Peripheral Vascular Resistance Index Research Articles

Study of effect of the newly developed artificial blood "Neo Red Cells (NRC)" on hemodynamics and blood gas transport in canine hemorrhagic shock.

The purpose of this study is to evaluate the newly developed liposome-encapsulated hemoglobin, named Neo Red Cells (NRC), in the treatment of hemorrhagic shock. The particle size of NRC is 180 +/- 88 nm, the hemoglobin concentration is 5.6 g/dl, the viscosity is 2 cp and P50 is 49.5 mmHg. The experiment was carried out on six mongrel dogs suffering hemorrhagic shock. Blood was extracted from the femoral artery and blood pressure became lower than 60 mmHg. NRC in amount equal to the amount of blood extracted was transfused immediately. Inhalating normal room air, the above manipulation was repeated 3-5 times. After 59% to 88% blood exchange using NRC, the total peripheral vascular resistance index (TPRI) was reduced and the cardiac index (CI) was increased, thereby alleviating the burden on the heart. The reduction of TPRI in the presence of hemorrhagic shock is presumed to be due to the small size of the NRC granules and their low viscosity. As the exchange rate increased, the oxygen consumption (VO2) increased remarkably, presumably due to the increase of CI and A-V difference of oxygen content. The conclusion of the study is that NRC is more suitable than natural blood for the treatment of hemorrhagic shock.

Blood pressure during sleep: Antihypertensive medication

To investigate whether excessive reduction of blood pressure (BP) by antihypertensive medications correlates with myocardial infarction, especially during steep in elderly patients, we used telemetry and cuvette dye-dilution methods to assess the direct BP and the hemodynamics of 68 inpatients with essential hypertension during wakefulness and steep. There were 25 patients ≥60 years old (OH-group) and 43 were ≤59 years old (YH-group). Of the OH-group, 36% showed high BP during the day, with marked decreases (minimum BP <110/70 mm Hg) during steep. Average cardiac index (CI) of the OH-group was low during wakefulness and extremely low during show-wave sleep. Changes of mean BP in the OH-group correlated with changes in total peripheral vascular resistance index (TPRI) during steep, but this correlation was not observed in the YH-group. The antihypertensive effects on nocturnal BP of the various medications was: central adrenergic inhibitors ≤ β blockers with intrinsic sympathomimetic activity ≤ α (αβ) blockers ≤ angiotensin-converting enzyme inhibitors ≤ calcium antagonists. Because BP and CI were found to be very low and TPRI seems to play an important role in BP regulation in sleeping elderly patients, excessive antihypertensive medication may be harmful to this subgroup. However, because the effects on nocturnal BP differ among various antihypertensive treatments, further research is required on the relation between antihypertensive medication and the hemodynamics of sleeping elderly hypertensive patients.

Electrocardiographic effects of zatosetron and ondansetron, two 5HT3 receptor antagonists, in anesthetized dogs

AbstractThe pharmacology of 5‐hydroxytryptamine3 (5HT3)‐antagonists is an area under active investigation, and several agents of this class are currently under development for multiple therapeutic indications. Recently, two 5HT3 receptor antagonists of a tropane derived series, ICS 205 930 and zatosetron, have been shown to alter electrocardiographic properties of heart muscle. A prototypical, but structurally distinct (imidazole) 5HT3‐antagonist, ondansetron, was examined for its comparative cardiovascular activity in anesthetized dogs at intravenous doses of 0.66–5.25 mg/kg. Similar to zatosetron, a significant, dose‐dependent prolongation of the duration of the action potential of the electrocardiogram (Q‐Tc interval) occurred following ondansetron exposure, with a maximum increase of 28%. Other cardiovascular parameters (heart rate, mean arterial pressure, pulmonary pressure, cardiac output, peripheral vascular resistance, stroke volume and work index) were essentially unchanged by ondansetron treatment. At equivalent 5HT3 blocking doses, both ondansetron and zatosetron prolonged the Q‐Tc interval in anesthetized dogs similarly. However, for both compounds, the doses required to increase Q‐Tc interval were higher than the doses required to demonstrate 5HT3 receptor blockade. The fact that ondansetron, an imidazole, exhibited electrophysiological effects on cardiac muscle like the 5HT3 receptor antagonists derived from tropane suggests that the electrocardiographic effects are related to some property shared by 5HT3 receptor antagonists rather than a property of the tropane structure.

