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H Schad

Publications and source records attributed to H Schad.

At least 37 records · Page 2Linked to original sources
PubMed1991

Action of benzene metabolites on murine hematopoietic colony-forming cells in vitro.

Five benzene metabolites--phenol, catechol, hydroquinone, parabenzoquinone, and trans,trans-muconaldehyde--were tested in vitro in murine hematopoietic cell cultures for erythrocytic (BFU-E and CFU-E) and granulocytic (CFU-C) colony growth. The dose range was 4 x 10(-4) to 4 x 10(-8) M. Of these compounds, phenol showed the lowest toxicity. In general, CFU-E cultures were far more sensitive than CFU-C and BFU-E. The results are discussed in relation to the test system used, the in vivo sensitivity of CFU-E, and the lack of knowledge about in vivo concentrations of these compounds.

Animals↗
PubMed1991

Global and regional ventricular function following intracoronary application of papaverine.

Intracoronary injection of papaverine is used to determine coronary flow reserve in patients. The present study was to investigate the effect of papaverine on the performance of myocardium with reduced flow reserve. In nine anaesthetized open-chest dogs a bypass from the aorta to the left circumflex coronary artery (LCX) was established. Left ventricular end-diastolic and aortic pressure, dP/dt, stroke volume, LCX blood flow, and ECG were monitored. The performance of a segment of subendocardial wall supplied by the LCX was assessed by sonomicrometry. Peak reactive hyperaemia after 15s bypass occlusion was 1.44 +/- 0.09 times the baseline flow (41 ml/min), indicating reduced coronary flow reserve. Papaverine was injected into the bypass (0.3, 0.6, 1.2, 2.5, 5.0 mg/ml, 1 ml in 15s). The maximum LCX flow following PAPA 0.3 mg was comparable to peak reactive hyperaemia, but 10-15% higher after injection of 0.6-5.0 mg papaverine. Systolic shortening of the myocardium (control: 17.5% of end-diastolic length) became reduced in a dose-dependent fashion (5-25%) for about 1 min following papaverine injection. Stroke volume (control: 0.94 +/- 0.12 ml/kg) was reduced by about 8%, left ventricular end-diastolic pressure (control: 6.2 +/- 0.8 mmHg) increased by 15%, and dP/dtmin (control: 1850 +/- 150 mmHg/s) was curtailed by 15-25%. The ECG showed a transient T inversion and S-T depression following papaverine administration and in one experiment ventricular fibrillation occurred after the injection of 2.5 mg papaverine. The observed effects of intracoronary papaverine are consistent with the theory of transient subendocardial ischaemia arising from a redistribution of blood flow from the subendocardial to the subepicardial layers, because of greater vasodilatory capacity in the latter than in the former.

Animals↗
PubMed1991

Significance of the subvalvular apparatus for left-ventricular dimensions and systolic function: experimental replacement of the mitral valve.

To study the significance of the subvalvular apparatus for left-ventricular performance in mitral valve replacement, a new experimental model was developed. In 21 dogs St. Jude prostheses were implanted in the mitral position preserving the chordae tendineae and the papillary muscles by plicating and fixing the mitral leaflets with the prosthesis on the valvular annulus. Flexible steel wires were slung around the chordae tendineae of the anterior and the posterior papillary muscle separately and passed through the left ventricular wall via insulating plastic cannulas. Left-ventricular dimensions and global systolic function were measured during volume loading with blood before and after severance of the chordae tendineae by external application of electrocautery to the steel wires. Thus the heart continued beating without any interference following loss of the subvalvular apparatus. The external left ventricular diameters in the major and minor axis were determined by sonomicrometry. Left-ventricular systolic and diastolic pressures were measured by catheter tip manometers, stroke volume by electromagnetic measurements of flow in the ascending aorta. When the chordae tendineae had been cut, left-ventricular end-diastolic diameters in the major axis were increased ( + 2%), in the minor axis decreased (-1%) at any left-ventricular end-diastolic pressure. Systolic shortening of the major axis diameter was considerably reduced (20-27%) at any left-ventricular end-diastolic pressure following severance of the chordae tendineae. Significant increase of the systolic shortening in the minor axis diameter occurred at preload levels of 3-6 mmHg (15-8%), while at higher left-ventricular end-diastolic pressure of 7-8 mmHg no significant changes were present.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Models of coronary artery disease: "critical" versus "functional" coronary artery stenosis.

