Pulmonary venous waterfall and perivenous pressure in the living dog

1975 ◽  
Vol 38 (2) ◽  
pp. 304-308 ◽  
Author(s):  
H. C. Smith ◽  
J. Butler
Keyword(s):  
Left Atrium ◽  
Lung Tissue ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Transpulmonary Pressure ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Living Animal ◽  
Alveolar Pressure ◽  
Flow Through

Evidence has been obtained that a waterfall effect occurs in the pulmonary veins of the living dog. Anesthetized open-chest dogs were used. Small catheters were passed from the left atrium retrogradely up the pulmonary veins and venous tributaries until they finally pierced the venous walls. They were then pulled out through the surface of the lung until their bellshaped inner ends wedged in small side branches of the vein. They were used to measure upstream venous pressures via the occluded tributary without occlusion of the vein. The pulmonary lymphatics and bronchial circulation were untouched. Alveolar pressure (transpulmonary pressure, Ptp) was held constant during the periods of measurement. We found that intrapulmonary (upstream) venous pressures did not rise with elevation of left atrial (downstream) pressures at any Ptp until a pressure of at least 7 cmH2O above the base of the lung was exceeded. This left atrial pressure (below which a venous waterfall or flow-limiting segment effect was present) increased with Ptp when Ptp exceeded about 15 cmH2O. The waterfall occurs in the larger veins at the lung surface. Its presence and location suggest that intrapulmonary veins in the living animal are held open by the surrounding lung tissue and that neither the flow through them nor their contained volume is influenced by left atrial pressure when this is low.

Effect of increased left atrial pressure on breathing frequency in anesthetized dog

1990 ◽  
Vol 69 (6) ◽  
pp. 1973-1980 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrium ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Left Heart ◽  
Breathing Frequency ◽  
Anesthetized Dogs ◽  
The Right

Distension or loading of the isolated canine left heart caused reflex tachypnea in prior studies. The object of the present effort was to explore the possibility that this depended primarily on atrial distension. Cardiopulmonary bypass perfusion and ligation of pulmonary veins were used to isolate the left-heart chambers of anesthetized dogs. Simultaneous distension of the beating left atrium and fibrillating ventricle stimulated breathing frequency (f), whereas isolated ventricular distension did not. At other times, intervals of atrial fibrillation were imposed under two different conditions: 1) while the right heart and lungs were bypassed and systemic perfusion was provided by the left ventricle using blood returned to the left atrium by pump and 2) while the ventricles fibrillated and systemic perfusion was supplied directly by the pump. Atrial fibrillation increased left atrial pressure and stimulated f in condition 1. In condition 2, f increased only if fibrillation was associated with a rise in left atrial pressure. Vagal cooling blocked the effect of fibrillation. I conclude that left atrial distension may initiate reflex tachypnea.

Pulmonary congestion enhances responses of lung rapidly adapting receptors to cigarette smoke in rabbit

1994 ◽  
Vol 77 (6) ◽  
pp. 2633-2640 ◽  
Author(s):  
K. Ravi ◽  
C. T. Kappagoda ◽  
A. C. Bonham
Keyword(s):  
Left Atrium ◽  
Cigarette Smoke ◽  
Left Atrial ◽  
Venous Congestion ◽  
Transient Increase ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Pulmonary Congestion ◽  
Stimulation Of

