Biomedical subjects

R G Gay

Publications and source records attributed to R G Gay.

18 recordsLinked to original sources

PubMed1990

Early and late effects of captopril treatment after large myocardial infarction in rats.

The early (after 21 days) and late (after 4 months) effects of continuous treatment with captopril on left ventricular performance, weight and volumes were studied in rats with myocardial infarction. Early effects were examined in rats subjected to coronary ligation and randomized to either immediate treatment with captopril (2 g/liter drinking water) starting 2 h after surgery or no treatment. After 21 days, the treated group showed reductions in mean arterial, left ventricular systolic and left ventricular end-diastolic pressures compared with untreated rats. Right and left ventricular weight and left ventricular volumes were decreased and the ejection fraction index was increased by captopril treatment. To study the late effects of captopril, a second group of rats was randomized to immediate captopril treatment (starting 2 h after surgery), delayed captopril treatment (starting 21 days after surgery) or no treatment. When studied after 4 months of treatment, rats started on captopril treatment 2 h after infarction showed no differences compared with rats started on treatment 21 days after infarction. Treatment with captopril for 4 months produced changes that were similar to those in rats treated for 21 days. Captopril treatment improved hemodynamic function after myocardial infarction in rats examined after either 21 days or 4 months of treatment. The extent of the benefit was similar in the two treatment periods. Initiation of captopril therapy immediately after infarction did not appear to produce a greater effect than treatment started at 21 days after infarction in rats studied after the drug had been administered for 4 months.

Animals↗

PubMed1990

Chronic propranolol treatment promotes left ventricular dilation without altering systolic function after large myocardial infarction in rats.

In rats with chronic myocardial infarction (MI), we have examined the effects of prolonged beta-adrenergic blockade with propranolol on left ventricular (LV) performance, weight, and volumes. Sham-operated rats and rats with large MI (greater than 30%) were evaluated. Four groups of rats were studied: control, sham-operated (n = 12); control, MI (n = 12); propranolol (500 mg/L of drinking water)-treated, sham-operated (n = 10); and propranolol treated, MI (n = 10). Treatment was started 3 weeks after coronary ligation. After 5-6 weeks, LV, systemic arterial, and right atrial pressures in addition to aortic blood flow before and during volume loading were measured. LV pressure-volume relations were measured ex vivo. The rats with chronic MI demonstrated expected decreases in LV systolic performance and increased LV end-diastolic and right atrial pressures. Propranolol had no independent effect on LV systolic pressure, LV end-diastolic pressure, resting cardiac index, stressed cardiac index during volume loading, peak developed aortic pressure during aortic occlusion, or ejection fraction index in either sham-operated or infarcted rats; however, heart rate was decreased. LV weight/body weight was 2.17 +/- 0.04 mg/g in control sham-operated rats, which was not different from the propranolol-treated sham-operated rats (2.09 +/- 0.04 mg/g). The LV weight/body weight was increased (p less than 0.01) to 2.21 +/- 0.08 mg/g in the propranolol-treated MI group from 1.94 +/- 0.06 mg/g in the control MI group. The LV pressure-volume relation was not altered by propranolol in the sham-operated rats but was shifted to the right by MI.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1990

Chronic inhibition of fatty acid oxidation: new model of diastolic dysfunction.

This study was designed to determine the changes in the heart that result from inhibition of long-chain fatty acid oxidation with 2-tetradecylglycidic acid (TDGA). Male Sprague-Dawley rats (n = 64) were treated with TDGA (20 mg.kg-1.day-1) or a comparable volume of vehicle by gavage feeding for 7 or 21 days. In conscious rats TDGA produced no changes in heart rate, left ventricular systolic or end-diastolic pressures, left ventricular pressure development (dP/dt), or the time constant of left ventricular relaxation. Left ventricular developed pressure was not changed at 21 days. TDGA increased left ventricular weight, left ventricular weight-to-body weight ratio, and total heart weight-to-body weight ratio. Left ventricular endocardial and epicardial myocyte volumes were increased by 53 and 65%, respectively. Myocardial triglyceride content was increased threefold. Left ventricular chamber stiffness constants between end-diastolic pressures of 0 and 30 mmHg were increased, and left ventricular end-diastolic volumes at operating end-diastolic pressures were decreased at both 7 and 21 days. The myocardial stiffness constant was also increased at 7 and 21 days. Thus inhibition of long-chain fatty acid oxidation with TDGA increased left ventricular mass and altered left ventricular chamber and muscle stiffness without changing left ventricular relaxation or systolic function. We conclude that inhibition of long-chain fatty acid oxidation produced an unusual model of left ventricular hypertrophy and diastolic dysfunction characterized by abnormalities of passive-elastic properties but preserved relaxation.

