 ppm CO for 24 h, and rats in a second group were injected with a bubble of pure CO ip. In both cases heart rate was sharply elevated and blood pressure depressed as HbCO saturation increased. Both parameters recovered on CO washout. There was no significant difference between the response to inhaled vs. injected CO.

MO746CARDIAC REMODELING AND PULMONARY HYPERTENSION IN HEMODIALYSIS PATIENTS

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Ekaterina Borodulina ◽  
Alexander M Shutov
Keyword(s):  
Pulmonary Hypertension ◽  
Left Ventricular Hypertrophy ◽  
Arterial Pressure ◽  
Ventricular Hypertrophy ◽  
Pulmonary Arterial Pressure ◽  
Hemodialysis Patients ◽  
Left Ventricular ◽  
Hemodialysis Treatment ◽  
Systolic Pulmonary Arterial Pressure ◽  
Pulmonary Arterial

Abstract Background and Aims An important predictor of cardiovascular mortality and morbidity in hemodialysis patients is left ventricular hypertrophy. Also, pulmonary hypertension is a risk factor for mortality and cardiovascular events in hemodialysis patients. The aim of this study was to investigate cardiac remodeling and the dynamics of pulmonary arterial pressure during a year-long hemodialysis treatment and to evaluate relationship between pulmonary arterial pressure and blood flow in arteriovenous fistula. Method Hemodialysis patients (n=88; 42 males, 46 females, mean age was 51.7±13.0 years) were studied. Echocardiography and Doppler echocardiography were performed in the beginning of hemodialysis treatment and after a year. Echocardiographic evaluation was carried out on the day after dialysis. Left ventricular mass index (LVMI) was calculated. Left ventricular ejection fraction (LVEF) was measured by the echocardiographic Simpson method. Arteriovenous fistula flow was determined by Doppler echocardiography. Pulmonary hypertension was diagnosed according to criteria of Guidelines for the diagnosis and treatment of pulmonary hypertension of the European Society of Cardiology. Results Pulmonary hypertension was diagnosed in 47 (53.4%) patients. Left ventricular hypertrophy was revealed in 71 (80.7%) patients. Only 2 (2.3%) patients had LVEF<50%. At the beginning of hemodialysis correlation was detected between systolic pulmonary arterial pressure and LVMI (r=0.52; P<0.001). Systolic pulmonary arterial pressure negatively correlated with left ventricular ejection fraction (r=-0.20; P=0.04). After a year of hemodialysis treatment LVMI decreased from 140.49±42.95 to 123.25±39.27 g/m2 (р=0.006) mainly due to a decrease in left ventricular end-diastolic dimension (from 50.23±6.48 to 45.13±5.24 mm, p=0.04) and systolic pulmonary arterial pressure decreased from 44.83±14.53 to 39.14±10.29 mmHg (р=0.002). Correlation wasn’t found between systolic pulmonary arterial pressure and arteriovenous fistula flow (r=0.17; p=0.4). Conclusion Pulmonary hypertension was diagnosed in half of patients at the beginning of hemodialysis treatment. Pulmonary hypertension in hemodialysis patients was associated with left ventricular hypertrophy, systolic left ventricular dysfunction. After a year-long hemodialysis treatment, a regress in left ventricular hypertrophy and a partial decrease in pulmonary arterial pressure were observed. There wasn’t correlation between arteriovenous fistula flow and systolic pulmonary arterial pressure.

Cardiorespiratory effects of rapid saline infusion in normal man

1975 ◽  
Vol 38 (5) ◽  
pp. 786-775 ◽  
Author(s):  
A. L. Muir ◽  
D. C. Flenley ◽  
B. J. Kirby ◽  
M. F. Sudlow ◽  
A. R. Guyatt ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Control Period ◽  
Lung Compliance ◽  
Saline Infusion ◽  
Tidal Range ◽  
Closing Volume ◽  
Rapid Infusion ◽  
Pulmonary Arterial

