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Biomedical subjects

H C Dittrich

Publications and source records attributed to H C Dittrich.

46 records · Page 3Linked to original sources

Furosemide during sustained left atrial hypertension in functionally anephric dogs: intravascular and extravascular pulmonary fluid volumes. V.

The response of intravascular (PBV) and extravascular (EVLW) pulmonary fluid volume was examined using double-indicator techniques (thermal-green dye) in 11 open-chest anesthetized dogs during the production of sustained left atrial (LA) hypertension by a LA balloon over a period of 195 min. In 6 of these animals data were also acquired after the intravenous administration of furosemide (1 mg/kg). The renal effects of the diuretic were blocked by tying off the ureters and the vascular supply of both kidneys. Left atrial pressure (N = 11) was abruptly increased from 2.2 +/- 2.1 mm Hg to 30.2 +/- 4.0 mm Hg (P less than 0.01) and maintained at that level for 120 min. Data were obtained prior to pressure elevation, immediately upon pressure elevation, and then every 60 min for a total of 120 min. At that point EVLW had increased (8.1 +/- 0.8 cc/kg at control to 21.7 +/- 2.0 cc/kg at 120 min, P less than 0.001), as had PBV (6.2 +/- 2.1 cc/kg to 9.1 +/- 3.1 cc/kg P less than 0.01). After furosemide injection (N = 6), LA pressure declined (mean peak reduction of approximately 6 mm Hg at 60-75 min, P less than 0.01), aortic and pulmonary arterial pressure both declined (P less than 0.01). However, EVLW remained unchanged, though PBV decreased significantly (peak decrease at 75 min after furosemide administration of 2.0 +/- 0.4 cc/kg, P less than 0.01). In the untreated dogs, EVLW continued to climb (P less than 0.05 vs treated dogs at 75 min postfurosemide).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of intracoronary and intravenous amrinone infusions in patients with cardiac failure and patients with near normal cardiac function.

The effects of intracoronary and intravenous infusions of amrinone were studied to distinguish the drug's direct cardiac actions from its peripheral vascular and neuroendocrine properties. Intracoronary infusions of amrinone were found to have no haemodynamic effect other than producing a slight reduction in the left ventricular ejection fraction and some suggestion of coronary vasodilatation in patients with impaired left ventricular function. They did not improve contractility, cardiac output, or filling pressures and had no significant effect on myocardial metabolism, although therapeutic concentrations of the drug were detected in coronary sinus blood. Intravenously administered amrinone reduced filling pressures and improved the cardiac index in all patients, but haemodynamic improvements were most pronounced in the patients with the worst cardiac function. These changes were accompanied by improvements in the indices of contractility only in patients in whom alterations in concentrations of free fatty acid, glycerol, and glucose suggested peripheral catecholamine release. In the patients with the best basal cardiac function intravenously administered amrinone produced a reduction in myocardial work and evidence of myocardial ischaemia, as a result of excessive reduction of coronary perfusion pressure and increased heart rate, without any appreciable increase in cardiac index. It is concluded that, at the concentrations of the drug that can be achieved in man without adverse effects, amrinone has no direct positive inotropic effect. Haemodynamic changes are predominantly the result of vasodilatation, although catecholamines may be released in some patients.

Adult↗

Radionuclide analysis of the forearm venous pressure-volume relationship: response to nitroglycerin.

By means of equilibrium radionuclide forearm venous occlusion plethysmography, we studied 12 adult men without heart failure. By using stepwise increases in venous occlusion pressure (0, 10, 20, and 30 mm Hg), we found that the relationship between venous cuff pressure and forearm radionuclide volume was consistently linear (r greater than 0.985). When sublingual nitroglycerin (NTG) was administered (0.8 mg), the venous pressure-volume relationship was consistently shifted rightward (reducing the slope and increasing the intercept). This resulted in large increases in venous capacitance, as shown by other workers using alternative techniques. Increased venous distensibility due to NTG was caused by an entire shift of the venous pressure-volume relationship rather than increased capacitance at one occlusion pressure. Equilibrium radionuclide venous occlusion plethysmography is a sensitive way to characterize venous pressure-volume relations. In addition, by using radionuclide blood pool component imaging to evaluate venous compliance, concern over fluid transudation seen with standard strain gauge venous plethysmographic techniques can be ignored, particularly at higher occlusion pressures.