Hemodynamic and respiratory effects of thyrotropin-releasing hormone and epinephrine in anaphylactic shock

Thyrotropin-releasing hormone (TRH) has been shown to increase mean arterial pressure during anaphylactic shock. The hemodynamic mechanism of action and the effect of TRH on the respiratory system during anaphylactic shock are not known. A rabbit model of anaphylaxis was used to determine the effect of TRH, epinephrine (EPI), and normal saline (NS) on various cardiovascular and respiratory parameters during anaphylactic shock. Anaphylactic shock was induced by antigen challenge in 31 sensitized animals. After a 25% decrease in mean arterial pressure, they were randomly treated with TRH (2 mg/kg), EPI (0.005 mg/kg), or NS (10 mL/kg). Blood was drawn at baseline and at the end of the experiment for laboratory analysis. Cardiac and respiratory parameters were monitored continuously and measured at baseline, at onset of shock (time zero), and at time intervals for 30 minutes. Animals were treated with repeated doses during the first 15 minutes as needed to maintain mean arterial pressure above shock level. Five of ten TRH-, five of 11 EPI-, and six of ten NS-treated animals survived. The TRH-treated group required fewer doses than the other groups and had increased heart rate, mean arterial pressure, peripheral vascular resistance, respiratory rate, and minute ventilation as well as decreased stroke volume index and lung compliance compared with the NS-treated group. EPI treatment resulted in increased minute ventilation and decreased pulmonary airway resistance compared with NS treatment. The EPI group also had a higher postsurvival epinephrine level than the other groups. No difference in right atrial pressure, cardiac index, acid-base status, pO2, A- a gradient, lung weight, lactate, or norepinephrine levels was found.(ABSTRACT TRUNCATED AT 250 WORDS)

Captopril in patients with type II diabetes and renal insufficiency: Systemic and renal hemodynamic alterations

Purpose: To our knowledge, clinical studies on the long-term use of angiotensin converting enzyme inhibitors in patients with type II diabetes mellitus and nephropathy with incipient renal failure are nonexistent. We therefore assessed the effects of long-term treatment with captopril on systemic and renal hemodynamics and urinary protein excretion in patients with type II diabetes mellitus and the clinical syndrome of diabetic nephropathy. Patients and methods: Twelve patients, 10 men and two women, with an average age of 52 years (range, 40 to 66), participated in the study. After the basal hemodynamic evaluation, the patients received captopril in two daily doses. The dosage was adjusted at weekly intervals in order to obtain normalization of blood pressure without exceeding the maximum allowable dosage. Four patients also received furosemide (20 to 40 mg/day). Results: After six months of treatment, the intra-arterial blood pressure fell (from 162 ± 17 103 ± 5 to 139 ± 26 89 ± 10 mm Hg) due to the reduction in total peripheral vascular resistance index (from 3,720 ± 658 to 3,190 ± 762 dynes/second/cm −5/m 2), with no change in cardiac index (2.78 ± 0.36 to 2.79 ± 0.47 liters/minute/m 2). No significant change was seen in renal vascular resistance (from 30,175 ± 5,371 to 30,173 ± 5,372 dynes/second/cm −5/1.73 m 2) and in filtration fraction (from 26 ± 8 to 27 ± 10 percent). A slight, not significant, decrease in renal plasma flow (from 243 ± 97 to 217 ± 108 ml/minute/1.73 m 2), in glomerular filtration rate (from 57 ± 17 to 51 ± 19 ml/minute/1.73 m 2), and in proteinuria (from 4.50 ± 3.10 to 3.40 ± 2.31 g/day) was also observed. Conclusion: Our findings suggest that captopril is an effective antihypertensive agent in patients with diabetic nephropathy, but the renal beneficial effects seem to be limited when this syndrome is complicated by renal insufficiency.

Increasing daytime vascular resistance with progressive hypertension in ambulant patients

Twenty-four-hour recordings of intra-arterial blood pressure, heart rate, and calculation of the index of peripheral vascular resistance were obtained in 20 untreated ambulant hypertensive patients during their routine activities outside the hospital. Blood pressures and heart rates were higher during the day, with a mean night-to-day increase of 22%, 34%, and 26%, for systolic, diastolic, and mean pressures, respectively. The average increase in the heart rate was 32%. Overall, the index of resistance was lower (12%) during the day. However, eight patients (40%) demonstrated no change or an increase in the peripheral vascular resistance. Six of these eight patients had an average daytime mean pressure above 120 mm Hg. There was a significant decrease in the index of resistance during exercise in all but one of the 16 subjects. Hemodynamic parameters of 1 hour before and 1 hour after awakening were similar to the values obtained during the entire night and the rest of the day, respectively. Our data suggest that in patients with “progressive” hypertension, the ability to decrease vascular resistance from night to day is compromised.

