Pulmonary Reflexes in Pulmonary Edema?

Abstract

The mechanism of pulmonary edema caused by stimulation of the central nervous system was studied in 33 dogs. Stimulation was obtained by the intracisternal injection of veratrine, or of air or saline under high pressure, or by electric stimulation of the hypothalamus. Pressure changes in the pulmonary artery, left atrium and left ventricle were recorded by means of three catheters introduced through the right external jugular vein and the left femoral artery. Experiments were performed with closed or open chest, and following ligation of the thoracic aorta and inferior cava. Lung opacity was studied as a means to estimate the blood content of this organ. Data obtained in closed-chest experiments suggest that a blood shift from the systemic to the pulmonary circulation may be a factor in veratrine-induced pulmonary edema. This was confirmed by the observation that, following mechanical exclusion of the systemic circulation, no pulmonary edema occurred while the changes of left ventricular pressure were minimal and inconstant. In these animals, pulmonary artery pressure still rose indicating vasoconstriction while an increase of lung opacity suggested that the vasoconstriction was greater in the pulmonary veins than in the arteries. Injection of air or saline under high pressure into the cisterna magna and faradic stimulation of the hypothalamus caused pulmonary hypertension, even after exclusion of the systemic circulation. In these experiments, a decreased lung opacity suggested that the pulmonary constriction was greater on the arterial than on the venous side. These findings are offered as evidence that the caliber of the pulmonary vessels may be influenced by central nervous system stimulation, an additional element to be considered in the mechanism of pulmonary edema.

Relative Mitral Insufficiency as a Factor of Paroxysmal Pulmonary Edema

“…Contrary to our previous experience in open chest experiments (8) and in agreement with studies of Wiggers (9,10), who proved that either increased venous return or increased peripheral resis tance is followed by increase in ventricular diastolic pressure in heart-lung preparations, it was actually noted that left ventricular diastolic pressure rose in most experiments. However, this rise usually started 20 or more m inutes alter the rise of systolic pres sure, indicating that other mechanisms were able to m aintain an increased left ventricular work for a relatively long time without requiring m arked dilatation.…”

“…(2) suggested that central stim ulation was fol lowed by neurogenic systemic vascular constriction and pulmonic dilatation. T hat the latter phenomenon may occur was dem onstrat ed in this laboratory (8).…”

“…The concurrent effect of direct or reflex changes in the caliber of the pulm onary vessels (constriction of the venules with further dilatation of the capillaries) seems also highly probable on the basis of previous studies (8), and may represent an addi tional factor.…”

Hemodynamic effects of elevated cerebrospinal fluid pressure: alterations with adrenergic blockade

“…Other investigators have found a similar elevation of systemic blood pressure and pulmonary venous pressure after elevating intracranial pressure with bags, balloons (5, 6, 10, 11), and mineral oil (12). Similar hemodynamic changes can be produced by the intracisternal injection of veratrine (13,14), kaolin (15), a thrombin-fibrinogen mixture (16)(17)(18), and the injection of aconitine in the preoptic areas (19). The mechanisms that have been suggested for these hemodynamic changes accompanying elevated intracranial pressure or intracisternal injections include: ischemia (1,20), release of a pressor material (21), venocontriction (22,23), a myocardial intoropic response (22), and somatic and splanchnic shunting (24).…”

Peripheral Circulation

“…Visscher et al (341) have reviewed the physiological and pharmacological aspects of pulmonary edema, while Luisada and co-workers (342,343) have shown that the pulmonary edema resulting from powerful stimulation of the vasomotor center of the central nervous system is probably caused by excessive shift of blood from the systemic to the pulmonary circulation. Hawthorne et al (344) have shown that acute pulmonary edema can be produced by simultaneous creation of aortic insu fficiency and renal artery constriction, but that this type of pulmonary edema can be prevented by prior construction of an atrial septal defect (345).…”