"Critical coronary stenosis" (reduction of coronary blood flow [Q] until reactive hyperaemia following 15s coronary occlusion is just abolished) and "functional stenosis" (reduction of Q until systolic shortening (dL) of post-stenotic myocardium is curtailed by 50%) were compared with respect to the reduction in Q necessary and the effect on regional myocardial and global ventricular function. In 9 anaesthetized (piritramide) dogs, enddiastolic length (edL) and dL of a myocardial area supplied by the left descending coronary artery (LAD) were measured by sonomicrometry. Left-ventricular end-diastolic pressure (LVEDP) and dP/dt, aortic pressure (AoP), stroke volume (SV), and heart rate (HR) were monitored. QLAD was stepwise reduced by a snare. Critical stenosis, present at a 25% reduction of QLAD, had no effect on regional and global ventricular function, but recovery of dL after release of 15s LAD occlusion was significantly delayed. Further obstruction of QLAD progressively impaired dL, reaching 50% dL (functional stenosis) by a flow reduction of about 50%. The decrease in dL was accompanied by an increase in edL. The haemodynamic effects of the functional stenosis were rather discrete (LVEDP + 5%, SV-12%, dP/dtmax-8%). Models of myocardial ischaemia used to study the effect of drugs or other haemodynamically effective interventions should be able to show functional impairment as well as improvement of the ischaemic myocardium. The critical stenosis does not impair myocardial function and, consequently, a favourable influence on the function and, consequently, a favourable influence on the function of ischaemic myocardium by any intervention may not become evident. However, in the presence of a functional stenosis the change in systolic shortening of the ischaemic myocardium is a very sensitive response to any intervention which affects the energy balance of the ischaemic myocardium. Therefore, this model should be preferred.

Animals↗
PubMed1991

Cyclic motion of ischemic ventricular wall area and hydrodynamics of the blood during ejection.

Analysis of dimensional changes of ischemic left ventricular wall segments evidenced a dilation immediately after onset of ejection; thereafter, contraction appears delayed but almost regular. This biphasic systolic wall motion was correlated in a retrospective study to parameters indicating local intramural disorders, intraventricular load changes, and hydrodynamics of the blood during ejection. Hemodynamic data stored on a 16-track tape recorder were analyzed from 12 consecutive experiments in anesthetized dogs in which the left circumflex coronary artery (LCX) was gradually narrowed (coronary flow restriction greater than or equal to 50%). Left ventricular and aortic pressure, aortic blood velocity (v), acceleration/deceleration (dv/dt), and instantaneous stroke volume (m = integral of v*dt), and segment lengths of normal and ischemic myocardial regions (sonomicrometry) were numerically evaluated with 5 msec resolution. Systolic shortening of the intact myocardium correlates with the diminution of the intraventricular volume during ejection (r greater than 0.98). In contrast, ischemic segments dilate early during systole when the blood is accelerated; the extent of dilation depends on the degree of coronary flow reduction. The time course of lengthening coincides with the development of force F = m*dv/dt (r greater than 0.90) originating from regularly contracting parts of the ventricle. During blood deceleration, ischemic wall segments shorten as F turns to negative (r greater than 0.95). Thus, the wall motion of ischemic myocardial regions is modulated by the hydrodynamic force resulting from acceleration and deceleration of blood consecutively impeding and supporting the systolic function of the ischemic myocardium in the course of ejection.

Animals↗
PubMed1991

Effect of the 'specific bradycardic agent' alinidine on the function of ischemic myocardium.

In patients with coronary artery disease, the reduction of heart rate (HR) by beta-blockers can further impair myocardial function by reducing the contractility and coronary perfusion. This is possibly not the case for "specific bradycardic agents" like alinidine (ALI). The effect of ALI on ischemic myocardium, therefore, was studied in anesthetized open-chest dogs measuring left ventricular end-diastolic pressure (LVedP), dP/dt, aortic pressure (AoP) by catheter tip manometers, coronary blood flow (Q) electromagnetically, end-diastolic length (edL) and systolic shortening (sdL in %edL) of ischemic (RISC) and non-ischemic (NISC) wall segments by sonomicrometry. Group A (n = 11): Left coronary artery constriction to reduce Q (-53%) and poststenotic sdL (-54%), then i.v. injection of ALI (0.25 + 0.25 + 0.5 + 1.0 mg/kg), thereafter atrial pacing at HR before ALI. Group B (n = 9): Installation of an aorto-coronary bypass, pump-perfused at 50% of free flow, infusion of ALI into the bypass. The results showed that ALI iv dose-dependently reduced HR from 135/min to 90/min, LVedP rose from 8.6 to 10.0 mmHg and NISC-edL from 14.1 to 14.6 mm indicating increased ventricular filling. Non-ischemic systolic shortening did not change. Ischemic systolic shortening was improved from 9.2% to 17.5%, which was not due to an increase in RISC-edL (14.8 versus 14.7 mm), enhanced RISC-Q (13 versus 12 ml/min), reduced AoP (86 versus 84 mmHg) or change in inotropy (dP/dtmax: 2290 versus 2240 mmhg/s), but the increase in RISC-sdl correlated closely (r greater than 0.85) to the reduction in HR (oxygen-demand).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Relation between epicardial electrograms and signal-averaged electrocardiograms after acute myocardial infarction in dogs.