Animals↗

PubMed1990

Captopril reduces left ventricular enlargement induced by chronic volume overload.

The effect of captopril treatment on left ventricular (LV) function, mass, and volume during chronic volume overload induced by production of aortic insufficiency (AI) was studied. AI was caused by mechanical disruption of the aortic valve in 175- to 225-g male Sprague-Dawley rats. At 24 h after surgery, AI and sham-operated rats were divided into control and captopril treatment (2 g/l drinking water) groups. After 2 mo of treatment, hemodynamics were measured in open-chest rats, and the LV pressure-volume relation was determined ex vivo. Compared with sham-operated rats, in the untreated AI rats, aortic pulse pressure was increased nearly 100%, LV end-diastolic pressure was 10 +/- 1 vs 3 +/- 1 mmHg, and LV end-diastolic volume was 1.25 +/- 0.07 vs 0.36 +/- 0.03 ml. LV weight was increased 43% and the LV pressure-volume relation was shifted rightward by AI. LV systolic and diastolic wall stress were increased in rats with AI. Peak LV pressure during aortic occlusion was decreased in AI rats, however, peak wall stress during aortic occlusion was not different compared with sham-operated rats. Captopril treatment decreased aortic pulse pressure and LV systolic pressure. Both LV weight and LV end-diastolic volume measured from the ex vivo pressure-volume relation at LV end-diastolic pressure were increased by 33% in untreated AI rats compared with captopril-treated AI rats. Captopril treatment of AI rats shifted the LV pressure-volume to the left compared with untreated rats. LV pressure and wall stress during aortic occlusion were not changed in captopril-treated AI rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1990

Selective vasopressin inhibition in rats with heart failure decreases afterload and results in venodilatation.

The hemodynamic effects of selective inhibition of arginine vasopressin (AVP) with a V1 antagonist, (CH2)5yreAVPa CL-1-4A, were studied in normal rats (n = 17) and in rats 4 weeks after coronary artery ligation with large myocardial infarctions and elevated left ventricular end-diastolic pressures (n = 22). In normal rats AVP inhibition with a 35-micrograms/kg bolus of AVP V1 antagonist did not change heart rate, right atrial, left ventricular systolic, left ventricular end-diastolic or aortic pressures. There were also no changes in mean circulatory filling pressure, unstressed vascular volume, blood volume or venous compliance. In rats with infarction and elevated left ventricular end-diastolic pressures, AVP inhibition did not change heart rate, right atrial pressure, mean circulatory filling pressure or blood volume, but mean aortic pressure decreased from 103 +/- 3 to 88 +/- 2 mm Hg (P less than .001), venous compliance increased (P less than .001) from 2.17 +/- 0.07 to 3.04 +/- 0.11 ml/mm Hg/kg and unstressed vascular volume decreased from 42.3 +/- 3.1 to 34.7 +/- 2.6 ml/kg (P less than .05). We conclude that inhibition of AVP with a specific V1 antagonist had no effect on the venous or arterial circulations in normal rats, but in rats with left ventricular dysfunction and heart failure after chronic myocardial infarction, AVP inhibition decreased arterial pressure and caused venodilatation.

Animals↗

PubMed1989

Atrial natriuretic peptide reverses angiotensin-induced venoconstriction in dogs.

To determine whether atrial natriuretic peptide (ANP) can reverse angiotensin (ANG II)-induced venoconstriction, ANP was infused (0.3 micrograms.kg-1.min-1) in the presence of ANG II-induced hypertension in six ganglion-blocked dogs. ANG II was initially administered to increase mean arterial blood pressure (MAP) 50% above control. ANG II did not change heart rate or left ventricular rate of pressure development (LV dP/dt) but increased total peripheral vascular resistance (TPVR) and left ventricular end-diastolic pressure (LVEDP). Mean circulatory filling pressure (MCFP) increased, whereas cardiac output and venous compliance decreased. Unstressed vascular volume did not change, but central blood volume increased. ANP infusion during ANG II-induced hypertension resulted in a decrease in MAP, but TPVR did not change. There were no changes in heart rate or LV dP/dt. ANP decreased cardiac output further. LVEDP returned to base line with ANP. ANP also decreased MCFP and normalized venous compliance. There was no significant change in total blood volume, but central blood volume decreased. In summary, ANP can reverse the venoconstriction but not the arterial vasoconstriction produced by ANG II. The decrease in MAP was due to a decrease in cardiac output that resulted from venodilatation and aggravation of the preload-afterload mismatch produced by ANG II alone. Because TPVR did not change when MAP fell, we conclude that the interaction between ANG II and ANP occurs primarily in the venous circulation.