We examined the effects of low-nicotine cigarette smoke, pulmonary venous congestion, and their combination on the activity of rapidly (RAR) and slowly adapting receptors (SAR) in anesthetized rabbits. Pulmonary venous congestion was achieved by inflating a balloon in the left atrium to increase left atrial pressure. We examined smoke effects on RARs (averaged over 15 breaths) at baseline left atrial pressure and at subthreshold and suprathreshold increases in left atrial pressure. At baseline, smoke significantly increased RAR activity from 12.1 +/- 4.2 to 16.2 +/- 4.2 impulses/breath (P < 0.05). At subthreshold increases in left atrial pressure (2.9 +/- 0.6 mmHg), smoke produced larger increases in RAR activity (12.3 +/- 3.3 to 22.5 +/- 4.1 impulses/breath; P < 0.05). Suprathreshold increases in left atrial pressure (9.2 +/- 1.1 mmHg) alone increased RAR activity from 10.9 +/- 3.2 to 19.8 +/- 5.9 impulses/breath (P < 0.05). Smoke had no additional effect (22.3 +/- 4.8 impulses/breath; P > 0.05). There was, however, a transient increase in RAR activity (1st 3 breaths of smoke) under all three conditions. Of nine SARs examined, only two were stimulated by smoke. We conclude that in the rabbit smoke-induced stimulation of RARs is augmented by mild pulmonary venous congestion. of RARs is augmented by mild pulmonary venous congestion.

Effect of lung-inflating pressure on pulmonary blood pressure and flow

1963 ◽  
Vol 205 (6) ◽  
pp. 1178-1186 ◽  
Author(s):  
E. F. De Bono ◽  
C. G. Caro
Keyword(s):  
Left Atrial ◽  
Perfusion Pressure ◽  
Pressure Ratio ◽  
Lower Lobe ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Alveolar Pressure ◽  
Perfusion Flow ◽  
The Relationship ◽  
Perfusion Flow Rate

In ten dogs the widely exposed left lower lobe of the lung was inflated to different static pressures over the range 5–20 cm H2O while being perfused with blood from a constant-flow source over a range of flows up to 300 ml/min. Left atrial pressure was kept below 3–4 cm H2O. The relationship between perfusion pressure and inflating pressure was linear and the slope independent of perfusion flow rate except at very low rates of flow. The Δ perfusion pressure-to-Δ inflating pressure ratio, with one exception, varied from 0.6 to 1.0, indicating that the major part of alveolar pressure was transmitted to the capillaries. At normal rates of flow the relationship between perfusion pressure and flow was linear. The findings, together with results obtained on a model, suggest that: 1) Calculation of pulmonary vascular resistance from the pulmonary artery-left atrial pressure gradient is misleading where inflating pressure exceeds left atrial pressure. In such circumstances the precapillary resistance can be measured. 2) At normal rates of flow the dominant resistance in the pulmonary vascular bed is precapillary. Despite the distensibility of pulmonary vessels this resistance does not vary with perfusion pressure or flow.

Lung microvascular pressure profile measured by micropuncture in anesthetized dogs

1988 ◽  
Vol 64 (2) ◽  
pp. 874-879 ◽  
Author(s):  
J. M. Shepard ◽  
M. A. Gropper ◽  
G. Nicolaysen ◽  
N. C. Staub ◽  
J. Bhattacharya
Keyword(s):  
Left Atrial ◽  
Left Lung ◽  
Lower Lobe ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Base Line ◽  
Alveolar Pressure ◽  
Pressure Zone ◽  
Isolated Lung ◽  
Anesthetized Dogs

We have micropunctured the lung in the open thorax of 17 anesthetized dogs to measure microvascular pressure. After intravenous pentobarbital sodium (25 mg/kg), we exposed the left lung through a wide left thoracotomy, which required rib excision. Through a double-lumen endotracheal tube, we ventilated the right lung to maintain normal blood gases and pH while we held the left lung motionless at an inflation pressure of 5 cmH2O. To reduce motion on the surface of the left lower lobe, we resected the left upper lobe, placed a Plexiglas baffle between the lobe and the heart, and held the lobe surface in a suction ring. In accordance with procedures we have previously described, we micropunctured subpleural vessels to measure microvascular pressure. At base line when alveolar pressure exceeded left atrial pressure (zone 2 conditions), 21, 38, and 41% of the total pressure drop occurred, respectively, in the arterial, microvascular, and venous segments. When we raised left atrial pressure above alveolar pressure (zone 3 conditions), the corresponding pressure drops were 30, 55, and 20% of total. The blood flow in the superficial layer of the lung averaged 15% less than the flow in the deeper layers as measured by distribution of 99mTc-albumin macroaggregates. We conclude that the intact and the isolated lung preparations in dog exhibit similar distributions of subpleural microvascular pressure.

