Elevated Systemic Arterial Pressure Research Articles

CLINICAL STUDIES ON PULMONARY ARTERIAL PRESURE OF THE PATIENTS WITH CHRONIC PULMONARY EMPHYSEMA

The Studies on pulmonary arterial pressure were made by the pulmonary arterial catheterization on 53 patients with chronic pulmonary emphysema, and the following results were obtained.1) The pulmonary arterial mean pressures of these patients were 9-66mmHg, the pulmonary arterial systolic pressures 9-121mmHg, the pulmonary arterial diastolic pressures 0-36mmHg.The fluctuation of the pulmonary arterial pressure by respiration was in the rarge of 0-20mmHg in systole and 0-25mmHg in diastole and was marked in the patients with high total pulmonary vascular resistance.No significant relation between the age of the patients and level of pulmonary arterial pressure was recognized.2) Many patients with high pulmonary arterial pressure had high ratioes of residual volume and dead space ventilation. However, the patients with high ratioes of residual volume and dead space ventilation had not high pulmonary arterial pressure.3) The relationships of the haematocrit, the O2 saturation and the CO2 pressure of the arterial blood with the pulmonary arterial pressure were nearly same as the reports of many other authors.The pulmonary arterial pressures increased during low O2 inhalation and decreased during high O2 inhalation.4) During the low O2 inhalation the elevated pulmonary and systemic arterial pressures were decreased by the injection of C6 and then the total pulmonary vascular resistances resulted in decrease hand in hand. From these results, it is considered that the autonomic nervous system would be concerned with the rise of pulmonary arterial pressure during low O2 inhalation.5) The degree of the elevation of the pulmonary arterial pressure compared with the decrease of the arterial blood O2 saturation were greater during exercise than during low O2 inhalation.The elevation of the pulmonary arterial pressure during exercise may be not only due to the influence of the low O2 saturation of the arterial blood, but also due to the increased pulmonary blood flow by exercise.6) The patients with pulmonary hypertension have not always systemic hypertension, and the patients with systemic hypertension have not always pulmonary hypertension.

Comparison of the effects of pressor and depressor agents and influences on pulmonary and systemic pressures of normotensive and hypertensive subjects

The comparative effects on the systemic and pulmonary arterial and capillary pressures of various pressor and depressor agents, including angiotonin, and psychogenic pressor influences have been studied. These measurements have been made on eleven patients with normal blood pressures and eleven patients with essential hypertension. Epinephrine, norepinephrine, Methedrine, ephedrine and angiotonin produced an elevation of systemic, pulmonary arterial, and pulmonary capillary pressures. The PA m-PC m gradient was not significantly changed as a result of any of the agents used. We interpret this to be due to either pulmonary vascular constriction beyond the tip of the catheter, pulmonary venous constriction, or both, rather than to an increased pulmonary blood volume secondary to left ventricular failure. We particularly wish to emphasize that angiotonin elevates the pulmonary artery and capillary pressures. It is further emphasized that pulmonary artery pressure in essential hypertension is normal. Pitressin does not cause an elevation of pulmonary artery pressure in either normotensive or hypertensive patients. All the depressor agents used caused a decrease in the systemic and pulmonary arterial pressures in both normotensive and hypertensive subjects. With the exception of Pitressin, the systemic and pulmonary arterial systems reacted similarly to both pressor and depressor drugs. The data presented do not support the concept that essential hypertension is due to angiotonin or epinephrine-like substances. The possibility that a humoral substance may cause essential hypertension is supported by the effects of Pitressin which causes selective elevation of systemic arterial pressure. The selective systemic hypertension produced under hypnosis is consistent with a possible central neurogenic mechanism for producing essential hypertension.