Angiotensin II↗

PubMed1989

Importance of venodilatation in prevention of left ventricular dilatation after chronic large myocardial infarction in rats: a comparison of captopril and hydralazine.

In rats with large myocardial infarctions, we compared the effects of captopril, a presumed arterial and venous vasodilator, with hydralazine, which is thought primarily to be an arterial vasodilator. To determine if the effects of captopril were dependent on the pathophysiological consequences of heart failure, we also studied a group of noninfarcted rats treated with captopril. In noninfarcted rats treated with captopril, left ventricular (LV) systolic and mean aortic pressures decreased from 132 +/- 12 to 107 +/- 15 mm Hg and 122 +/- 1 to 100 +/- 2, respectively (p less than 0.01). In noninfarcted rats, captopril decreased LV weight, LV weight/body weight, and total heart weight/body weight but produced no effects on the peripheral venous circulation. Rats subjected to coronary artery ligation were selected by ECG criteria to have large myocardial infarctions and were treated for 4 weeks with captopril (n = 8), hydralazine (n = 5), or placebo (n = 9). In infarcted rats treated with captopril, LV systolic, mean aortic pressures and LV end-diastolic pressure (LVEDP) decreased (p less than 0.01) from 115 +/- 4 to 86 +/- 3 mm Hg, 106 +/- 4 to 74 +/- 3 mm Hg, and 23 +/- 2 to 11 +/- 2 mm Hg, respectively. Mean circulatory filling pressure decreased (p less than 0.05) from 11.2 +/- 0.6 to 8.7 +/- 0.8 mm Hg and venous compliance increased (p less than 0.05) from 2.04 +/- 0.07 to 2.70 +/- 0.20 ml/mm Hg/kg. Blood volume decreased (p less than 0.05) from 67.3 +/- 0.9 to 58.2 +/- 1.8 ml/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1989

Cardiac hypertrophy induced by thyroid hormone is independent of loading conditions and beta adrenoceptor blockade.

This study was designed to determine whether thyroid hormone (T4) produces cardiac hypertrophy and alters ventricular function by direct effects on the heart or by alterations in adrenergic stimulation or changes in the peripheral circulation. Rats were treated with captopril (4 mg/ml of drinking water), propranolol (0.5 mg/ml of drinking water), hydralazine (80 mg/l of drinking water) or the combination of captopril and propranolol with and without T4 (15 micrograms/100 g b.w. i.p.). After 10 days, T4 increased (P less than .01) heart rate, left ventricular (LV) dP/dt and LV weight/body weight, but did not alter LV systolic pressure (SP) or enddiastolic pressure (EDP). Compared to treatment with T4 alone, captopril plus T4 decreased LV SP (P less than .05) and LV EDP (P less than .01); however, heart rate, LV dP/dt and LV weight/body weight were unchanged. Treatment with T4 plus propranolol decreased heart rate and LV EDP (P less than .05) compared to T4 alone; however, LV SP, LV dP/dt and LV weight/body weight were unchanged (P greater than .05). Hydralazine did not alter (P greater than .05) heart rate, LV SP, LV EDP or prevent the development of increased LV weight/body weight when given with T4; however, LV dP/dt was slightly decreased (P less than .05). Treatment with the combination of captopril and propranolol did not alter (P greater than .05) heart rate, LV SP, LV EDP or LV dP/dt and also failed to prevent the development of increased LV weight/body weight and LV dP/dt when given with T4.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Use of acetylcholine to measure total vascular pressure-volume relationship in dogs.

