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Biomedical subjects

C F Vahl

Publications and source records attributed to C F Vahl.

At least 73 records · Page 4Linked to original sources
PubMed1998

Triiodothyronine reverses depressed contractile performance after excessive catecholamine stimulation.

BACKGROUND: Conflicting results have been reported regarding the acute effects of triiodothyronine (T3) on myocardial contractile performance. The present study analyzes the role of T3 in reversing the depressant effect of excessive catecholamine stimulation in isolated porcine left ventricular myocardium. METHODS: Thirty-six left ventricular trabeculae (0.4 x 6.0 mm) obtained from 6 pigs were used for measurements of isometric force development, isotonic shortening, and intracellular calcium in three experimental series (measurement conditions: 37 degrees C; optimal length; supramaximal electrical stimulation, 1 Hz; calcium measurement, fura-2 ratio method; frequency, 225 Hz). In series 1, isometric force development was measured before and after a 60-minute incubation with 10(-7) mol/L epinephrine in preparations with (n = 6) and without (n = 6) preceding fura-2 loading for calcium measurements. In series 2, the acute effects of a 30-minute administration of T3 (10(-9) mol/L) on isometric force and intracellular calcium were analyzed (n = 6). In series 3, after simultaneous fura-2 loading and a 6-hour 10(-7) mol/L epinephrine exposure the effects of T3 (10(-9) mol/L, 30 minutes) on force development, shortening, and intracellular calcium transient were analyzed. RESULTS: Long-term and high-dose epinephrine exposure induced a severe contractile depression with a significant reduction of isometric force development (p < 0.05) and increased diastolic (p < 0.001) and systolic calcium (p < 0.001). In normal porcine myocardium T3 had no effect on the extent of isometric force generation but accelerated the time course of force development (p < 0.05) and increased the calcium transient (p < 0.001). After induction of myocardial depression by epinephrine exposure T3 accelerated the intracellular calcium transients and reduced diastolic calcium. Triiodothyronine increased the shortening amplitude and the force amplitude (p < 0.01). CONCLUSIONS: Triiodothyronine reverses depressed contractile performance after preceding high-dose epinephrine exposure in isolated porcine myocardium. Increased force amplitudes and unaltered or even reduced intracellular calcium transients argue in favor of a resensitization of the contractile apparatus for calcium by T3. The study supports a potential role for T3 treatment in depressed myocardium after previous excessive catecholamine exposure (eg, brain death, catecholamine treatment, ischemia).

Animals↗
PubMed1998

Endothelin-A and -B antagonists protect myocardial and endothelial function after ischemia/reperfusion in a rat heart transplantation model.

OBJECTIVE: Previous studies suggested that endothelin-1 (ET-1) may play a pathophysiological role in myocardial ischemia/reperfusion injury. This study was designed to investigate the effects of the selective ET-A receptor antagonist BQ123 and the selective ET-B receptor antagonist BQ788 on myocardial and endothelial function after reversible deep hypothermic ischemia in a heterotopic rat heart transplantation model. METHODS: Isogenic intraabdominal heterotopic transplantation was performed in Lewis rats. After 1 h of cold ischemic preservation reperfusion was started either after application of placebo (control), BQ123 (3 mumol/kg/min). BQ788 (3 mumol/kg/min), ET-1 (8 pmol/kg/min) or simultaneous infusion of BQ123 or BQ788 and ET-1, respectively (n = 12 each). An implanted balloon was used to obtain pressure-volume relations of the transplanted heart. Myocardial blood flow (MBF) was assessed by the hydrogen-clearance method. Measurements were taken after 1 and 24 h of reperfusion. Endothelium-dependent vasodilation to acetylcholine (ACH) and endothelium-independent vasodilation to sodium nitroprusside were also determined. RESULTS: Both BQ123 and BQ788 significantly improved myocardial and endothelial functional recovery during early reperfusion, whereas ET-1 significantly impaired myocardial and endothelial function. Simultaneous infusion of ET-1 diminished the effects of BQ123 and BQ788. Although myocardial function and baseline MBF were similar in all groups after 24 h of reperfusion, endothelium dependent vasodilation to ACH was still significantly higher in the BQ123 and BQ788 groups and lower in the ET-1 groups (p < 0.05). CONCLUSIONS: These results suggest that endogenous ET release is involved in the pathogenesis of reperfusion injury after heart transplantation. ET-A and ET-B receptor antagonists may be useful to reduce ischemia/reperfusion injury.