Hemodynamic effects of naloxone in anaphylactic shock.

Recent reports suggest that endorphins may contribute to hemodynamic depression in septic and hemorrhagic shock. There is also evidence that reversal of endorphin effects with high dose naloxone may improve hemodynamic function and improve survival in shock states. The purpose of this study was to examine the effects of naloxone on hemodynamic parameters in anaphylactic shock. Anaphylactic shock was induced in sensitized rabbits with horse serum. Three minutes after serum challenge, rabbits were treated with a 3 mg/kg bolus of naloxone followed by a 3 mg/kg per h infusion (group I, n = 8), or by injection with an equal volume of saline (group II, n = 8). Cardiac output, blood pressure, heart rate and body temperature were monitored continuously for 60 min and the experiment was terminated. There was a significant increase in cardiac index in group I animals at 10 min (P less than 0.01) and 15 min (P less than 0.01). Stroke volume index was also higher in naloxone treated animals at 10 min and 15 min (P less than 0.05). Although mean blood pressure was higher in group I animals at all time intervals after naloxone was begun, the difference was statistically significant only at 60 min (P less than 0.05). Peripheral vascular resistance index was not significantly different for the two groups.

An index of peripheral vascular resistance.

An index of peripheral vascular resistance, derived from directly measured arterial pressure, has been developed and tested in an animal model. Assuming a mono-exponential character for diastole, the time constant for direct arterial pressure decay in the central aorta was obtained with high-fidelity recording techniques from six anaesthetized dogs. Changes in peripheral resistance were induced by infusion of phenylephrine or nitroprusside. The time constant correlated well with resistance determined from 1-min averages of pressure divided by integrated electromagnetic flow (r = 0.845). A portable system used for direct arterial pressure recording in ambulant outpatients yielded a mean correlation of 0.822 with resistance. In a study of patients undergoing cardiac catheterization, a time constant obtained from the brachial artery (the site of pressure recording in the ambulant subjects) correlated well with the aortic time constant (n = 6, r = 0.964). The results of the present work suggest that the time constant derived from direct arterial pressure waveform may be a useful index in the evaluation of the peripheral vascular resistance. Furthermore, with the help of the portable system it might be used for the continuous monitoring of resistance changes in ambulatory subjects.

Evaluation of an index of peripheral vascular resistance in human subjects.

Based on evidence in animal studies, an index of resistance in man has been evaluated. In 10 human subjects, ranging in age from 31 to 60 years, direct brachial arterial pressure was measured, and a computer program using linear regression calculated the index of resistance from the slope of the logarithm of the pressure versus time during the second half of diastole. Resistance was independently calculated from 20-s averages of pressure and cardiac output obtained by thermodilution. Resistance was varied by infusion of phenylephrine and nitroprusside. The values of the index of resistance were compared with independently calculated resistance by linear regression and correlation. The index of resistance was variably correlated with independently calculated resistance. However, when the comparison was limited to points with a model correlation coefficient greater than or equal to 0.98 (i.e. a good fit of a straight line to the logarithm of pressure versus time), the correlation of the index of resistance with calculated resistance approached or exceeded 0.9 in eight of 10 subjects. In the two subjects showing poor correlation of the index with calculated resistance, estimated compliance from the same model was much lower than in the other subjects. In the same two subjects pressure dependence of estimated compliance was much higher than in the other subjects, suggesting the presence of significant atherosclerosis. We concluded that the diastolic decay of pressure may be used to calculate a useful index of resistance, provided that a single exponential decay fits the observed diastolic waveform well, and arterial compliance is not significantly reduced by atherosclerosis.

Effects of sublingual nifedipine on hemodynamics and systolic and diastolic function in patients with hypertrophic cardiomyopathy.