Aged↗

Sustained venous occlusion plethysmography: effects on protein osmotic pressure, intravascular volume, and capillary filtration.

In six acutely anesthetized, mechanically ventilated mongrel dogs, we evaluated sequential changes (over 30 minutes) of sustained forelimb venous occlusion (occlusion pressures 30 to 65 mm Hg) on strain gauge dimension, radionuclide blood pool emissions, and venous, subcutaneous, and intramuscular pressures (Wick technique). Forelimb intravascular volume (assessed by decay-corrected radionuclide counts/unit time) changed by a mean of only -1.2 +/- 2.8% (+/- SEM) and thus was ignored in the calculation of filtration rate. Forelimb (distal to the occlusion site) hematocrit changed insignificantly (45.3 +/- 1.4% at the control point to 48.2 +/- 1.1% at 30 minutes), colloid osmotic pressure rose slightly 19.4 +/- 1.4 mm Hg to 22.7 +/- 1.6 mm Hg, p less than 0.01), and serum osmolality remained unchanged. During sustained occlusion, venous pressure remained constant, subcutaneous pressure rose (-0.7 +/- 1.2 mm Hg control vs 0.5 +/- 1.4 mm Hg at 30 minutes, p less than 0.05), and intramuscular pressure also rose (-0.4 +/- 1.1 mm Hg to 2.6 +/- 1.6 mm Hg, p less than 0.01). Driving pressure, defined by venous pressure - oncotic pressure less the average of intramuscular and subcutaneous pressure declined slightly over the 30 minutes of the study (27.8 +/- 5.5 mm Hg to 23.3 +/- 1.3 mm Hg, p less than 0.05). The relationship between either the initial driving pressure or the initial difference between venous and protein osmotic pressure correlated (r = 0.83 for both) well with strain gauge estimates of capillary fluid flux (evaluated by the change in forelimb strain gauge dimension over time and given as cc/100 cc forelimb volume/min).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Cellular sodium concentration and vasoconstrictor state in hypertension.

The sodium content of peripheral blood leucocytes was estimated in two separate investigations of the relationship between cellular sodium content and the vasoconstrictor state. In the first study various parameters of forearm blood flow were measured in a group of 31 normal subjects. A positive correlation was found between peripheral vascular resistance and leucocyte sodium content (p less than 0.05), and a negative correlation between venous compliance (VV60) and leucocyte sodium content (p less than 0.001). In the second study the leucocyte sodium content of 14 patients with essential hypertension was investigated before and after treatment with the calcium antagonist verapamil. The sodium content was found to be abnormally high, as previously described, and treatment with verapamil was found to reverse the defect. Both studies indicate a link between cell sodium content and the vasoconstrictor state, and the results are discussed in light of current theory.

Adult↗

Analysis of ventricular emptying and filling indexes during acute increases in arterial pressure.

Using equilibrium radionuclide angiography, an evaluation was made of the response of left ventricular ejection and filling rates at rest and during acute increases in afterload in 8 normal volunteer subjects and 10 patients with previous transmural myocardial infarctions. Using the postatropine point for comparison, normal patients increased ejection time and decreased peak ejection rate (-3.90 +/- 0.49 vol/s to -3.41 +/- 0.95 vol/s) and peak filling rate (3.94 +/- 0.88 vol/s to 3.51 +/- 0.38 vol/s). Infarct patients had similar responses, although all indexes were lower than the corresponding values in the normal subjects. At rest, the ratio of peak filling to emptying rate was similar in the normal subjects and the infarct patients (1.01 +/- 0.24 versus 0.99 +/- 0.25, respectively) and maintained that relationship after atropine (0.91 +/- 0.11 versus 0.81 +/- 0.21) and at the peak increase in arterial pressure (1.07 +/- 0.21 versus 1.02 +/- 0.32). The ratio of time to peak filling/time to peak emptying behaved in similar fashion regardless of the differences in the absolute values. In this study, left ventricular filling and emptying behaved in a similar fashion in response to the alteration in arterial pressure in normal subjects and in patients with previous myocardial infarctions.

Adult↗

Increased in blood flow to ischemic myocardium caused by a new dopamine analog.

