Stimulus—response curves for the pulmonary vascular bed to hypoxia and hypercapnia
TL;DR: In anaesthetized open‐chest cats and dogs, blood flow and gas tensions were measured in a circuit inserted into a pulmonary vein while ventilating the lobe which it drained with low O2 and high CO2 mixtures.
Abstract: 1. In anaesthetized open-chest cats and dogs, blood flow and gas tensions were measured in a circuit inserted into a pulmonary vein while ventilating the lobe which it drained with low O2 and high CO2 mixtures.
2. Both hypoxic and hypercapnic mixtures caused a reduction in blood flow from the lobe.
3. Stimulus—response curves relating blood flow to pulmonary venous PO2 and PCO2 were obtained. Those for hypoxia were usually asymptotic in shape; the curves became steep below 100 torr and flow sometimes fell to zero. The mean reduction in blood flow for every 20 torr fall in PO2 was 15·7% in cats and 11·8% in dogs. Those for hypercapnia were steep at first but levelled out at high PCO2 values; the maximum reduction in flow was 40–60% as vasoconstriction was only observed over a limited PCO2 range.
4. Hypoventilation of the lobe led to a reduction in blood flow. This was mainly attributable to hypoxia though other factors such as hypercapnia may sometimes have contributed.
5. Total occlusion of the bronchus of an O2-filled lobe caused blood flow to fall in two phases. The first phase could be attributed to a rise in PCO2 and the second to a fall in PO2.
6. The results confirm the hypothesis that hypoxia is an important factor regulating local blood flow in relation to local ventilation.
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TL;DR: In patients participating in regular physical exercise and low-fat diet, coronary artery disease progresses at a slower pace compared with a control group on usual care.
Abstract: BACKGROUNDSignificant regression of coronary and femoral atherosclerotic lesions has been documented by angiographic studies using aggressive lipid-lowering treatment. This study tested the applicability and effects of intensive physical exercise and low-fat diet on coronary morphology and myocardial perfusion in nonselected patients with stable angina pectoris.METHODS AND RESULTSPatients were recruited after routine coronary angiography for stable angina pectoris; they were randomized to an intervention group (n = 56) and a control group on "usual care" (n = 57). Treatment comprised intensive physical exercise in group training sessions (minimum, 2 hr/wk), daily home exercise periods (20 min/d), and low-fat, low-cholesterol diet (American Heart Association recommendation, phase 3). No lipid-lowering agents were prescribed. After 12 months of participation, repeat coronary angiography was performed; relative and minimal diameter reductions of coronary lesions were measured by digital image processing. Cha...
1,289 citations
TL;DR: Evidence regarding the contribution of HPV to the physiological and pathophysiological processes involved in the transition from fetal to neonatal life, pulmonary gas exchange, high-altitude pulmonary edema, and pulmonary hypertension is evaluated.
Abstract: It has been known for more than 60 years, and suspected for over 100, that alveolar hypoxia causes pulmonary vasoconstriction by means of mechanisms local to the lung. For the last 20 years, it has been clear that the essential sensor, transduction, and effector mechanisms responsible for hypoxic pulmonary vasoconstriction (HPV) reside in the pulmonary arterial smooth muscle cell. The main focus of this review is the cellular and molecular work performed to clarify these intrinsic mechanisms and to determine how they are facilitated and inhibited by the extrinsic influences of other cells. Because the interaction of intrinsic and extrinsic mechanisms is likely to shape expression of HPV in vivo, we relate results obtained in cells to HPV in more intact preparations, such as intact and isolated lungs and isolated pulmonary vessels. Finally, we evaluate evidence regarding the contribution of HPV to the physiological and pathophysiological processes involved in the transition from fetal to neonatal life, pulmonary gas exchange, high-altitude pulmonary edema, and pulmonary hypertension. Although understanding of HPV has advanced significantly, major areas of ignorance and uncertainty await resolution.
576 citations
Book•
01 Jan 1977
TL;DR: The inequality of blood flow and ventilation in the normal lung and ventilation-perfusion ratio inequality and regional gas exchange are studied.
Abstract: Introduction Oxygen transport from air to tissues Inequality of blood flow and ventilation in the normal lung Ventilation-perfusion ratio inequality and regional gas exchange Ventilation-perfusion ratio inequality and overall gas exchange Methods of measuring ventilation-perfusion ration inequality Distributions of ventilation-perfusion ratios Appendixes: How to talk the Va/Q language How to draw a Va/Q line Suggestions for further reading References Index
300 citations
TL;DR: Patients with edema due to chronic obstructive pulmonary disease have severe retention of salt and water, reduction in renal blood flow and glomerular filtration, and neurohormonal activation similar to that seen in patients with edma due to myocardial disease.
