Increase in the calculated resistance of anatomically fixed stenosis in vitro in association with decrease in distal resistance.

The effects of changes in distal resistance on stenotic resistance were studied in vitro. Physiological saline was passed through the left carotid artery obtained from the dog, flexible rubber tubing, or through solid polyethylene tubing with a constant perfusion pressure or with a constant flow rate. Various stenotic resistances were established using a screw type constrictor and the distal resistance was varied by allowing physiological saline to pass through either a 23 gauge hypodermic needle (high peripheral resistance) or 23 and 20 gauge needles (low peripheral resistance ). For arteries with anatomically fixed stenosis, the calculated resistance was increased in association with reduction of the distal resistance. The stenotic resistance in the flexible rubber tubing changed in the same manner as that of the carotid artery, while the solid polyethylene tubing showed no significant stenotic resistance changes due to altering the distal resistance. These findings suggest that the stenotic resistance change of the artery correlates with the elasticity of the vessel wall and also indicate that resistance values were of little usefulness for evaluating the effects of vasodilating stimuli on the vessel segment with a significant stenosis.</p

Increase in stenotic resistance following a brief coronary occlusion in the anesthetized open-chest dog.

Changes in the stenotic resistance of a coronary artery following brief coronary occlusion were studied in the anesthetized open-chest dog. A critical coronary stenosis was constructed by tying a thick string around the circumflex coronary artery (LCx) near its origin. The LCx was occluded for 5, 10, 15, 20 and 30 seconds with and without coronary stenosis then the reactive hyperemia was observed. In the absence of the stenosis, resistance of the segment of the large coronary artery remained unchanged during the reactive hyperemia independent of the duration of occlusion. In the presence of the stenosis, however, stenotic resistance increased for a certain time after the release of occlusion. This increased resistance lasted longer with more severe stenosis and with longer duration of coronary occlusion. These results suggest that stenotic resistance can increase dynamically, and that the duration of increased resistance may reflect the severity of the stenosis.</p

Increase in the resistance of stenotic coronary segment by intravenous infusion of isoproterenol.

The effects of intravenous infusion of isoproterenol on stenosis resistance were studied in the anesthetized open-chest dog. The circumflex coronary artery (LCx) was isolated near its origin and an electromagnetic flow transducer was placed around the vessel for measuring coronary flow. A polyethylene catheter was inserted into the small branch of LCx for monitoring distal coronary pressure. LCx was constricted with a thick cotton string to a degree of obstruction that eliminated reactive hyperemia following a 20-second coronary occlusion. The coronary resistance across the stenotic segment (RL) was calculated as the pressure gradient across the stenosis divided by coronary flow. Isoproterenol was infused intravenously in a dose to keep the heart rate at a level 25-30% above the control with and without coronary constriction. For maintaining the ascending aortic pressure at the pre-isoproterenol level, the descending thoracic aorta was constricted with a tape. In the absence of coronary constriction, the vascular resistance of large coronary arteries was not affected by isoproterenol with a significant increase in coronary flow. In the presence of coronary stenosis, isoproterenol markedly increased RI regardless of additional aortic constriction. The magnitude of the increase in RL during aortic constriction varied directly with the percent increase in the pressure gradient across the coronary stenosis. Pacing-tachycardia essentially did not affect RL. These results suggest that isoproterenol increased the vascular resistance of the stenotic segment with fixed caliber.</p

Effect of Chlorpromazine on myocardial contractility and hemodynamics.

Hemodynamic effects of Chlorpromazine(CP) were studied in anesthetized open-chestdogs. Intravenous injection of 1.0mg/kg CP increased heart rate by 20.7 % , cardiac output by 14.7% , LVdp/dt/50 by 11.3% and QTc by 0.012, respectively. Systolic shortening of a segment of the heart muscle increased by 9.8% with decreases in end-diastolic length. These changes were inhibited completely by Propranolol and incompletely by Reserpine pretreatment. Blood pressure was lowered by CP, but no response to intravenous Methoxamine was observed 10 min after CP. However, with 10mg/kg of CP injected intravenously, heart rate and LVdp/dt/50 initially decreased markedly, and systolic shortening decreased in association with increases in end-diastolic length. Ten min later, the measurements increased above the control. These results suggested that CP has α-blocking and β-stimulating action mimicking an α(2)-blocker

Effects of intracoronary infusion of Chlorpromazine on myocardial performance, regional QTc and coronary hemodynamics in the anesthetized open-chest dog.

The direct effects of CP on the heart muscle were studied in anesthetized open-chest dogs by intracoronary infusion of chlorpromazine (CP) to LAD in doses of 0.01 and 0.1 mg at the flow ste of 1 ml/min. At 0.01 mg/ml/min of CP, no significant changes in the measurements were observed. At 0.1 mg/ml/min, CP caused a gradual increase in heart rate and CBF of LAD without changes in systemic blood pressure and cardiac output. In the LAD area, systolic expansion of the heart muscle (systolic bulge) occurred in 6 out of 14 dogs (43%). In 8 dogs having no bulge, systolic shortening of segmental myocardium of the infused area decreased by 9.4% and end-systolic length increased, while in the control (LCX) area, systolic shortening of the heart muscle increased markedly with a reduction in the end-diastolic length. Local QTc was prolonged in the LAD area, but did not change in the LCX area. In the LAD area, more prolongation of QTc was observed in the dogs with bulge than the dogs without bulge. Pretreatment with CoQ(10) completely prevented CP-induced bulge. No significant changes in other measurements including QTc were observed in comparison with dogs without CoQ(10) pretreatment. These results suggest that the effects of CP are of direct myocardial suppression and are incompletely preoented by CoQ(10) pretreatment

Correlation between QT interval and RR interval on the epicardial electrogram in open-chest dog.

Correlation between QT interval and RR interval on epicardial electrogram in anesthetized open-chest dog was studied. The aortic blood pressure was kept above 70mmHg during the course of the experiment. RR interval was changed by left atrial pacing in the range of 0.243-0.870sec (0.412±0.119, mean±SD). In association with the change in RR interval, QT interval varied in the range of 0.190-0.360sec (0.253±0.028). The relation of QT interval to RR interval was statistically significant (r=0.744, p<0.01), though QT interval varied widely when the heart rate was under 100beat/min. QT interval correlated more closely to √RR interval than RR interval. The correlation equation was as follow: QT interval(sec)=0.24√RR interval (sec)+0.102, r=0.760, p<0.01. The data suggest that QT interval obtained by epicardial electrogram would be of use as an index of local electrical systole

A case of primary pulmonary hypertension treated with yearlong administration of oral phenoxybenzamine

A 26 year old woman with primary pulmonary hypertension received oral phenoxybenzamine, 15-30 mg daily, over a year without serious side effects. The patient was discharged after phenoxybenzamine therapy for 6 months, because her subjective complaints improved gradually with reduction of the Cardiac Thoracic Ration of chest X-ray films from 60% to 54% . However, she was readmitted for right heart failure precipitated by a common cold. It is suggested that oral phenoxybenzamine for primary pulmonary hypertension is effective in alleviating subjective complaints, but the effects may only be temporary