In the anesthetized, open-chest dog, intravenous infusion 8-13 microgram . kg-1. min-1) of a new dopamine analog 5,6-dihydroxy-2-methylaminotetralin hydrobromide (M-8) demonstrated potent coronary vasodilator properties. Blood flow to normal myocardium was increased an average of 53% above control flow values and this was associated with a decrease in coronary vascular resistance of 50%. The increase in blood flow was distributed uniformly to all portions of the myocardium (left ventricular free wall, right ventricular free wall, and septum). Subendocardial/subepicardial (endo/epi) flow ratios of the left ventricle, right ventricle, and septum were not significantly changed from control. In dog hearts subjected to acute, sudden occlusion of portions of the left anterior branch of the left coronary artery, M-8 produced a 93% increase in flow to the whole heart over postocclusion flow values. Flow to tissues of the heart made ischemic by the occlusive procedure in creased by an average of 94% during M-8 administration despite the fact that the occlusive ligatures remained in place. The vasodilation produced by M-8 was accompanied by a 22-24% increase in myocardial capillary surface area available for exchange of lipid-insoluble substances, fructose and sucrose. Hemodynamic changes associated with M-8 include a transient decrease in aortic pressure, but no change in heart rate, left ventricular (dP/dt)/P, or central venous pressure. Propranolol blocked the vasodilator activity of M-8. It was concluded that M-8 is a beta2-adrenergic receptor agonist having potent coronary vasodilator properties which also has the ability to open preexisting collateral blood flow channels and provide nutritive flow to ischemic, marginally ischemic, and normal myocardium. The cardiovascular actions of M-8 increase blood flow and oxygen delivery to the myocardium while decreasing the work and oxygen utilization by the heart, suggesting that it may have important antianginal characteristics.

Animals↗

Myocardial contrast echocardiography in experimental coronary artery occlusion with a new intravenously administered contrast agent.

A new intravenously administered ultrasound contrast agent was studied in eight dogs during intermittent coronary artery occlusion. The area of the myocardial contrast defect was compared with that of the acute wall motion abnormality induced by coronary occlusion. A close correlation was found between these two independent measures of acute myocardial ischemia. The peak change in myocardial intensity during coronary occlusion was significantly less than for the same segment before ischemia and for a remote nonischemic segment. This new, intravenously administered ultrasound contrast agent can be used to evaluate the spatial distribution of hypoperfused myocardium and should therefore prove valuable in the clinical evaluation of ischemic syndromes.

Animals↗

Diagnostic pitfalls in transesophageal echocardiography.

The technology of transesophageal echocardiography is now widely available and has proved extremely useful in evaluating cardiovascular anatomy and pathology. Unfortunately, the enhanced echocardiographic detail and multiple transesophageal imaging planes may sometimes be confusing and cause misinterpretations. The majority of these problems are simply the result of operator inexperience. To help prevent misdiagnoses, we have collected a series of the more common diagnostic and technical "pitfalls" of transesophageal echocardiography.

Aorta↗

Influence of Doppler sample volume location on the assessment of changes in mitral inflow velocity profiles.

Previous studies that have validated Doppler indexes of mitral inflow have used pulsed wave sample volume locations either at the level of the mitral valve anulus or at the tips of the mitral valve leaflets. Although significant differences between absolute values for peak velocities and velocity time integrals at these sample volume locations have previously been reported, no information exists that has compared changes in inflow profiles after an intervention to improve left ventricular filling. To address this question, 13 patients with severe pulmonary hypertension (mean pulmonary artery pressure, 50 +/- 13 mm Hg) caused by chronic thromboembolic disease were studied with use of Doppler echocardiography immediately before and after surgical reduction of pulmonary hypertension (pulmonary vascular resistance decreased from 916 +/- 413 to 233 +/- 89 dynes.sec.cm5). This clinical model has been shown to have abnormal mitral inflow velocity profiles that improve markedly after surgery. Doppler measures of early and late peak velocities were significantly lower both before and after surgery when sampling at the mitral anulus compared with the leaflet tips, although late filling parameters and the deceleration of early flow velocity tended to differ little. With surgery, the significant increase in peak early velocity and the ratio of early to late velocity was present regardless of the sample volume location (peak E at leaflet tips, 47.1 +/- 16.0 to 68.9 +/- 15.4 [p less than 0.001], and at anulus, 40.7 +/- 11.3 to 56.2 +/- 14.6 cm/sec [p less than 0.001]; peak E/A at leaflet tips, 0.95 +/- 0.4 to 1.55 +/- 0.9, and at anulus, 0.78 +/- 0.3 to 1.32 +/- 0.7 [both p less than 0.02]).(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Flow Velocity↗