Signal-averaged electrocardiograms allow the non-invasive detection of late potentials which represent locally delayed conduction in the myocardium. To validate this method, it is necessary to compare the signal-averaged data with electrograms recorded directly from the heart. However, the studies performed to date involve only a consecutive collection of the invasively and non-invasively obtained data. To obtain a more direct comparison, we examined this relation at operation by simultaneous epicardial and signal-averaged measurements. Acute infarction in animals was chosen, because the ischemic area is a zone of delayed conduction whose presence can be verified in a signal-averaged electrocardiogram. For this purpose, the left anterior descending artery, proximal of large septal and diagonal branches, was tied off in nine mongrel dogs after thoracotomy. Before infarction, a signal-averaged electrocardiogram was recorded from the body surface. At the same time, epicardial electrograms were performed using bipolar electrodes both from the supply area of the left anterior descending artery and from that of the circumflex artery. Five minutes after coronary ligation, both the epicardial measurements and the signal-averaged electrocardiogram were repeated on the open thorax. Before occlusion of the left anterior descending artery, narrow activation complexes occurred in general in the epicardial electrograms and no late potentials were recorded in any dog by the signal-averaged electrocardiogram. Five minutes after coronary ligation, fractionated and prolonged electrograms occurred in the epicardial recordings from the ischemic zone, while the activation complexes in the uninfarcted supply area of the circumflex artery remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Effects of Nd: YAG laser coagulation of myocardium on coronary vessels.

Laser coagulation of arrhythmogenic myocardium proved to be an effective surgical therapy for refractory arrhythmias. To determine the influence of Nd: YAG laser coagulation of myocardium on coronary vessels, a total of 48 transcatheter laser impacts (10 W, 10 sec, 7 W mm2) were directed to the left ventricular free wall via endocardial (24 lesions in 2 dogs) or epicardial (24 lesions in 2 dogs) approach. In 8 of 24 endomyocardial lesions (2 and 6 months old) coronary vessels with a diameter of greater than 50 microns were found within the coagulation zones. The volume of these lesions was significantly (P less than 0.01) smaller (139 +/- 43 mm3) than those (n = 16) with coronary vessels measuring less than 50 microns (311 +/- 87 mm3). Volumes of epimyocardial lesions (1-2 hours old) produced by transcoronary irradiation with normal coronary blood flow were significantly (P less than 0.01) smaller (31 +/- 17 mm3) than with reduced (73 +/- 22) or interrupted (119 +/- 34 mm3) blood flow (n = 8, each). Both directly irradiated coronary vessels and those found within the coagulation zones and scars appeared histologically normal through all layers with an intact intima without fibrosis or thrombosis. The ultrastructure of irradiated arteries, even with total interruption of blood flow, was no different from that of non-irradiated controls. Thus, coronary artery blood flow significantly reduces the volume of coagulated myocardium, whereas the vessels themselves appear to remain undamaged by laser irradiation as used for myocardial coagulation.

Animals↗
PubMed1990

Preservation versus severance of the subvalvular apparatus in mitral valve replacement: an experimental study.

Preservation of the subvalvular apparatus in mitral valve replacement has been suggested to improve postoperative left ventricular performance. As it is difficult to quantify the change in left ventricular performance clinically, an experimental model was devised to demonstrate the contribution of the subvalvular apparatus to left ventricular function. In eight dogs mitral valve replacement (St. Jude prostheses) was performed, preserving the subvalvular apparatus by plicating the leaflets with the prosthesis on the mitral annulus. Left ventricular function was assessed during volume loading with blood before and after cutting the chordae tendineae by means of electrocautery applied via flexible wires slung around the chordae and exteriorized through the left ventricular wall. Left ventricular internal diameters were measured by sonomicrometry. End-diastolic volume (LVedV) and stroke volume were determined by dye dilution and left ventricular pressure (LVP) by cathter tip manometer. The results showed that after cutting the chordae the heart rate did not differ from the pre-cut values at any LVedP. The peak left ventricular pressure was only significantly reduced at an LVedP of 5 mmHg and minor axis diameters were only increased at an LVedP of 9-12 mmHg. Significant changes were observed, however, in LV dP/dtmax (= maximum rise of LVP) (-15%), major axis end-diastolic diameter (+10%) and systolic shortening (-40%), end-diastolic volume (+18%) and ejection fraction (-16%) at any LVedP, and stroke volume (-24%) at any LVedV.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of urapidil on the performance of ischaemic myocardium in anaesthetized dogs.