The hemodynamic effects of sublingual nifedipine were examined in 36 patients with hypertrophic cardiomyopathy. Twenty-one patients were initially given 20 mg and 15 patients were given 10 mg of the drug; 30 min after this first dose 26 patients received 10 mg and one patient 20 mg as a second dose. Hemodynamic findings in patients who received different doses of the drug were similar. Peak effects included an increase in heart rate from 79 +/- 12 to 91 +/- 14 (mean +/- 1 SD) beats/min (p less than .01), and a decrease in mean blood pressure from 89 +/- 12 to 77 +/- 10 mm Hg (p less than .01). Cardiac index increased after nifedipine (2.8 +/- 0.6 to 3.3 +/- 0.8 liters/min/m2; p less than .01); stroke volume index, however, did not change (36 +/- 7 to 36 +/- 8 ml/beat/m2; NS). Peripheral vascular resistance index fell significantly from 822 +/- 261 to 610 +/- 197 dynes X sec X cm-5 (p less than .01). Overall, left ventricular outflow tract gradient (LVOTG) did not change in patients with significant (greater than or equal to 30 mm Hg) basal LVOTG (75 +/- 22 to 83 +/- 22 mm Hg; NS), but it increased significantly in those six patients in whom peripheral vascular resistance fell by 25% or more (73 +/- 28 to 99 +/- 22 mm Hg; p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

Hemodynamic effects of naloxone in anaphylactic shock

Recent reports suggest that endorphins may contribute to hemodynamic depression in septic and hemorrhagic shock. There is also evidence that reversal of endorphin effects with high dose naloxone may improve hemodynamic function and improve survival in shock states. The purpose of this study was to examine the effects of naloxone on hemodynamic parameters in anaphylactic shock. Anaphylactic shock was induced in sensitized rabbits with horse serum. Three minutes after serum challenge, rabbits were treated with a 3 mg/kg bolus of naloxone followed by a 3 mg/kg per h infusion (group I, n = 8), or by injection with an equal volume of saline (group II, n = 8). Cardiac output, blood pressure, heart rate and body temperature were monitored continuously for 60 min and the experiment was terminated. There was a significant increase in cardiac index in group I animals at 10 min (P less than 0.01) and 15 min (P less than 0.01). Stroke volume index was also higher in naloxone treated animals at 10 min and 15 min (P less than 0.05). Although mean blood pressure was higher in group I animals at all time intervals after naloxone was begun, the difference was statistically significant only at 60 min (P less than 0.05). Peripheral vascular resistance index was not significantly different for the two groups.

Increased Cardiovascular Responses to Norepinephrine and Calcium Antagonists in Essential Hypertension Compared with Normotension in Humans

The responses to a supine rest, norepinephrine (NE) and angiotensin II (Ang II) were investigated in the absence and presence of calcium antagonist nifedipine or diltiazem in essential (genetic, arterial) hypertension and normotension in humans. A supine rest significantly decreased blood pressure (BP), heart rate (HR), stroke volume index (SI), and cardiac output index (CI). On the contrary, the rest increased total peripheral vascular resistance index (TPRI) in both normotensives and hypertensives. The decrease in BP was significantly greater in hypertensives than in normotensives. NE significantly increased BP and TPRI, whereas it decreased HR, SI, and CI. The increase in BP was greater in hypertensives than in normotensives. Nifedipine and diltiazem inhibited the NE-induced increases in BP and TPRI. Ang II increased BP and TPRI, but it decreased HR, SI, and CI. Diltiazem did not inhibit the Ang-II-induced increases in both BP and TPRI. The increased responses to a rest and NE were observed in the early stage of essential hypertension. The increased responses may contribute to both the increase in BP and the induction of high blood pressure in essential hypertension. The calcium antagonists inhibited the NE-induced increases in BP and TPR. The results suggest that the antagonists inhibit the NE-dependent calcium influx and calcium release in the arterial smooth muscle. The observed responses to Ang II suggest that the antagonists may not inhibit Ang-II-dependent calcium-channel activity in the smooth muscle.

Induced low P 50 in anesthetized rats: Blood gas, circulatory and metabolic adjustments

In anesthetized, normoxic or hypoxic rats the hemodynamic, metabolic and O 2 transport characteristics following exchange transfusion with human erythrocytes containing a high O 2 affinity hemoglobin (Hemoglobin Creteil, β 89 Ser → Asp) have been studied. The in vivo oxygen partial pressure at 50% oxygen hemoglobin saturation (P 50) decreased from 37.4 ± 2.1 to 12.7 ± 0.7 mm Hg; the arterial oxygen tension was reduced significantly from 109.9 ± 7.7 to 87.3 ± 12.0 mm Hg. There was a decrease in right ventricular partial pressure of oxygen (Pv̄O 2), ( P < 0.001), oxygen consumption (V̇ O2), ( P< 0.001), arterio-venous difference, ( P < 0.001), and peripheral vascular resistance index, ( P < 0.01). Exchange transfusion with normal rat blood ( P 50 = 37.2±2.4 mm Hg) or with 2,3-diphosphaglycerate-enriched human red blood cells ( P 50 = 34.7±2.2 mm Hg), did not modify these variables in normoxic rats. In hypoxia, the reduction in P 50 was associated with a further decrease in Pv̄ O2 an increase in serum lactate concentration and a V̇ O2 decrease.