Acetylcholine↗
PubMed1998

Right ventricular function after brain death: response to an increased afterload.

OBJECTIVE: A major cause of early postoperative morbidity and mortality after cardiac transplantation is right ventricular (RV) failure which is attributed to the inability of the donor's RV to acutely compensate for the recipient's elevated pulmonary vascular resistance. This study was performed to determine: (1) the acute effects of brain death on the RV function; and (2) the adaptation potential of the RV to a progressive increase in RV afterload. METHODS: In 13 anesthetized, open-chest dogs (eight with brain death vs. five control with sham operation), brain death was induced by inflation of a subdural balloon catheter. Heart rate, RV systolic and end-diastolic pressure (RVSP, RVEDP), pulmonary arterial pressure (PAP), and cardiac output (CO), and pressure-length loops (sonomicrometry) were recorded. Afterload increase was induced 2 h after brain death induction by constriction of the pulmonary artery with an increase in RVP from 25 to 50 mmHg in 5 mmHg steps. RESULTS: Cushing phenomenon occurred within a few minutes after brain death induction, with a significant increase of HR (229 +/- 10 vs. 89 +/- 6 min(-1), P < 0.001), CO (3.2 +/- 0.2 vs. 1.7 +/- 0.1 l/min, P < 0.001), PAP (30.4 +/- 2.5 vs. 15.5 +/- 1.3 mmHg, P < 0.01) RVSP (55 +/- 5 vs. 23 +/- 2 mmHg, P < 0.001) and RVEDP (7.4 +/- 0.9 vs. 3.3 +/- 0.6 mmHg, P < 0.001). All these values were also significantly (P < 0.01) higher than the time corresponding values of the control group. The analysis of the pressure-length loops showed a hypercontractile state. Within 15-60 min, all parameters turned to baseline and remained stable for up to 2 h. When afterload was increased progressively, RVEDP increased markedly in the brain death and slightly in the control group (9.4 +/- 0.7 vs. 4.2 +/- 1.1 mmHg, P < 0.01, at RVSP = 50 mmHg). On the other hand, the increase of peak positive dP/dt was significantly higher in the control group (430 +/- 37 vs. 644 +/- 55 mmHg/s, P < 0.01, at RVP = 50 mmHg). However, global RV pump function characterized by CO and stroke work was similar in both groups. While regional RV contractility remained unchanged in the brain death group in terms of pressure-length relationships, RV contractility significantly increased in the control group. CONCLUSION: (1) Brain death per se does not result in an acute impairment of RV function. (2) While control animals adapt to an increased afterload by the homeometric, as well as the heterometric regulation, after brain death, an increase in RV preload follows elevations in RV afterload by the Frank-Starling mechanism subserving the increased stroke work required to ensure unchanged pump function.

Adaptation, Physiological↗
PubMed1998

Endothelin-A receptor antagonist BQ123 protects against myocardial and endothelial reperfusion injury.

BACKGROUND: This study was designed to investigate the effects of the selective endothelin-A receptor antagonist BQ123 on myocardial and endothelial function after reversible deep hypothermic ischemia and reperfusion. METHODS: Isogenic intra-abdominal heterotopic heart transplantation was performed in Lewis rats. After one hour of cold ischemic preservation reperfusion was started after application of either saline vehicle or BQ123 (1 micromol/L). Left-ventricular pressure-volume relations and myocardial blood flow were assessed after one and 24 hours of reperfusion. Responses to endothelium-dependent vasodilator acetylcholine and endothelium-independent vasodilator sodium nitroprusside were also determined. RESULTS: BQ123 significantly improved myocardial contractility, as indicated by the leftward shift of the systolic pressure-volume relation and significantly increased myocardial blood flow during early reperfusion (p < 0.05). Although myocardial function and baseline myocardial blood flow were similar in both groups after 24 hours of reperfusion, endothelium-dependent vasodilatation was still significantly higher in the BQ123 group (p < 0.05). CONCLUSIONS: These results suggest that endothelin-A receptor antagonists may be useful in reducing ischemia/reperfusion injury after heart transplantation by preservation of myocardial and endothelial function.

