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Biomedical subjects

J K Vyden

Publications and source records attributed to J K Vyden.

At least 19 recordsLinked to original sources
PubMed1984

Lack of effect of cyclandelate in peripheral arterial disease.

While cyclandelate is widely used in the therapy of peripheral arterial disease, objective evidence of its efficacy remains controversial. For this reason, 12 patients with intermittent claudication (average age of 66.8 years) received both cyclandelate 400 mg qid and placebo in a double-blind crossover trial lasting two months. During the cyclandelate and placebo periods, the following peripheral hemodynamic measurements were obtained using a plethysmograph and treadmill claudication testing: mean calf blood flow, vascular resistance and venous capacitance; finger and toe blood flow, pulsation amplitude and temperature before and after vasodilating maneuvers; arm and leg arterial pulsation amplitudes, one and ten minute calf reactive hyperemia reaction; 30 pound/30 second calf active hyperemia reactions and times of onset of claudication as measured on a treadmill. No major significant difference could be demonstrated between placebo and cyclandelate on any subjective symptom or any objective measurement. It is concluded that cyclandelate 400 mg qid for 4 weeks was of little objective value in treating this group of 12 patients with peripheral arterial disease and suffering from intermittent claudication.

Aged↗
PubMed1983

Peripheral hemodynamics in patients with Fabry's disease.

Altered vasomotor activity has been reported as a clinically prominent feature of Fabry's disease (angiokeratoma corporis diffusum universale). While symptomatic cardiovascular involvement occurs eventually in most patients with this disorder, little is known concerning the effect of Fabry's disease on peripheral hemodynamics. Peripheral hemodynamics in the extremities and digits were studied in eight patients with Fabry's disease by means of segmental and venous occlusion pneumoplethysmography and thermal probes, and the results obtained were compared with those of 10 normal subjects. Forearm vascular resistance in Fabry's disease patients was significantly higher (p less than 0.01) than that in normal subjects. Forearm venous capacitance in Fabry's disease was significantly lower (p less than 0.01). Segmental pulse volume amplitudes showed no significant difference in any segments (upper arm, wrist, thigh, above and below knee, and the calf) between the two groups. Finger and toe blood flow, finger and toe pulse volume, and temperature in the resting state were all significantly less (p less than 0.01, p less than 0.05: p less than 0.01, p less than 0.01: p less than 0.05, p less than 0.05, respectively) than those in normal subjects. Finger and toe blood flow and pulse volume after vasodilation procedures were significantly less (p less than 0.05, p less than 0.01: p less than 0.05, p less than 0.01, respectively) than those in normal subjects despite equal elevation of digital temperature obtained after vasodilation in both groups. These findings indicate the presence of vasoconstrictive process in both resistance vessels and capacitances vessels in cutaneous and skeletal muscular beds. A limited response in the cutaneous circulation to vasodilation procedures also was seen. These data suggest the possibility that latent enhanced sympathoadrenal discharge as well as the accumulation of glycolipid in the autonomic nervous system and vessel walls plays an important role in the disturbed pathophysiology of this disorder.

Adolescent↗
PubMed1983

Observations on the relationship between digital heat loss and systemic hemodynamics in patients with heart disease.

A concomitant study of finger heat discharge and systemic hemodynamics was undertaken in a series of 19 patients (mean age 54 years) suffering from various forms of heart disease. Finger heat discharge, as measured by calorimetry, was found to correlate significantly with mean circulation time (-0.760), cardiac index (+0.649), systemic vascular resistance (-0.615), stroke work index (+0.649), mean pulmonary artery pressure (-0.596), mean pulmonary capillary wedge pressure (-0.554), stroke index (+0.541), appearance time (-0.502) and mean right atrial pressure (-0.453). There was no significant correlation between finger heat discharge and mean arterial blood pressure, LV dp/dtmax, and heart rate. An effect of heart failure on finger heat discharge was found. When evidence of forward failure and also possibly backward failure was found, mean finger heat discharge was significantly diminished. When both forward and backward failure were present together, mean finger heat discharge fell still further.

Blood Circulation Time↗
PubMed1983

Unloading effects of molsidomine on peripheral circulation and cardiac hemodynamics in patients with acute myocardial infarction.