Hemodynamic response to volume depletion in acutely uremic dogs.

Hemodynamic response to volume depletion by isolated ultrafiltration was compared in uremic (U) and nonuremic (N) conscious dogs. Fluid was removed at a constant rate until mean arterial pressure (MAP) decreased to less than 80 mmHg. Initial MAP was higher in the uremic dogs [132 +/- 8.6 (SD) mmHg] than in nonuremic controls (106 +/- 12, P less than 0.001). Initial cardiac index [U 4.97 +/- 0.831 X min-1 X m-2, N 4.44 +/- 0.62] and total peripheral vascular resistance index [(TPRI) U 2,160 +/- 353 dyn X s X cm-5 X m-2, N 1,976 +/- 420] were slightly, but not significantly, higher in uremic animals. Initial central venous pressure, wedge pressure, and plasma norepinephrine level were greater in the uremic dogs. At the end point of volume depletion, both uremic and nonuremic animals had achieved similar levels of TPRI, despite greatly attenuated or absent increases in plasma renin activity in the uremic group. At end point, blood volumes and plasma norepinephrine levels were comparable. The increase in pulse rate was higher in the uremic animals (59 +/- 37 pulses/min) compared with controls (25 +/- 52, P less than 0.05). In an additional group of uremic dogs, cardiovascular responses to hemorrhage and isolated ultrafiltration were compared and found to be similar, after allowance for blood viscosity changes had been made. The data suggest that in acutely uremic conscious dogs, despite reduced renin-angiotensin responses, hemodynamic adaptation to rapid volume depletion is not impaired.

Echocardiographic hemodynamic study during ultrafiltration sequential dialysis.

4 patients on regular dialysis were studied by the echocardiographic method during ultrafiltration and dialysis performed sequentially according to two different protocols. Blood pressure, heart rate, cardiac output, stroke volume, systolic and diastolic dimension of the left ventricle, systolic and diastolic volumes of the left ventricle, ejection fraction, shortening fraction and total peripheral vascular resistance index were measured. During ultrafiltration there is an increase of the total peripheral vascular resistance index. Myocardial contractility improves only during dialysis. Physiopathologic implications are discussed.

Haemodynamic effects of angiotensin converting enzyme inhibition after cardiopulmonary bypass in dogs.

Recent studies have suggested a possible causative relationship between elevated plasma levels of Angiotensin II (AII) and the vasoconstriction associated with conventional cardiopulmonary bypass. The haemodynamic effects of SQ14225, a specific angiotensin converting enzyme inhibitor, have been studied in a group of five dogs submitted to a 60 min period of cardiopulmonary bypass (CPB). A 20 min infusion of SQ14225 in a dose of 2 microgram .kg-1 .h-1 was administered to each dog 2 h after the end of the period of CPB. Measurements of peripheral vascular resistance index (PVRI), cardiac index (CI) and plasma levels of Angiotensin II were obtained at the start and end of the infusion period. The results in the five blocked dogs were compared with a control series of ten unblocked dogs submitted to an identical cardiopulmonary bypass regine. In the blocked dogs, PVRI fell significantly during infusion of SQ14225 from 38.27 units to 21.70 units (P <0.01). There was a simultaneous significant increase in cardiac index from 3.00 to 3.98 litre.m2 .min-1 (P <0.01). Plasma Angiotensin 11 levels fell in the blocked dogs from 57 to 11.5 pg.cm-2 during the infusion period (normal levels <15 pg.cm-3). In the control unblocked dogs, there was no corresponding fall in PVRI, no rise in cardiac index, and no fall in elevated plasma AII levels. The difference between the groups were statistically highly significant (P <0.005). These results indicate that reduction in elevated plasma AII levels after CPB using converting enzyme inhibitor SQ14225 is associated with a significant fall in peripheral vascular resistance and a significant rise in cardiac index. In addition, the study confirms the causative relationship between elevated plasma levels of Angiotensin II and the increased vasoconstriction associated with non-pulsatile CPB.

Role of angiotensin II in the development of peripheral vasoconstriction during cardiopulmonary bypass.