Animals↗
PubMed1998

Heterogeneity of myocardial edema in isolated pig hearts after perfusion with different types of cardioprotective solutions.

The extent and distribution of myocardial edema induced by perfusion with cardioprotective solutions is of great interest. Domestic pig hearts (n = 12) were perfused in situ after aortic cross clamping either with Bretschneider's cardioplegic solution (HTK, 4 degrees C, n = 3), with a heparinized Krebs-Henseleit solution containing 30 mmol/L 2,3 Butanedionemonoxime (BDM, 4 degrees C, n = 3) or with heparinized pig blood (HPB, 24 degrees C, n = 3). After a three-hours storage period, magnetic resonance tomography (MRI) was carried out. The acquired T1-weighted data were used for the subsequent three-dimensional reconstruction based on the "Heidelberg ray-tracing technique". The small myocardial tissue blocks (n = 216) were excised from these hearts for dry weight measurements for 9 preselected regions in duplicate including ventricular papillary muscle, ventricular free wall, ventricular septum, apex, and atrial tissue. In control hearts (n = 3), dry weight was measured immediately after explantation (no MRI). The results of dry-weight measurements and three dimensional visualization were compared. Dry-weight measurements revealed that considerable myocardial edema is induced by any of the experimental procedures. The effects were most pronounced after BDM perfusion. Regardless how the edema was induced, there were significant differences of the water content within the heart: the water content in the heads of the papillary muscles and in the interventricular septum was always smaller than that of the free left- and right-ventricular walls. The heterogeneity of myocardial edema and its spatial distribution pattern could be qualitatively visualized. The experimental data (biophysical data and 3D visualization) clearly show a heterogeneity of myocardial edema induced by different types of cardioprotective solutions. As the presence of myocardial edema represents one of the crucial events in the pathophysiology of myocardial dysfunction occurring during myocardial infarction, ischemia, heart transplantation, and extracorporeal circulation, the present study represents an interesting contribution towards intravital detection and distribution of myocardial edema.

Animals↗
PubMed1998

The role of coronary perfusion changes in cardiac dysfunction associated with brain death.

BACKGROUND: Previous studies described a hemodynamic instability in the potential organ donor which has clinical relevance for cardiac transplantation. The possible pathophysiological link between altered loading conditions, coronary perfusion, and cardiac function after brain death has not been investigated yet. Therefore this study was undertaken to investigate the role of coronary perfusion changes during brain death in cardiac dysfunction. METHODS: Dogs on cardiopulmonary bypass provided iso-volumetric left-ventricular (LV) contractions. By protocol, coronary perfusion pressure was kept at the level of mean aortic pressure. LV pressure, LV dP/dt, the slope of end-systolic pressure-volume relationship (Emax), coronary blood flow (CBF), and myocardial oxygen consumption (MVO2) were measured. Brain death was induced by a subdurally placed balloon-catheter. RESULTS: Induction of brain death led to a transient hyperdynamic response with a significant increase of aortic and LV pressure, dP/dt, Emax, CBF, and MVO2. Thereafter, aortic pressure and, parallelly, LV pressure, dP/dt, Emax, CBF, and MVO2 decreased significantly. However, if coronary perfusion pressure was decoupled from aortic pressure and elevated to pre-brain death level, CBF and myocardial contractility were restored to baseline level. CONCLUSION: The impairment of coronary blood flow may contribute to decreased contractility after brain death.

Animals↗
PubMed1998

Effects of nitric oxide synthesis on reperfusion injury and catecholamine responsiveness in a heterotopic rat heart-transplantation model.