The effect of urapidil on the ischaemic myocardium was studied in eight anaesthetized dogs. Stenosis of the left descending coronary artery reduced blood flow and systolic contraction of the post-stenotic myocardium by about 50%; the end-diastolic length of the post-stenotic myocardium and the end-diastolic pressure increased, while aortic pressure slightly decreased. Subsequent administration of urapidil (0.25 + 0.25 + 0.5 + 1.0 mg/kg intravenously) did not affect the systolic shortening and end-diastolic length of the myocardium supplied by the left circumflux coronary artery, while the stroke volume and the systolic shortening of the ischaemic myocardium increased. The latter was correlated with a decrease in the heart rate (r = -0.92), but not with the reduction in aortic pressure. Urapidil by itself does not impair the performance of the ischaemic myocardium, but might be beneficial in decreasing the heart rate or suppressing reflex tachycardia during reduction of the afterload.

Adrenergic alpha-Antagonists↗
PubMed1987

Thoracic duct lymph and PEEP studies in anaesthetized dogs. I. Lymph formation and the effect of a thoracic duct fistula on lymph flow.

The effect of positive end-expiratory pressure ventilation (PEEP, 11-12 mmHg, 60-90 min without, 19 h with circulatory support) on fractional escape rate of plasma proteins (FER), and on thoracic duct lymph flow draining against jugular venous (LFJVP) or atmospheric pressure (LFAP) was studied in anaesthetized dogs. FER was 10.8%/h, 15.3%/h, and 8.5%/h before, during, and after PEEP, respectively, indicating augmented lymph formation probably due to the increase in venous pressure from 4.8 to 10.8 mmHg during PEEP. LFJVP was 39 microliter/min per kg before PEEP, decreased transiently during PEEP but the steady state value (up to 19 h) was not different from control, and increased transiently after PEEP. LFAP was 37, 80, and 38 microliter/min per kg before, during, and after PEEP, respectively. Long-term PEEP increased LFAP fourfold. Changing the drainage mode during PEEP yielded an immediate increase from LFJVP = 34 to LFAP = 79 microliter/min per kg and an instantaneous reduction from LFAP = 95 to LFJVP = 35 microliter/min per kg. Lymph protein concentration and protein lymph/plasma ratio increased concomitantly with LFAP during PEEP suggesting augmented hepatic contribution to LFAP, augmented intestinal contribution was revealed by labelling intestinal lymph using olive oil orally, muscular lymph flow was not increased as shown by i.m. Evans blue. In conclusion, the augmentation of venous pressure by PEEP promotes capillary filtration but obstructs lymph drainage from the thoracic duct into the jugular vein. PEEP imbalances formation and return of lymph and affects the development and removal of oedema.

Animals↗
PubMed1987

Thoracic duct lymph and PEEP studies in anaesthetized dogs. II. Effect of a thoracic duct fistula on the development of a hyponcotic-hydrostatic pulmonary oedema.

PEEP impedes thoracic duct drainage (LF). This can be counteracted by a thoracic duct fistula. Consequently, lung oedema (LOE) should develop during PEEP more slowly with LF at atmospheric pressure (LFAP) than with LF against jugular venous pressure (LFJVP). In 12 anaesthetized dogs LOE was produced by Ringer's solution i.v. (2.5 ml/min per kg) for 6 h during PEEP (10 mmHg) with either LFAP or LFJVP. Ringer's + PEEP greatly increased aortic, pulmonary artery and wedge pressures, JVP, and cardiac output. Colloid osmotic pressures in plasma and lymph were drastically reduced, pulmonary effective filtration pressure (EFP) rose by about 20 mmHg. LFJVP increased 7-fold, LFAP about 19-fold, the respective loss of plasma proteins was 1.83 and 1.06 g/kg during 6 h. Thermal-dye extravascular lung water showed an increment of 68 with LFJVP versus 43 microliter/h/g per mmHg with LFAP. Final lung water content was at any delta EFP (12.8-31.9 mmHg) lower with LFAP than with LFJVP amounting 512 with LFJVP versus 377 microliters/g/per mmHg with LFAP. LFAP decreased the development of LOE during PEEP by bypassing the PEEP-induced high JVP and thus facilitating the removal of interstitial fluid. It is hypothesized that a thoracic duct fistula might aid the treatment of patients with LOE due to ARDS and therefore requiring high levels of PEEP.