To define total vascular capacitance, we used acetylcholine to arrest the heart and measured mean circulatory filling pressure (MCFP) during controlled hemorrhage and volume loading in 12 splenectomized dogs after ganglion blockade with hexamethonium. We also examined the gross pathological and histological changes in the lungs. Controlled hemorrhage (n = 12) of 5 and 10 ml/kg decreased MCFP from 6.8 +/- 0.1 to 4.9 +/- 0.3 and 3.6 +/- 0.2 mmHg, respectively. Volume loading of 5 (n = 8) and 10 ml/kg (n = 4) increased MCFP to 9.3 +/- 0.2 and 12.1 +/- 0.1 mmHg, respectively. At MCFPs below 5 mmHg, the pressure (P)-volume (V) relationship was not linear [(P = P0ekV, where k is slope of ln (MCFP) vs. V, k = 0.061, R2 = 0.998]. At MCFPs between 5 and 12 mmHg, the pressure-volume relationship was linear (slope = 0.479 mmHg.ml-1.kg-1, R2 = 0.992) and total vascular compliance was 2.09 ml.mmHg-1.kg-1. There were no changes in heart rate, cardiac output, right atrial, pulmonary artery, and pulmonary artery wedge pressures when values at base line were compared with those measured 15 min after each arrest. There were no changes in arterial gas measurements or acid-base balance, and there was no evidence of atelectasis or interstitial or intra-alveolar edema. We conclude that the total body pressure-volume relationship in the presence of ganglion blockade had a nonlinear configuration. The use of acetylcholine to arrest the heart, four times with hexamethonium in reflex-blocked animals, did not result in changes in hemodynamics or pulmonary function.

Acetylcholine↗

PubMed1988

Effects of thyroid state on venous compliance and left ventricular performance in rats.

The cardiovascular system of hypothyroid, normal, and hyperthyroid rats was studied by evaluation of the peripheral venous circulation and left ventricular (LV) systolic and diastolic performance in rats. Cardiac index (CI) and CI during a volume load were measured in open-chest rats. When compared with control, hypothyroid rats showed a decrease in heart rate, aortic pressure, LV systolic pressure, first derivative for LV pressure (LV dP/dt), CI, and CI during a volume load. LV pressure-volume relation was shifted to the right, muscle stiffness was unchanged, and LV relaxation was prolonged. There was a decrease in mean circulatory filling pressure (MCFP) to 6.3 +/- 0.2 from 7.6 +/- 0.2 mmHg in control rats. This was associated with an 11% decrease in unstressed vascular volume and 12% decrease in total blood volume but no change in venous compliance. In hyperthyroid rats there was an increase in heart rate, LV systolic pressure, LV dP/dt, CI, and CI during a volume load. LV chamber stiffness was increased, but muscle stiffness and LV relaxation were unchanged. There was an increase in MCFP to 9.5 +/- 0.3 mmHg and a decrease in venous compliance to 2.65 +/- 0.12 compared with 3.20 +/- 0.09 ml.mmHg-1.kg-1 in control rats. Unstressed vascular volume and total blood volume were unchanged. In conclusion, hyperthyroid rats have augmented LV systolic function and altered diastolic function which, combined with changes in the venous circulation, result in increased venous return and thus cardiac output. In hypothyroid rats both LV systolic and diastolic function are altered. When combined with changes of the venous circulation the changes result in a decrease in cardiac output.

Algorithms↗

PubMed1988

Effects of 10- to 12-day treatment with L-thyroxine in rats with myocardial infarction.

The effects of treatment with L-thyroxine (T4) for 10-12 days on left ventricular (LV) function and myosin isoenzyme content in rats with LV dysfunction after myocardial infarction were studied. Electrocardiogram (ECG) criteria were used to select animals with large myocardial infarctions. These animals were divided into six groups: control and five treatment groups that received daily subcutaneous injections of T4 (1.5, 3, 6, 10, or 15 micrograms/100 g body wt) for 10-12 days. Intravascular pressures were then measured with micromanometer-tipped catheters, and the hearts were analyzed for myosin isoenzyme distribution. The lowest dose of T4 (1.5 micrograms) produced no changes in heart rate, LV pressure or aortic pressure (AoP), myosin isoenzyme composition, or serum T4 levels. Larger doses of T4 (3, 6, 10, and 15 micrograms) produced increases in LV rate of pressure development (dP/dt), heart rate, and T4 levels but did not change LV pressure or AoP. Myosin isoenzyme composition in the control group showed increases in the proportion of the V3 form and decreases in the V1 form compared with the normal pattern. T4 administration produced dose-dependent increases in the V1 myosin isoform and corresponding decreases in the amount of the V2 and V3 forms. Heart rate increases observed with larger doses of T4 could be prevented by addition of propranolol (500 mg/l) to the drinking water. However, in rats treated with T4 and propranolol, LV pressure, AoP, LV dP/dt, and myosin isoenzyme composition were unchanged compared with T4-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Serial changes in left ventricular relaxation and chamber stiffness after large myocardial infarction in rats.