Global myocardial ischemia and reperfusion injury play a major role in early postoperative graft dysfunction. In this study, the influence of nitric oxide (NO) on reperfusion injury and catecholamine sensitivity after ischemia was investigated in a heterotopic rat heart-transplantation model. After a 1-h ischemic preservation, reperfusion was started either after application of saline vehicle (control, n = 8) or nitro-L-arginine methyl ester (L-NAME; 10 mg/kg, n = 8) for inhibition of NO synthesis or NO-precursor L-arginine (L-Arg; 40 mg/kg, n = 8), or L-NAME plus L-Arg (n = 8), respectively. After 60 min of reperfusion, continuous dobutamine infusion (5 microg/kg/min) was started. Myocardial blood flow was assessed by the hydrogen-clearance method. An intraventricular balloon was used to measure pressure-volume relations: peak left ventricular pressure, the rate of pressure development (dP/dt), end-diastolic pressure, and isovolumic relaxation constant. Myocardial blood flow was significantly reduced after L-NAME and increased after L-Arg in comparison with control (p < 0.05). The L-NAME group showed decreased systolic and diastolic functional recovery in comparison with control. Simultaneous infusion of L-Arg and L-NAME reversed these effects. L-Arg alone led to a further improvement of cardiac functional recovery. Whereas myocardial blood flow remained unchanged in the L-NAME group with dobutamine infusion, it significantly increased in the control group (p < 0.05). L-Arg antagonized this effect of L-NAME. Dobutamine increased peak left ventricular pressure and dP/dt and shortened the isovolumic relaxation constant in all groups; however, the changes of systolic hemodynamic indices were significantly smaller in the L-NAME group (p < 0.05) and significantly higher in the L-Arg group (p < 0.05). These results indicate that (a) NO production within the graft during reperfusion has a significant beneficial effect on graft function, and (b) NO formation may play an important role in beta-adrenergic responses after heart transplantation.

Adrenergic beta-Agonists↗
PubMed1998

Effects of brain death on myocardial function and ischemic tolerance of potential donor hearts.

BACKGROUND: An increasing number of experimental and clinical studies reports hemodynamic instability in the donor organism after brain death. However, the relative importance of brain death-related cardiac dysfunction on posttransplantation cardiac function and the reversibility of the observed changes remain controversial. In this study a load-independent analysis of cardiac function after brain death was performed. Special interest was focused on a possible interactive influence of brain death and cardiac preservation on postischemic cardiac function. METHODS: In 12 anesthetized dogs, brain death was induced by inflation of a subdural balloon; 12 sham-operated animals served as control subjects. After a 2-hour observation in situ, the hearts were explanted and perfused parabiotically either immediately or after hypothermic ischemic preservation (4 hours, 4 degrees C). Heart rate, cardiac output, left ventricular pressure, the maximum of left ventricular pressure development and aortic pressure were measured in situ. In addition, the slope of the end-systolic pressure-volume relationship, coronary blood flow, and myocardial oxygen consumption were estimated in the cross-circulated hearts. RESULTS: In spite of a brain death-associated hemodynamic deterioration in situ (expressed as low mean aortic pressure and significant decrease of maximal dP/dt), myocardial function was similar to control after explantation, if assessed ex vivo. Furthermore, after hypothermic ischemic preservation and reperfusion, complete functional recovery of control and brain-dead hearts could be observed. CONCLUSIONS: These data indicate that hemodynamic instability after brain death may rather reflect altered loading conditions than irreversible myocardial damage or primary cardiac dysfunction. Furthermore, there is no evidence for a brain death-related impairment of ischemic tolerance.

Animals↗
PubMed1998

The effect of triiodothyronine on myocardial contractile performance after epinephrine exposure: implications for donor heart management.