Animals↗
PubMed1987

A new technique for the cannulation of small lymph vessels.

A method is described which allows rapid cannulation of small lymph vessels using a modified, in-dwelling cannula and a tissue glue. The method was used to cannulate hilar lymph vessels of the kidney but should but appropriate to cannulate small lymph vessels at other locations as well.

Animals↗
PubMed1987

[Determination of plasma volume with indocyanine green].

In 31 anesthetized dogs, the distribution volume (Vd) of indocyanine green (ICG, Cardiogreen) was compared to that of Evans blue (EB), which is considered to represent plasma volume. Vd was computed from the injected amount of indicator and the indicator concentration in plasma at time zero, which was obtained by extrapolation of the monoexponential decay of the indicator concentration. The decay was assessed by eight plasma samples from 10-60 min and from 5-12 min after injection of EB and ICG, respectively. EB was measured in a spectrophotometer at 640 and 720 nm; ICG was measured in a spectrophotometer at 805 nm or in a cuvette densitometer with two light sources (LEDs) of 800 and 900 nm. The decay of EB had a half-life of about 330 min, corresponding to a disappearance rate of about 13%/h; the half life of ICG was about 8.0 min, equivalent to a fractional disappearance of about 9%/min. Vd (EB) was 55 +/- 11 (n = 31) ml.kg-1 (mean +/- SD), Vd (ICG) was 55 +/- 12 (n = 20) and 56 +/- 10 (n = 20) ml.kg-1 when ICG was measured in the densitometer or spectrophotometer, respectively. The ICG clearance was about 5 ml.min-1 per kilogram. The accuracy of the determination of plasma volume by ICG was tested in four experiments in two splenectomized dogs. Changes in plasma volume by volume load, enforced diuresis, hemorrhage, and reinfusion were determined by ICG and compared to the theoretical changes calculated from the hematocrit and removed volumes. The mean difference between measured and calculated values was 1.3 +/- 3.4% (n = 14).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Renin-angiotensin system responses of acute graded hemorrhage in dogs.

The effect of acute hemorrhage on hemodynamics and the renin-angiotensin system (RAS) was studied in eight anesthetized dogs. Stepwise blood loss to 17 +/- 6.2 ml/kg within 9 to 33 min decreased cardiac output (CO) to 42.8% of control. Mean arterial blood pressure was decreased to 35%, peripheral vascular resistance (PVR) was 1.58-fold increased, plasma renin activity (PRA) and plasma renin concentration (PRC) were increased 3.6-fold and 4.3-fold, respectively, angiotensin I (A I) concentration in plasma was 3.7-fold increased, angiotensin II (A II) was 3.8-fold increased, and A I-degrading enzyme was strongly decreased. Angiotensinogen, A I-converting enzyme, and A II-degrading enzyme activities into blood circulation were not significantly changed. The minimal blood loss to activate the RAS was 3 ml/kg. The rate of plasma active renin (PRA and PRC) increase depended on the velocity of blood withdrawn. PRA was correlated inversely to CO. PVR correlated linearly to increased plasma angiotensin concentrations. The experiments conducted demonstrate the high sensitivity and prompt activation of RAS to blood loss and suggest that RAS is involved in the regulating mechanisms of hemodynamics during acute graded hemorrhage. The stimulation of RAS supports survival of grave blood loss.

Acute Disease↗
PubMed1986

[Effect of hyperoncotic volume administration on capillary protein filtration and lymph flow in the thoracic duct].

The effect of an intravenous injection (2 ml/kg) of hyperoncotic (30 g%) Dextran (MW 60000) or Albumin on lymph formation and thoracic duct lymph flow was studied in 16 dogs. As a result of the injection, plasma colloid osmotic pressure increased, plasma volume increased due to fluid reabsorption from the extravascular compartment, and thus cardiac output became enhanced. Total body lymph formation was not affected as shown by an unchanged transcapillary disappearance rate of macromolecules. Thoracic duct lymph flow, however, was increased. The concomitant augmentation of lymph protein concentration and the elevated hepatic blood flow following the injection of hyperoncotic Dextran show that the increased thoracic duct lymph flow was probably brought about by an increase in hepatic lymph flow.

Animals↗