To determine the time course of changes in left ventricular diastolic properties after a large myocardial infarction, we serially measured left ventricular relaxation, chamber stiffness, and the ratio of left ventricular cavity to wall volume (V/VW) after coronary artery ligation in rats. Left ventricular relaxation was measured during the occlusion and then both relaxation and chamber stiffness were measured at 3 hr, 24 hr, and 3, 5, and more than 22 days after infarction. Left ventricular pressures and left ventricular dP/dt were recorded with micromanometer-tipped catheters. Left ventricular relaxation was measured by computer digitization of the left ventricular pressure tracings and averaged over 100 to 150 cardiac cycles. Five chamber stiffness constants were calculated from pressure-volume curves that were obtained ex vivo. We found ventricular relaxation prolonged for the first hour after coronary occlusion; relaxation was maximally prolonged at 10 to 15 min after onset of occlusion. After 1 hr relaxation returned to normal. However, by 5 days ventricular relaxation was again prolonged. Left ventricular stiffness constants were increased at 3 and 24 hr, resulting in a shift of the left ventricular pressure-volume relation to the left. At 3 days after coronary artery ligation, all stiffness constants and the pressure-volume relation returned to normal. At more than 22 days the pressure-volume relation was shifted to the right and the stiffness constant for low filling pressures was decreased. V/VW was significantly decreased from 0.603 +/- 0.021 at 3 and 24 hr to 0.379 +/- 0.024 and 0.362 +/- 0.032, respectively. V/VW was significantly increased at more than 22 days (0.921 +/- 0.094).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Atrial natriuretic peptide levels during development of chronic heart failure after myocardial infarction in rats.

Serum levels of atrial natriuretic peptide (ANP) are elevated in chronic heart failure presumably due to dilatation of the left atrium resulting from increases in intracardiac pressures. To define the time course of changes in serum ANP levels and to determine the relationship to left ventricular end-diastolic pressure, rats were subjected to coronary artery ligation to produce myocardial infarction and left ventricular failure. Atrial natriuretic peptide levels were measured weekly for four weeks thereafter. In rats with myocardial infarction and elevation of left ventricular end-diastolic pressure there was no change in ANP levels at 7 and 14 days. However, at day 21 and 28, ANP levels were elevated more than 3 fold. There was a correlation between ANP levels and left ventricular end-diastolic pressures. There was no correlation between ANP levels and right atrial pressures or serum sodium concentrations. We conclude that the chronic elevation of left ventricular end-diastolic pressure is required to produce an increase in ANP after myocardial infarction which results in chronic heart failure.

Animals↗

PubMed1987

Cardiac catheterization for patients with postinfarction angina.

A retrospective review was conducted to determine the incidence of cardiac catheterization for postinfarction angina, the associated coronary anatomy, and the subsequent clinical course. Over one year, 30 of 178 myocardial infarctions were complicated by postinfarction angina resulting in cardiac catheterization. This was 18% of cardiac catheterizations for evaluation of coronary artery disease. Among the 30 patients, 3 had left main disease, 3 had triple-vessel disease, 11 had double-vessel disease, 11 had single-vessel disease, and 2 had no significant disease. Nine patients had proximal left anterior descending disease without left main disease. In contrast to previous autopsy or surgical series, the extent of coronary artery involvement was less severe and followed a distribution similar to that found in uncomplicated myocardial infarctions. Nevertheless, 17 of the 30 patients underwent revascularization with angioplasty or bypass surgery compared with 41 of 137 without postinfarction angina (p = 0.01). Clinical characteristics of the patients with postinfarction angina did not predict who would ultimately require revascularization. Cardiac catheterization is necessary for management of patients with postinfarction angina, because a majority of them will require revascularization.

Angina Pectoris↗

PubMed1987

Quinidine-induced reactive lymphadenopathy.

This report describes a patient who presented with extensive inguinal lymphadenopathy while taking quinidine for the treatment of arrhythmias. An excisional lymph node biopsy specimen demonstrated atypical, reactive, follicular hyperplasia. Immunologic assessment utilizing 20 monoclonal antibodies indicated a reactive process with follicles shown to be polyclonal B cell. The patient's adenopathy resolved within one month of discontinuation of quinidine and he remains well 15 months later. The histologic and immunologic findings as well as the clinical response are typical for a drug-induced reactive lymphadenopathy.