BACKGROUND: This study analyzes in the experimental model of isolated human atrial myocardium whether the myocardial contractile depression occurring after high-dose/long-term catecholamine exposure (as typically occurring in brain-dead organ donors) can be reversed by thyroid hormone administration. METHODS: Isolated trabeculae were prepared from atrial myocardium from patients undergoing coronary artery bypass (n = 15). Initial measurements of isometric force were carried out (measurement conditions of 37 degrees C, Krebs Henseleit solution, supramaximal electrical stimulation, 1 Hz, at optimal length). Then the trabeculae were incubated for 6 hours at 26 degrees C in a Krebs Henseleit solution containing epinephrine 10(-7) mol/L and the fluorescent dye FURA-2/AM for calcium measurements. At the end of the incubation period, isometric force, isotonic shortening, and intracellular calcium transient (FURA-2 "ratio method") were measured. After 30 minutes administration of triiodothyronine (5 x 10(-9) mol/L), the measurements were repeated. Control groups included 6 hours incubation in 4 degrees C Krebs Henseleit solution (n = 5); 6 hours incubation in 26 degrees C FURA-2/AM (n = 5); and 6 hours incubation in epinephrine 10(-7) mol/L (n = 5). RESULTS: After 6 hours catecholamine exposure isometric force declined significantly to 56.8% (p < .0001) and isotonic shortening to 54% of its initial value (p < .01). Administration of triiodothyronine was associated with a significant recovery of the isotonic shortening amplitude (p < .005), of isometric force development (p < .01), an increased velocity of force development (p < .0001), and of diastolic force decay (p < .005). At the same time the shape of the intracellular calcium transient became smaller as a result of an accelerated diastolic decay. The amplitude of the calcium transient remained unaltered, whereas the calcium time integral was reduced (p < .05). CONCLUSION: In the model of isolated human myocardium, experimental depression of the contractile performance resulting from long-term catecholamine exposure could be reversed by a 30-minute triiodothyronine incubation. The experimental data showing increased force amplitudes at unaltered amplitudes of the intracellular calcium transient and an even-reduced calcium time integral provide strong evidence for a sensitization of the contractile apparatus for calcium by triiodothyronine. The data provide additional knowledge to explain the successful administration of triiodothyronine in donor heart management.

Calcium↗
PubMed1997

Is the brain death related endocrine dysfunction an indication for hormonal substitution therapy in the early period ?

Experimental studies in animals have suggested that brain death (BD) -- related endocrinological dysregulations lead to a significant depression of cardiac pump and muscle function, however, the discussion about the relative extent of this influence remains controversal. The aim of the present study was to assess in an open chest animal model the short time course (5 hours) of hormonal (epinephrine, norepinephrine, T3, T4, ACTH, cortisol, insuline) and metabolic (glucose, lactate) changes in 10 brain dead dogs with special respect to the hemodynamic stability and myocardial pump function. After the onset of BD the concentrations of all hormonal parameters showed a significant decrease. Despite these changes, and in contrast to other studies, an adequate pump function (filling pressures, cardiac output) and muscle function (LVdp/dt) could be maintained by exclusive volume substitution without the use of hormonal or pressor agents. We conclude that in the present model a sufficient pump and muscle function can be maintained by adequate volume substitution, exclusively. The significant fall in adrenal and thyroid hormones had no direct effects on heart functional parameters in the first 5 hours after experimental BD induction.

Animals↗
PubMed1997

Dual effect of digitalis glycosides on norepinephrine release from human atrial tissue and bovine adrenal chromaffin cells: differential dependence on [Na+]i and [Ca2+]i.

It was the aim of the present study (1) to characterize the influence of Na+/K(+)-ATPase inhibition by the digitalis glycoside ouabain on both spontaneous and nicotine-evoked norepinephrine release from the human heart; and (2) to further investigate the role of glycoside-induced changes in [Na+]i and [Ca2+]i (determined by microfluorimetry) for catecholamine release. The latter experiments were performed in bovine adrenal medullary chromaffin cells (BCC), an established cell culture model for sympathetic nerves. Ouabain (1-1000 mumol/l) exerted a dual effect on norepinephrine release (determined by HPLC) from incubated human atrial tissue: (I) Ouabain induced a concentration-dependent increase in norepinephrine release, that was calcium-independent and almost completely prevented by blockade of the uptake1-carrier by desipramine (1 mumol/l). The characteristics of this release process are consistent with a non-exocytotic mechanism. (II) In addition, ouabain augmented the nicotine-evoked (1-100 mumol/l) calcium-dependent norepinephrine release, which can be considered to be exocytotic. Na+/K(+)-ATPase inhibition also reduced the threshold concentration of nicotine from 10 to 1 mumol/l and it delayed the rapid tachyphylaxis of its norepinephrine releasing effect in human atrial tissue. In BCC, ouabain increased [Na+]i, [Ca2+]i and [3H]-norepinephrine release in parallel. Under calcium-free conditions, not only the ouabain-induced increase in [Na+]i, but also [3H]-norepinephrine release were enhanced. The ouabain-induced [3H]-norepinephrine release was always closely related to changes in [Na+]i, indicating a key role of [Na+]i for this calcium-independent non-exocytotic norepinephrine release. In addition, pretreatment with ouabain (1 mmol/l) augmented the nicotine-evoked (0.1-10 mumol/l) increments in [Na+]i, [Ca2+]i and [3H]-norepinephrine release. As nicotine-induced norepinephrine release depends on an increase in both [Na+]i and [Ca2+]i, these findings are indicative of an ouabain-mediated facilitation of exocytosis. In conclusion, increasing [Na+]i and [Ca2+]i inhibition of Na+/K(+)-ATPase by ouabain triggers non-exocytotic norepinephrine release, and facilitates nicotine-evoked exocytotic norepinephrine release.