The possible relationship between angiotensin II -- the end product of the renin-angiotensin system, and the increase in peripheral vasoconstriction associated with cardiopulmonary bypass, has been investigated in 12 patients undergoing elective open-heart surgical procedures. Plasma angiotensin II (AII) levels were measured by radio-immunoassay at the start and the end of the period of cardiopulmonary bypass. Measurements of peripheral vascular resistance index were made at the times of AII sampling. Plasma AII levels rose during CPB from 78.0 to 231.3 pg.cm-3 (normal values less than 35 pg.cm-3). Peripheral vascular resistance index also rose during perfusion from 20.87 to 27.83 units. The rise in plasma AII levels and in peripheral vascular resistance index were correlated for each of the 12 patients. A highly significant correlation was obtained (r = 0.91; P less than 0.001). These results confirm the presence of parallel rises in plasma angiotensin II levels and in peripheral vasoconstriction during conventional non-pulsatile cardiopulmonary bypass, and suggest that increased plasma AII levels may be principal causative factor in the increased vasoconstriction associated with open-heart surgical procedures.

Hemodynamic changes during sequential ultrafiltration and dialysis

Seven patients on regular dialysis were studied to elucidate the hemodynamic changes during ultrafiltration and dialysis, performed sequentially, the period of ultrafiltration (1 hour) either preceding or following dialysis (3 hours). During dialysis ultrafiltration was prevented by applying positive pressure in the dialysate compartment. Cardiac index (dye dilution: indocyanine green), heart rate, stroke volume index, blood pressure, and total peripheral vascular resistance index were measured. During ultrafiltration, cardiac index and stroke volume index decreased, but heart rate was not significantly changed. Total peripheral vascular resistance increased, resulting in unchanged blood pressure. During dialysis, the total peripheral vascular resistance decreased, but cardiac index and heart rate increased. BP decreased when the increase in cardiac index was insufficient to compensate for the decrease in total peripheral vascular resistance. PRA increased during ultrafiltration due to hypovolemia and decreased during dialysis, presumably due to decreased sympathetic activity which may also be a cause of dialysis-induced vasodilation.

Carotid baroreceptor function in hypertensive patients.

Carotid baroreceptor function has been studied in twenty-five patients with essential hypertension and in ten normotensive control subjects of corresponding age. The carotid baroreceptors were stimulated by increasing the transmural pressure over the carotid arteries by the application of negative pressure in a box enclosing the neck. Stimulation elicited significant decreases in intra-arterial blood pressure, heart rate and cardiac index in both hypertensive and normotensive subjects. Both groups also showed a significant decrease in stroke index and a significant increase in total peripheral vascular resistance index. The response to carotid sinus stimulation did not differ significantly between the two groups. In fourteen of the hypertensive subjects, carotid baroreceptor function was studied after 4 months of saluretic therapy, mefruside, and in nine of these patients after additional treatment with a beta-receptor blocking drug, alprenolol, for another 4 months. Both mefruside and alprenolol induced a significant decrease in mean arterial blood pressure but the response to the carotid baroreceptor stimulation was not significantly altered. The findings indicate that the carotid baroreceptor is re-set to the actual blood pressure level, with little or no change in gain in hypertensive subjects both without and during hypotensive therapy.

The long-term hemodynamic effect of fusaric acid in elderly hypertensive patients.

The hemodynamic effect of fusaric acid calcium salt (calcium salt of 5-butylpicolinic acid), an inhibitor of dopamine beta-hydroxylase, was studied in long-term administration of this agent in 10 elderly hypertensive patients. The hemodynamic items were measured by dye-dilution method before and 3 months, 6 months and one year after administration of fusaric acid calcium salt. The main hemodynamic changes observed were as follows: 1) Heart rate did not show any consistent change. 2) Systolic, diastolic and mean blood pressure decreased. The mean values of these pressures after fusaric acid calcium salt administration were significantly lower than the mean values before administration of this agent. 3) Total peripheral vascular resistance index decreased. The mean values of this index at 3 months, 6 months and one year after fusic acid calcium salt administration were significantly lower than the mean value before administration of this agent. 4) Cardiac index showed various changes throughout administration of fusaric acid calcium salt. The changes in this index might be secondary following the changes in total peripheral vascular resistance index, an inverse correlation being existed between them. 5) Stroke volume index showed almost a similar pattern of change as observed in cardiac index. An inhibitory action of fusaric acid calcium salt on the inotropism of the heart could be hardly found. 6) Plasma volume showed no tangible changes after fusaric acid calcium salt administration throughout one year. It might be concluded that fusaric acid calcium salt elicited the hypotensive response primarily through the reduction of total peripheral vascular resistance index.