Biopsy↗

PubMed1987

Beta-2 adrenoceptor control of the venous circulation in intact dogs.

The effects of beta-2 adrenoceptor stimulation on the peripheral circulation in 10 dogs were evaluated. All studies were done during ganglion blockade with hexamethonium. Venous capacitance was assessed by measuring mean circulatory filling pressure, venous compliance and unstressed vascular volume. Beta-2 stimulation was achieved with terbutaline (27 micrograms/min) after beta-1 blockade with metoprolol (0.75 mg/kg). At a dose of terbutaline that decreased mean aortic pressure from 80.4 +/- 3.5 to 58.9 +/- 1.9 mm Hg (P less than .01), there was no change in cardiac index (155.8 +/- 10.5 vs. 161.1 +/- 9.1 ml/kg/min) despite an increase in heart rate from 118.6 +/- 5.2 to 132.6 +/- 5.0 beats/min. Right atrial pressure, left ventricular end-diastolic pressure and dP/dt did not change. Systemic vascular resistance decreased from 0.52 +/- 0.02 to 0.39 +/- 0.03 mm Hg . min . kg . ml (P less than .01). Arterial compliance increased from 0.067 +/- 0.003 to 0.088 +/- 0.007 ml/mm Hg/kg and the volume of blood shifted out of the larger arteries was 1.8 +/- 0.4 ml/kg. Mean circulatory filling pressure did not change but venous compliance decreased from 1.90 +/- 0.04 to 1.47 +/- 0.06 ml/mm Hg/kg and unstressed vascular volume increased from -14.5 +/- 0.5 to -8.4 +/- 0.5 ml/kg. Central blood volume increased from 22.8 +/- 1.1 to 27.4 +/- 2.2 ml/kg. There was an increase in total blood volume from 81.1 +/- 2.7 to 90.5 +/- 3.7 ml/kg. To determine the extent to which changes in the spleen were responsible for these observations, five dogs were studied 2 weeks after splenectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Dog model to study the effects of pharmacologic agents on the peripheral circulation: effects of milrinone.

To study the effects of an inotropic agent, milrinone, on the entire cardiovascular system, we developed an intact dog model to assess the responses of the heart, arterial and venous circulations. At a dose that increased left ventricular dP/dt by 30% (P less than .001) from 2033 +/- 133 to 2688 +/- 140 mm Hg/sec, milrinone caused a decrease (P less than .001) in mean aortic pressure from 88.4 +/- 3.5 to 73.1 +/- 3.0 mm Hg and cardiac output from 148.0 +/- 14.6 to 134.5 +/- 13.9 ml/kg/min. Heart rate increased (P less than .01) from 124 +/- 8 to 135 +/- 8 beats/min. Systemic vascular resistance did not change. Right atrial pressure and left ventricular end-diastolic pressure decreased (P less than .01). Total blood volume did not change but central blood volume decreased (P less than .01) from 26.1 +/- 0.9 to 22.3 +/- 0.5 ml/kg. After milrinone administration, mean circulatory filling pressure decreased (P less than .01) by 30% from 7.4 +/- 0.4 to 5.0 +/- 0.2 mm Hg. Vascular or venous compliance increased (P less than .05) slightly from 1.96 +/- 0.4 to 2.20 +/- 0.1 ml/mm Hg/kg. This was accompanied by an increase (P less than .01) in unstressed vascular blood volume of 3.3 +/- 0.6 ml/kg. Arterial compliance also increased (P less than .05). In summary, milrinone produces an increase in inotropy, arterial vasodilatation and venodilatation as evidenced by the increased venous compliance and unstressed vascular volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1985

Severe pulmonary hypertension in a patient with Whipple's disease.

Rapidly progressive heart failure, in part related to severe pulmonary hypertension, developed in a patient with biopsy-proved Whipple's disease. The patient's pulmonary hypertension progressed despite antibiotic therapy and histologic remission of his intestinal disease. The combination of oral nifedipine and low-flow continuous oxygen led to both short- and long-term increases of at least 2 liters per minute in cardiac output and reductions of more than 10 mm Hg in mean pulmonary artery pressure. Accompanying these hemodynamic changes was an improvement of more than 10 percent in right ventricular ejection fraction. The relationship between this patient's pulmonary hypertension and his Whipple's disease is not known.

Drug Combinations↗