We have studied the cardiorespiratory effects of the rapid infusion (100 ml/min) of 2 liters of saline in four normal seated subjects. Cardiac output and pulmonary arterial pressure increased, while vital capacity (VC) and total lung capacity (TLC) decreased. There was an increase in closing volume (CV) without any detectable change in lung compliance or flow-volume characteristics. There was an increase in Pao2 during infusion period which can be related to better matching of ventilation to perfusion and to improved hemoglobin transport. In the recovery stage as cardiac output, pulmonary arterial pressure, TLC, and VC all returned toward control values CV remained high. In two subjects CV occurred within the normal tidal range of ventilation and in these two subjects Pao2 fell significantly below values obtained in the control period. The results suggest that rapid saline infusion in man can cause interstitial edema and lead to premature airway closure and hypoxemia.

Pulmonary pressor response after prostaglandin synthesis inhibition in conscious dogs

1982 ◽  
Vol 52 (3) ◽  
pp. 705-709 ◽  
Author(s):  
B. R. Walker ◽  
N. F. Voelkel ◽  
J. T. Reeves
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Conscious Dogs ◽  
Pulmonary Pressure ◽  
Time Control ◽  
Mean Pulmonary Arterial Pressure ◽  
Before And After ◽  
Pulmonary Arterial

Recent studies have shown that vasodilator prostaglandins are continually produced by the isolated rat lung. We postulated that these vasodilators may contribute to maintenance of normal low pulmonary arterial pressure. Pulmonary pressure and cardiac output were measured in conscious dogs prior to and 30 to 60 min following administration of meclofenamate (2 mg/kg iv, followed by infusion at 2 mg . kg-1 . h-1) or the structurally dissimilar inhibitor RO–20–5720 (1 mg/kg iv, followed by infusion at 1 mg . kg-1 . h-1). The animals were also made hypoxic with inhalation of 10% O2 before and after inhibition. Time-control experiments were conducted in which only the saline vehicle was administered. Meclofenamate or RO–20–5720 caused an increase in mean pulmonary arterial pressure and total pulmonary resistance. Cardiac output and systemic pressure were unaffected. The mild hypoxic pulmonary pressor response observed was not affected by meclofenamate. Animals breathing 30% O2 to offset Denver's altitude also demonstrated increased pulmonary pressure and resistance when given meclofenamate. It is concluded that endogenous vasodilator prostaglandins may contribute to normal, low vascular tone in the pulmonary circulation.

Mechanism and pharmacology of endotoxin shock in sheep

1963 ◽  
Vol 18 (3) ◽  
pp. 544-552 ◽  
Author(s):  
D. F. J. Halmagyi ◽  
B. Starzecki ◽  
G. J. Horner
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Arterial Oxygen Saturation ◽  
Lung Compliance ◽  
Systemic Arterial Pressure ◽  
Endotoxin Shock ◽  
Arterial Oxygen ◽  
Marked Rise ◽  
Pulmonary Arterial ◽  
Pressure Fall

The cardiopulmonary consequences of coli-lipopolysaccharide and staphylococcus toxin administration were studied in sheep. Circulatory changes consisted mainly of a marked rise in pulmonary arterial and pulmonary arterial wedge pressure (with left atrial pressure unchanged), and a fall in cardiac output and in systemic arterial pressure. Fall in the latter closely followed the onset of pulmonary hypertension. The respiratory response consisted mainly of a severe fall in lung compliance produced by terminal airway closure. Continued perfusion of the nonventilated alveoli resulted in venous admixture. Premedication with antihistaminic, antiserotonin, or adrenolytic agents failed to affect the response. Norepinephrine or hypertensin administered after toxin injection had virtually no effect while isoproterenol treatment reduced pulmonary arterial pressure, increased cardiac output, arterial oxygen saturation, and, in cases of endotoxin shock, promptly raised systemic arterial pressure. Endotoxin-resistant sheep proved nonresponsive to minor pulmonary embolism and to incompatible blood transfusion. It is suggested that a common mediator agent is responsible for the similar cardiopulmonary consequences of these three diverse conditions. Submitted on November 26, 1962

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