This is a report of echocardiographic features of high altitude cardiac disease. The authors examined 25 healthy men at sea level as a control, 45 healthy male inhabitants at 3658 meters and 25 male inhabitants at the same high level but with high altitude cardiac disease. The results showed that the internal diameter of right ventricle and right pulmonary artery in healthy inhabitants was larger as compared with that seen in the control group. However, there was no significant difference in the internal diameter of the left ventricle, the value of stroke volume, cardiac index or ejection fraction between these two groups. These findings suggest that the left ventricle of the healthy inhabitants adapts to the high altitude well. The echocardiographic features of the male inhabitants suffering from high altitude cardiac disease showed several peculiarities. There was an enlargement of the internal diameters of the right ventricle and the right pulmonary artery; the pulmonary valves showed typical echocardiographic patterns of pulmonary hypertension; the internal diameters of the left ventricle and the values of stroke volume are also increased but their ejection fractions decreased significantly as compared with the healthy inhabitants. Prolapse of mitral valve was observed in four patients. Left ventricular dilatation and dysfunction may be the result of systemic hypertension, polycythemia, increase of cardiac output or hypoxia. Echocardiographic criteria for diagnosis of high altitude cardiac disease are outlined.

This experiment was designed to observe the changes of the functions of the two ventricles during acute hypoxia and to determine the efficacy of sodium ni-troprusside on the pressor response of the pulmonary artery under hypoxic condition. 14 piglets were anesthetized and force to inspire a gas mixture containing 10% or 5 %O2 in nitrogen respectively.During moderate hypoxia, there were increase of the dp/dt max, the systolic pressures and the develope pressures of the two ventricles, and shortening of the R-dp/dt time but there was no significant change of the end diastolic pressures of the ventricles. At the end of the ten-minute hypoxia, 7 piglets were given intravenous infusion of sodium nitroprusside. Then the pressures in the pulmonary artery and aorta were found to be reduced promptly but no change occurred in the dp/dt max and the systolic pressures of the ventricles.During severe hypoxia, 4 piglets showed a progressive falling of the cardiac functions while the remaining 9 showed a preliminary compensatory augmentation followed with a gradual falling of the cardiac functions. The survival time of the latter was longer than that of the former.These results indicate that the contractility of the myocardium is augmented during moderate hypoxia, the existence of cardiac compensatory response is one of the important factors determining the survival time of the animal, and sodium nitroprusside can markedly reduce the pulmonary arterial hypertession due to hypoxia.

Hemorrhagic shock was studied in 9 sheep living and born at 3658m above sea level. It was found that cardiac pump function and isovolumic systolic and diastolic function of biventricles were reduced. There were no significant changes of peripheral and pulmonary vascular resistance as compared with the control values. After reinfused shed blood, all above parameters immediately return to the control values, the results suggest that impaired systolic and diastolic function is due to the decreased preload. Two hours after reinfused shed blood, At Ci, Si, carotide blood flow fell obviously, later mean aortic arterial pressure and dp/dtmax of LV decreased while LV diastolic pressure and T constant increased, At last dp/dtmax of RV diminished and diastolic pressure of RV raised. These results indicate that the dysfunction of biventricles may be produced by the reduced myocardial contractility, and left ventricle impaired earlier than right ventricle. Two hours after reinfused shed blood, pulmonary arterial pressure and pulmonary vascular resistance were increased but aortic arterial pressure was reduced.

The response of breathing 100% oxygen was studied in 9 anesthetized piglets, born and living at 3658m high altitude. After breathing pure oxygen at highland piglets right ventricular systolic pressure, dp/dt max of the right ventricle, stroke index, pulmonary vascular resistance and pulmonary arterial pressure were decreased obviously, but no significant changes were seen in the dp/dt max of left ventricle and cardiac index, peripheral vascular resistance and aortic pressure. These results suggested that the main factor responsiable for the increase in pulmonary resistance of highland piglets was hypoxic vasoconstriction. Breathing pure oxygen decreased dp/dt max of right ventricle, it appeared to show that chronic hypoxia might augment the right ventricular performance. The percent physiologic shunt was decreased by the inspirated pure oxygen. This fact implied that VA/Q mismatching occurred in highland piglets.

The combined effect of stepwise intermittent hypoxia and physical training was investigated with ultrasonic cardiography on 12 bikers who were permanent inhabitants at 1895 meters above sea level and were subjecting to physical training under hypoxic condition in a hypobaric chamber. It was found that the internal diameters of the right ventricle and right pulmonary artery of the bikers increased proportionally with the increase of both the altitude and the duration of the physical training. At a simulated altitude of 4000 meters, the cardiac stroke volume and cardiac cutput, the internal diameter of the left ventricle and the left ventricular mass increased markedly as compared with those at sea level. The thickness of the interventricular septum and the posterior wall of the left ventricle also increased. The stroke volume and cardiac output of the bikers increased more significantly at the simulated altitude of 4000m., that at the altitude of 3000m. All these change are still within the physiologic ranges and can be considered as adaptation changes to highaltitude training. NO case of acute mountain sickness occurred in any of the trained bikers.These findings suggest that this intermittent stepwise hypoxic physical training can improve the cardiac function and increase its adaptibility towards hypo-xic conditions.