The unloading mechanisms and side of peripheral action of the new antianginal drug molsidomine was compared with isosorbide dinitrate (ISDN) in 14 patients with acute myocardial infarction using a Swan-Ganz catheter and venous occlusion plethysmography. Sublingual molsidomine (2-4 mg) increased calf venous capacitance (CVC) (0.42 +/- 0.18 to 0.64 +/- 0.09 ml/100 ml, p less than 0.05) from 30 to 240 minutes, while simultaneously lowering of PCWP (25.9 +/- 4.9 to 15.8 +/- 7.3 mmHg, p less than 0.05) and CVP (9.3 +/- 3.7 to 5.8 +/- 3.5 cmH2O, p less than 0.05). Calf blood flow (CBF), calf vascular resistance (CVR), CI, TSPR and SWI were not affected significantly. Molsidomine reduced preload more than 240 minutes after its administration. Sublingual ISDN increased CBF into the initial 15 minutes (1.19 +/- 0.49 to 1.83 +/- 0.98 ml/100ml/min, p less than 0.05) and CVC from 5 to 60 minutes (0.42 +/- 0.19 to 0.68 +/- 0.24 ml/100ml p less than 0.01) while simultaneously lowering PCWP (24.3 +/- 2.2 to 14.6 +/- 4.5 mmHg, p less than 0.01) and CVP (9.0 +/- 2.8 to 5.5 +/- 3.5 cmH2O, p less than 0.05). Neither drug affected cardiac index, blood pressure or systemic vascular resistance. These data suggest that molsidomine significantly lowered elevated preload (PCWP/PCP) by dilating venous capacitance vessels. Its length of action was 240 minutes compared with 60 minutes obtained with ISDN, which suggests this new agent may be of marked benefit in the AMI patients suffering from backward failure uncomplicated by forward failure in whom continued preload reduction is necessary. (Results are expressed as the mean +/- standard deviation).

Adult↗
PubMed1982

Unloading effects of vasodilators on peripheral circulation and cardiac hemodynamics in patients with acute myocardial infarction.

Effects of three representative vasodilators on peripheral and cardiac hemodynamics were studied in 20 patients with heart failure due to acute myocardial infarction (PCWP greater than 18 mmHg, C1 greater than 2.20 L/min/m2) using venous occlusion plethysmography and a Swan-Ganz catheter. Sublingual isosorbide dinitrate (ISDN) significantly increased calf venous capacitance (CVC) from 5 to 60 min (p less than 0.01) and calf blood flow (CBF) in the initial 15 min (p less than 0.05), while simultaneously lowering PCWP (p less than 0.05) and central venous pressure (p less than 0.05). Calf vascular resistance (CVR), cardiac index, blood pressure, and total systemic peripheral resistance (TSPR) were not affected significantly. Nitroglycerin ointment (NGO) significantly decreased CVR (p less than 0.05) and increased CVC (p less than 0.05) from 60 to 240 min, simultaneously with lowering of PCWP (p less than 0.01), central venous pressure (p less than 0.05), and TSPR (p less than 0.05). Oral prazosin (Pz) increased CBF (p less than 0.01) and CVC (p less than 0.05) from 60 to 240 min, simultaneously with significant lowering of PCWP (p less than 0.01) and TSPR (p less than 0.05), resulting in increased stroke work index (p less than 0.05). These data confirm that ISDN predominantly causes capacitance vessel dilatation and reduce excessive venous return, while Pz and NGO dilate not only capacitance vessels but also resistance vessels, consequently reducing systemic vascular resistance and resulting in increased peripheral blood flow and cardiac performance. It was observed that the higher the base-line calf vascular resistance rose, the better the response to the vasodilator treatment appeared in terms of a decrease in calf vascular resistance.

Adult↗
PubMed1977

Effect of sex difference and pregnancy on the normal reactive hyperemia curve.

The 10-min reactive hyperemia reaction was studied in a group of normal males, 10 normal females, 10 females in each trimester of pregnancy, and 10 females 6 wk postpartum. Sex difference had a marked effect on the hyperemic reaction, in that 5 and 15 s after release of circulatory arrest, the mean forearm blood flow in normal males was significantly reduced below that of normal females. During pregnancy there was a shift in the reaction of the pregnant female toward that in the normal male. In the 1st trimester of pregnancy, 5 s after circulatory arrest the mean forearm blood flow was diminished below that of the normal female; in the 2nd and 3rd trimesters at 5 s, the reaction was significantly diminished below that of the normal female. At 6wk postpartum, the reaction was essentially the same as in the nonpregnant female. Although these changes may be explained by a hormonal difference, they portray that there may be a marked difference in vascular reactivity due to sex difference only.