Adrenal Medulla↗
PubMed1997

Myocardial length-force relationship in end stage dilated cardiomyopathy and normal human myocardium: analysis of intact and skinned left ventricular trabeculae obtained during 11 heart transplantations.

UNLABELLED: The Frank-Starling-mechanism (FSM) was analyzed in isolated intact and skinned human left ventricular myocardium obtained from 11 heart transplantations (normal donor hearts (NDH), n = 8; dilated cardiomyopathy (DCM), n = 11). The new technique to utilize muscle strips from normal donor hearts which were actually implanted is described in detail. METHODS: I) In electrically stimulated left ventricular trabeculae (37 degrees C, oxygenated Krebs-Henseleit solution, supramaximal electrical stimulation, frequency 1 Hz) force development was analyzed as a function of muscle length (NDH = 8; DCM = 11). II) In an additional series left ventricular myocardium was demembranized ("skinned") by Triton-X-100. At different sarcomere lengths and calcium concentrations corresponding to pCa values of 4.3, 5.5, and 8.0 force development was measured (DCM = 11; NDH = 9). RESULTS: I) Developed force increased up to an optimum as a function of muscle length in intact NDH- and DCM-myocardium. However, the relative increment of developed force after any length step was smaller in DCM than in NDH. Near "Lmax" (muscle length associated with maximum developed force) passive resting tension was considerably elevated in DCM, indicating significantly increased diastolic stiffness. II) In skinned left ventricular DCM- and NDH-myocardium developed force depended on sarcomere length with an optimum near 2.2 microns. However, a reduction of activator calcium concentration from pCa 4.3 to pCa 5.5 produces a smaller percent decline in force at short sarcomere lengths in DCM than it does in NDH. CONCLUSION: The present study shows that except for diastolic stiffness and a smaller relative force increment after any length step in DCM the Frank Starling mechanism is still present in isolated human left ventricular DCM- as in NDH-myocardium. The current study does not allow to decide whether in skinned myocardium the smaller percent decline in force after reduction of activator calcium concentrations in DCM is caused by an increased calcium sensitivity at short sarcomere lengths or decreased sensitivity at long sarcomere lengths.

Calcium↗
PubMed1997

[Calibration of clinical databanks with "virtual patients"].

The scientific value of multicenter studies is still questionable, as there are no methods available that allow to determine whether in fact identical items are recorded in the same way in different centers. Subjective classifications (for example according to the New York Heart Association (NYHA)), definitions of items, documentation habits and procedures may not be comparable in different hospitals. For that reason the concept of a "virtual patient" for calibration of database systems was developed as a new methodological approach. The "virtual patients" describes a computer program that includes and uses multimedia-tools to represent an exactly defined patient. A sound card enables a patient to talk and to represent intracardial and intrapulmonary sounds. Additional information including echocardiographic sequences, perioperative video sequences, x-ray analysis, angiograms, etc. is represented in the program. Thus during the perioperative course of a patient the complete relevant pre-, intra- and postoperative information regarding the patient is provided. Any physician participating in a multicenter study is asked to record the data of this virtual patient and to store it in a database system using the sheets applied in a multicenter study. As the patient is exactly defined (virtual patient) incorrect classifications and incomplete recordings, etc. can easily be detected and discussed. The virtual patient is a tool that allows calibration of database systems by direct comparison of the documentation technique between different physicians and different hospitals participating in multicenter studies. It is thus a multimedia-instrument to support standardization and quality assurance of database systems.