The changes of pulmonary rheography of 12 bikers were investigated after they had been physically trained under hypoxic condition in a hypobaric chamber simulating altitudes of 2000 m, 3000m, and 4000m respectively. All the bikers were permanent inhabitants at 1895 meters above sea level.The changes were most marked on the rheographies taken at the simulated altitude of 4000m. Comparing with the control values at the sea level, the authors found that tonic interval (Q-a interval) on the bikers' pulmonary rheographies was prolonged. The amplitude, the mean rate of filling and the rate of maximal ascending of the systolic wave were decreased.The results showed that hypoxic physical training could result in the contraction of pulmonary vessels. In turn it caused pulmonary arterial hypertension and reduced the amount of blood circulating through the lungs. Pulmonary arterial hypertension could further increase the afterload of the right ventricle.Eight days after the bikers returned to the sea level, all the indices also returned to their original levels except the tonic interval. It is apparent that these changes are most likely to be functional rather than organic.

The left and right cardiac function of 11 patients with chronic mountain sickness was studied before and after oxygen administration. It was found that after pure oxygen was inhaled, the internal diameter of the right ventricle, the ratio between right and left ventrcular diameters, and the heart rate were decreased significantly, while the ?-wave excursion of the pulmonary valve and the EF slope of the mitral valve were increased obviously. However there was no change of the systolic time interval of both the ventricles and of the left ventricular systolic function. The results suggest that oxygen inhalation could relieve hypoxic pulmonary hypertension and improve left ventricular diastolic function.

The main pathological changes of hypoxia in the myocardium were lysis or necrosis of the myocardium.hyperplasia or swelling of myocardial mitochondria,and swelling.increase of pinocytic vesicles in number,and appearance of tubules and villus-like eminences in the endothelial cells of myocardial capillaries:And those in the lungs were thickening of the wall and narrowing of the lumen of pulmonary arterioles,and swelling or appearance of proteinous material in the connec- tive tissue around pulmonary venules.After the treatment with dilthiazem.the pathological lesions were decreased in number or diminished in severity.In addition,the pathological mechanisms of hy-poxia and the therapeutic efficacy of dilthiazem were discussed.

The dynamic changes of the functions and the weight index of the 2 ventricles and the density of ?-adrenoceptors in the myocardium were observed and the correlation between the changes of ?-adrenoceptors of the myocardium and.the peripheral lymphocytes was investigated during and after intermittent chronic hypbxia in rabbits.The fingings were as follows.(1)Chronic hypoxia resulted in an increase of systolic pressure,dp/dtmas and weight index of the right ventricle.25 days after the restoration of normal oxygen supply,systolic pressure and dp/dtomas of the right ventricle became normal but its weight index remained increased.(2)The density of ?-adrenoceptors of the 2 ventricles was reduced on the 7th,15th and 30th day of hypoxia as compared with that of the control.25 days after the restoration of oxygen supply,the density of ?-adrenoceptors became normal in the left ventricle but remained decreased in the right ventricle.(3)There was a positive correlation between the changes of ?-adrenoceptors in the 2 ventricles and peripheral lymphocytes.The findings suggest that hypoxia-induced hypertrophy of the right ventricle is usually accompanied with a decreased density of its ?-adrenoceptors and thedensity of ?-adrenoceptors of peripheral lymphocytes can reflect the changes of ?-adrenoceptors in the myocardium.

AIM:To investigate the roles of nitric oxide (NO) and endothelin-1(ET-1) in regulation of coronary vascular reserve (CVR) during hypoxia.METHODS: CVR were measured with 99m TC radiolabelled frog RBC, the changes of NO - 2,ET-1 contents, nitric oxide synthase(NOS) activity and the myocardial morphometry were observed. RESULTS: (1) Acute hypoxia caused an increase in left and right ventricular myocardial blood flow,myocardial NO - 2,ET-1 contents,NOS activity,but CVR in the left and right ventricle were decreased compared with the control group.(2) Intermittent hypobaric hypoxia for 90 days did not lead to significant change in left ventricular CVR,myocardial ET-1/NO - 2 ratio. However, right ventricular myocardial ET-1 contents,ET-1/ NO - 2 ratio were increased,right ventricular CVR and myocardial NO - 2 contents were decreased. We also observed that perivascular collagen,arterial wall thickness in right ventricle, hematocrit,RV weight index were augmented. CONCLUSION: Rest myocardial blood flow was increased,CVR was decreased;The decreased coronary vascular reserve during chronic hypoxia might be resulted from the increased hematocrit,arterial wall thickness,perivascular collagen,ET-1 content, the decreased NO content and right ventricular hypertrophy.