Wedge pressure in large vs. small pulmonary arteries to detect pulmonary venoconstriction

1985 ◽  
Vol 59 (4) ◽  
pp. 1329-1332 ◽  
Author(s):  
A. Zidulka ◽  
T. S. Hakim
Keyword(s):  
Blood Flow ◽  
Left Atrial ◽  
Venous Pressure ◽  
Pulmonary Veins ◽  
Atrial Pressure ◽  
Left Atrial Pressure ◽  
Large Artery ◽  
Small Artery ◽  
Proximal Site ◽  
Wedge Pressure

Pulmonary arterial wedge pressure measures the pressure where blood flow resumes on the venous side. By occlusion of a large artery, the point where blood flow resumes will be in or near the left atrium. However, by occlusion of a small artery, it is possible to shift the point where flow resumes to a more proximal site in the veins and thus measure a pressure within the small veins. Increased pulmonary venous pressure, as a result of partial obstruction in the large veins, may not be detected by wedging a Swan-Ganz catheter in a large artery but may be detected by wedging in a small artery. We demonstrated this phenomenon in open-chest dogs by mechanically obstructing the left lower lobar vein or by infusing histamine to cause a generalized pulmonary venoconstriction. The wedge pressure measured by a 7-F Swan-Ganz catheter, with its balloon inflated in the main left lower lobar artery, nearly equaled left atrial pressure. On the other hand, the wedge pressure measured with a 7-F, 5-F, or a PE-50 catheter advanced into a small artery (without a balloon) was considerably higher than left atrial pressure. These results suggest that high resistance in the pulmonary veins can be demonstrated with the Swan-Ganz catheter by comparing the pressures obtained with the catheter wedged in a small and large artery.

Left atrial pressure-clamp servomechanism demonstrates LV suction in canine hearts with normal mitral valves

1994 ◽  
Vol 267 (1) ◽  
pp. H354-H362 ◽  
Author(s):  
N. B. Ingels ◽  
G. T. Daughters ◽  
S. D. Nikolic ◽  
A. DeAnda ◽  
M. R. Moon ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Left Atrium ◽  
Left Atrial ◽  
Left Ventricular Pressure ◽  
Left Ventricular ◽  
Rate Of Change ◽  
Atrial Pressure ◽  
Left Atrial Pressure

A novel technique is presented to study suction of the in situ left ventricle in open-chest experimental animals without requiring cardiopulmonary bypass or disturbing the native mitral valvular apparatus. In 17 dogs, left ventricular pressure (LVP) and left atrial pressure (LAP) were measured, the left atrium was cannulated and connected to a servo pump, and LAP was controlled to a setpoint near 0 mmHg by withdrawing blood from the left atrium. Heart rate [103 +/- 17 (SD) min-1], peak pressure (100 +/- 13 mmHg), minimum pressure (1.4 +/- 0.8 mmHg), and maximum rate of change of pressure with respect to time during isovolumic contraction and relaxation (2,506 +/- 775 and -1,761 +/- 855 mmHg/s, respectively) were normal. Servo control of LAP was possible to +/- 1 mmHg. LV suction was demonstrated in each heart (mean negative LVP -2.3 +/- 1.1 mmHg; P < 0.0001). This new technique demonstrates that the left ventricle can generate negative diastolic suction pressures when examined in vivo and in situ with an undisturbed mitral valve and physiologically normal preload and afterload. This adds to a growing body of evidence that, under appropriate circumstances, the heart can suck blood into itself and thereby aid in its own filling.

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