Abstract: BACKGROUNDThe pathogenesis of salt and water accumulation in patients with chronic obstructive pulmonary disease is unclear and may differ from that in patients with congestive heart failure due to myocardial disease. This study was undertaken to investigate some of the mechanisms involved.METHODS AND RESULTSHemodynamics, water and electrolyte spaces, renal function, and plasma hormone concentrations were measured in nine patients with edema due to chronic obstructive pulmonary disease and in six patients after recovery. Mean cardiac output (3.8 +/- 0.26 l/min.m2) was normal, but right atrial (11 +/- 1 mm Hg) and mean pulmonary arterial (41 +/- 3 mm Hg) pressures were increased. Mean pulmonary arterial wedge pressure (11 +/- 1 mm Hg) was normal. Pulmonary vascular resistance (8.6 +/- 1.3 mm Hg.min.m2/l) was increased, but systemic vascular resistance (19.3 +/- 1.3 mm Hg.min.m2/l) and mean arterial pressure (83 +/- 4 mm Hg) were low. All patients were hypoxemic (PaO2, 40 +/- 2 mm Hg) and hypercapnic (PaCO2...
238 citations
TL;DR: The sections in this article are: Steady-State Relations Between Stimulus and Response, Dynamic Properties of Respiratory Control System, Stability of Alveolar and Arterial CO2 and O2 Tensions, and Concluding Remarks.
Abstract: The sections in this article are:
1
Feedback Loop
11
Metabolic Hyperbola
12
Steady-State Relations Between Stimulus and Response
13
Sites of Interaction Between Hypercapnic and Hypoxic Drives
14
Apnea Point: Carbon Dioxide-Acid Thresholds
2
Dynamic Properties of Respiratory Control System
21
Dynamics of Receptors
22
Dynamic Properties of Overall System
23
Respiratory Oscillations and Whole-System Responses
3
Pattern of Breathing
31
Mean Values in Steady States
32
Changing States: Dynamic Responses
33
Nonclassic Dynamic Stimuli
4
Potassium
5
Stability of Alveolar and Arterial CO2 and O2 Tensions
6
Concluding Remarks
214 citations
References
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TL;DR: The relationship between the degree of pulmonary vascular response and the level of hypoxia has received only little attention, and usually a constrictor response to a single low oxygen gas inhalation has been reported.
Abstract: Considerable controversy regarding the effects of hypoxia on the pulmonary vasculature has arisen over the past few decades. The literature has been extensively reviewed by Fishman (1), and it is now generally accepted that hypoxia is a pulmonary vasoconstrictor. Much of the controversy has centered around the interpretation of a small elevation of pulmonary arterial pressure in the face of an increase in cardiac output related to the hypoxic stimulus. Some investigators calculated a small increase of pulmonary vascular resistance, whereas others could not confirm this observation. Most studies were performed in adult animals, or in adult humans, but more recently attention has been directed to hypoxic responses in the newborn animal, in view of the greater responsiveness of the pulmonary vasculature at this age. The relationship between the degree of pulmonary vascular response and the level of hypoxia has received only little attention, and usually a constrictor response to a single low oxygen gas inhalation has been reported. Recently Thilenius, Hoffer, Fitzgerald, and Perkins (2) attempted to relate pulmonary vascular resistance change to the level of inspired gas oxygen tension, but no obvious relationship could be demonstrated. Liljestrand (3) in 1958 suggested that the pulmonary vascular response to hypoxia may be related to the production of local Ho ion concentration changes in the lung. More recently Enson and as-
490 citations
TL;DR: Inhaled radioactive CO2 is rapidly taken up by pulmonary blood and by external counting over the chest during breath holding, the clearance rate of radioactiveCO2xs from the counting field can be cleared.
Abstract: Inhaled radioactive CO2 is rapidly taken up by pulmonary blood. By external counting over the chest during breath holding, the clearance rate of radioactive CO2xs from the counting field can be rec...
451 citations
TL;DR: Measurements of regional ventilation and blood flow using radioactive CO2 show that both increase from apex to base of the lung; the results are used to build an integrated picture of gas exchange.
Abstract: Measurements of regional ventilation and blood flow using radioactive CO2 show that both increase from apex to base of the lung; the results are used to build an integrated picture of gas exchange....
263 citations
240 citations
TL;DR: It is assumed that the effects of reactivity of the vascular compartment to various stimuli will be more readily discernible in the presence of a restricted bed because of the high degree of correlation between the level of pulmonary artery pressures and the degree of hypoxemia.
Abstract: Pulmonary hypertension has been found to be reversible in certain patients with, cor pulmonale due to chronic bronchitis, bronchiolitis, and/or emphysema. In these individuals, as disturbances in gas exchange are corrected, pulmonary artery pressures fall (1). The high degree of correlation between the level of pulmonary artery pressures and the degree of hypoxemia (2, 3) as well as the pressor response to acutely induced hypoxia (4, 5) has implicated a reduced oxygen tension within the lungs as a major factor in the appearance of pulmonary hypertension (6). Since these patients almost invariably demonstrate hypercapnia, carbon dioxide tension has also been invoked as a cause of pulmonary hypertension (3). Anatomic reduction of the pulmonary vascular bed cannot be assigned a dominant role in the genesis of this hypertension because of its reversibility. Nonetheless, we may assume that the effects of reactivity of the vascular compartment to various stimuli will be more readily discernible in the presence of a restricted bed. Liljestrand has recently come to the conclusion that an increased hydrogen ion concentration in the blood is the chemical stimulus for pulmonary
237 citations