Adolescent↗
PubMed1976

Cardiovascular effects of ajmaline.

Ajmaline, a rauwolfia derivative, has been found to possess potent antiarrhythmic effects. The present study has been designed to define the cardiovascular effects of this drug. Hemodynamic studies performed in anesthetized and conscious dogs demonstrated no significant changes in measured hemodynamic parameters at doses equal to or less than 2 mg. per kilogram. Studies in isolated papillary muscle demonstrated no negative inotropic effects until concentrations of 1 X 10(-4). Disparate results were obtained with regard to heart rate reflecting the state of autonomic tone. Electrophysiologic studies in both anesthetized and conscious dogs demonstrated a significant depression of intraventricular conduction with no significant effect on AV nodal conduction; ventricular automaticity was not affected. Ajmaline did not alter digitalis-induced AV nodal conduction prolongation. However, ajmaline dramatically altered or abolished ventricular arrhythmias secondary to acute ischemia. In conclusion, these studies demonstrate that ajmaline specifically depresses intraventricular conduction, suggesting that this drug would be particularly effective in the treatment of re-entrant ventricular arrhythmias.

Ajmaline↗
PubMed1975

The effect of lidocaine on peripheral hemodynamics.

Lidocaine was given in increasing step-wise dose concentrations of 1, 2, 3, 4, and 5 mg/minute and the resulting serum concentrations correlated with the effect of this agent on the peripheral vasculature of seven patients. Lidocaine infusion causes an immediate sustained increase in mean calf venous capacitance but little effect on mean diastolic blood pressure. In high concentration levels this agent causes an increase in mean calf blood flow and systolic blood pressure. Its effect on calf vascular resistance is variable, but there is a tendency to reduce resistance, particularly at a high concentration level. The effect of lidocaine infusion rate on serum lidocaine levels was such that the greater the infusion rate, the higher the resultant serum lidocaine levels.

Adult↗
PubMed1975

Hemodynamic and metabolic effects of isosorbide dinitrate in chronic congestive heart failure.

To assess the potential beneficial effects of a nonparenteral vasodilator, sublingual isosorbide dinitrate (5 to 15 mg.) was administered in 12 patients with chronic congestive heart failure refractory to conventional therapy. Hemodynamic measurements were performed before and at 15 minute intervals after drug administration for 90 minutes. Venous capacitance was measured at 5 minute intervals. Myocardial metabolism was also studied in five patients before and after drug administration. Hemodynamic effects were characterized by a modest decrease in mean arterial pressure (85 +/- 3 to 78 +/- 2 [S.E.M.] mm. Hg) and substantial decrease in right atrial (10 +/- 1 to 6 +/- 1), pulmonary arterial (39 +/- 4 to 30 +/- 4) and pulmonary capillary wedge pressures (28 +/- 2 to 21 +h- 2). These changes were accompanied by an increase in venous capacitance (2.46 +/- 0.16 to 3.99 +/- 0.24 c.c./100 c.c. of tissue). Along with a decrease in left ventricular filling pressure, cardiac index increased (1.99 +/- 0.13 to 2.37 +/- 0.15 L./min/M.2). No significant effect on heart rate was seen. Delta P/delta t, an index related to left ventricular dp/dt, increased in all but one patient (253 +/- 31 to 298 +/- 39 mm. Hg/sec.) (p less than 0.02 for all changes) in the face of decreased preload and afterload and unchanged heart rate, suggesting improved contractile state. A decrease in coronary blood flow (165 +/- 13 to 131 +/- 15 c.c./min.) and myocardial oxygen consumption (18.1 +/- 1.6 to 14.5 +/- 1.6 c.c./min.) was noted (p less than 0.02). No change in arterial-coronary sinus oxygen difference or lactate extraction was observed. These data demonstrate that the objectives of therapy in congestive heart failure, namely improved forward output and decreased ventricular filling pressures, can be achieved without metabolic deterioration by using sublingual isosorbide. The mechanisms responsible are related to diminished impedence to ventricular ejection and peripheral pooling of blood. Since the duration of action does not usually exceed 90 minutes, frequent drug administration may be a source of patient inconvience.

Administration, Oral↗