Calibration↗
PubMed1997

Successful revascularisation for unstable angina of a patient with asymptomatic bilateral internal carotid occlusion, 70% stenoses of the external carotid arteries, and other circulation disturbances.

Nowadays, advanced surgical and anaesthesiological techniques of coronary artery bypass grafting minimize the risk of severe complications in patients with advanced arteriosclerotic cerebrovascular disease. Nevertheless, in case of highly compromised cerebrovascular status, the decision whether to undertake coronary artery bypass grafting or not requires special patient-related consideration. A severe, unstable angina made it necessary to perform coronary bypass grafting in a patient with bilateral internal carotid occlusion, a bilateral mid-stage stenosis of both external carotid arteries, a diminished flow within the right vertebral artery, and a subsequently impaired intracranial blood flow. Intraoperatively, besides the usual hemodynamic measurements, laser-Doppler flow probes were placed on the left and right upper temple to monitor relative changes of the cerebral blood supply. Using an individual perioperative management, the patient experienced a normal postoperative course and was discharged in good condition.

Aged↗
PubMed1997

Contractile behaviour and intracellular calcium during afterloaded contraction in mitral valve disease.

It was the aim of the present study to analyze left-ventricular contractile behaviour (force development, shortening) and intracellular calcium handling using afterloaded contractions of papillary muscle fibres from patients operated upon for mitral valve stenosis (MVS, n = 12) or mitral valve incompetence (MVI, n = 15). Isometric force development and passive resting tension at Lmax were similar in MVI and MVS (n.s.). Isotonic shortening amplitudes were reduced in MVI (p < 0.0001) compared to MVS. The peak intracellular calcium transient (ICT) preceeded the maximum force- and shortening amplitude in MVI and MVS. The amplitude of the ICT rose with decreasing afterload, became broader during shortening and presented a prolongation of the diastolic decay. Those differences were much more pronounced in MVI. The calcium-time integral (CTI) at minimal load (isotonic contraction) was 119 +/- 5% in MVS and 165 +/- 14% in MVI (p < 0.0001). The data reveal a severe diastolic calcium overload during shortening in left-ventricular MVI myocardium. An increased dissociation rate of calcium from the contractile proteins during shortening, a depressed calcium re-uptake into the sarcoplasmic reticulum during shortening, or altered mechanosensitive ion channels in MVI may be involved.

Calcium↗
PubMed1997

[Internal quality assurance or Hawthorne effect?].

The tendency of study participation per se to affect outcome is described by the term Hawthorne effect. This process defines the first step for internal quality assurance. However, whenever an attempt is made to describe the effects of quality assurance in more detail specific mathematical tools are required, including a database system that allows the calculation of clinical profiles, problem profiles, time-related variance of variables, univariate and multivariate statistics, calculation of scores and application of the hazard function. However, it has to be considered that any mathematical model is a way to present a hypothesis and not a proof. Whenever a proof is required, one should not ask for internal quality assurance, but design a randomized study.

Cardiac Surgical Procedures↗
PubMed1997

Hemodynamic consequences of replacing the aorta by vascular grafts simulated in a mathematical model.

OBJECTIVE: Replacing parts of the aorta by a noncompliant vascular prosthesis results in marked alterations of the aortic input impedance and influences arterial hemodynamics. We propose a mathematical model of circulation able to predict hemodynamic changes after simulation of vascular grafting. METHODS: Using a mathematical 128-branch model of the human arterial system a digitized aortic flow wave was chosen as the input signal to this system. After determination of the modules of elasticity of native vascular tissue and customary prostheses in technical experiments, replacement of any part of the aorta with a prosthesis was simulated by increasing the elasticity in the parts desired. RESULTS: During control conditions, the model displayed a physiologic distribution of flow and pressure waves throughout the arterial system. Simulated replacement of the aorta resulted in an increase of pressure amplitude and a partial loss of the aortic "Windkessel" function. Calculation of the aortic input impedance showed an increase of the characteristic impedance, while the peripheral resistance remained unaltered. CONCLUSION: This mathematical model of the arterial circulation proves to be useful to simulate hemodynamic changes after implantation of vascular grafts. The results of the model analysis are consistent with previous work done in experimental setups.

Aorta↗