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Biomedical subjects

L Priebe

Publications and source records attributed to L Priebe.

At least 19 recordsLinked to original sources
PubMed2000

The ultrarapid and the transient outward K(+) current in human atrial fibrillation. Their possible role in postoperative atrial fibrillation.

Atrial fibrillation (AF) causes distinct changes in atrial conduction, characterized as electrical remodeling. Experimental data on the possible significance of alterations of specific K(+)outward currents in this process are still limited in human AF. The ultra-rapid delayed rectifier current (I(Kur)) has not been studied in AF with respect to its sensitivity to 4-Aminopyridine (4-AP). To clarify the role of (1) the 4-AP sensitive I(Kur)current, compared to recordings without using 4-AP (I(Kur*)), and (2) the transient outward current (I(to)) in changes of atrial repolarization associated with AF, whole cell voltage-clamp recordings were obtained from atrial myocytes of patients undergoing elective cardiac surgery, with and without a history of atrial fibrillation (AF/non-AF). Further, a possible relation between experimental data and postoperative AF was studied. In AF patients, I(Kur*)was reduced by 40% [5.00+/-0.32 pA/pF (non-AF) and 2.91+/-0. 45 pA/pF (AF) at +50 mV, P<0.0001, n=22/11], I(Kur)by 55% [3.81+/-0. 30 pA/pF (non-AF) and 1.71+/-0.20 pA/pF (AF) at +50 mV, P<0.0001, n=22/11]. The mean amplitude of I(Kur)was significantly smaller than I(Kur*). Consistently, I(to)was reduced by 44% [11.57+/-0.77 pA/pF (non-AF) and 6.51+/-1.31 pA/pF (AF), P<0.01, n=25/11]. In 48% of non-AF patients, postoperative AF was detected. The corresponding voltage-clamp recordings showed a trend to reduced I(Kur*)and I(Kur)currents, although it did not reach statistical significance. The consistent reduction of all three K(+)currents investigated due to the presence of AF indicates an important association of abnormalities in cellular repolarization with the onset and the self-sustaining nature of human AF.

4-Aminopyridine↗
PubMed1999

[Chylothorax as a postoperative complication of aortocoronary bypass operation].

HISTORY AND CLINICAL FINDINGS: One month after a coronary bypass grafting operation, pericardial- und pleural effusions were found in a 75-year-old woman. Dressler-syndrome was assumed and an antiphlogistic and cortisone were prescribed. Under this therapy, the pericardial effusion disappeared, but the pleural effusion increased in size. After thoracocentesis, the diagnosis of a chylothorax could be confirmed. Three days later, the thoracic radiography was inconspicuous and the patient was discharged without changes in medication. As dyspnea occurred two weeks later, the patient was admitted to our hospital. INVESTIGATIONS: The thoracic radiography showed a reappearance of the pleural effusion. DIAGNOSIS, THERAPY AND COURSE: The laboratory test confirmed a relapse of the chylothorax. After a pleurodesis by drainage and a prescription of a high-caloric, fat-reduced diet the patient could be discharged two weeks later. The diet could be terminated two months later after a recurrence of the chylothorax had been excluded in the thoracic radiography. In the follow-up examinations, there was no evidence for a relapse of the chylothorax. CONCLUSIONS: The chylothorax is an uncommon postoperative complication of the aortocoronary bypass surgery. A relapse is likely and it can result in life-threatening cachexia. Therefore, a early and adequate therapy is important.

Aged↗
PubMed1998

Increased availability and open probability of single L-type calcium channels from failing compared with nonfailing human ventricle.

BACKGROUND: The role of the L-type calcium channel in human heart failure is unclear, on the basis of previous whole-cell recordings. METHODS AND RESULTS: We investigated the properties of L-type calcium channels in left ventricular myocytes isolated from nonfailing donor hearts (n= 16 cells) or failing hearts of transplant recipients with dilated (n=9) or ischemic (n=7) cardiomyopathy. The single-channel recording technique was used (70 mmol/L Ba2+). Peak average currents were significantly enhanced in heart failure (38.2+/-9.3 fA) versus nonfailing control hearts (13.2+/-4.5 fA, P=0.02) because of an elevation of channel availability (55.9+/-6.7% versus 26.4+/-5.3%, P=0.001) and open probability within active sweeps (7.36+/-1.51% versus 3.18+/-1.33%, P=0.04). These differences closely resembled the effects of a cAMP-dependent stimulation with 8-Br-cAMP (n= 11). Kinetic analysis of the slow gating shows that channels from failing hearts remain available for a longer time, suggesting a defect in the dephosphorylation. Indeed, the phosphatase inhibitor okadaic acid was unable to stimulate channel activity in myocytes from failing hearts (n=5). Expression of calcium channel subunits was measured by Northern blot analysis. Expression of alpha1c- and beta-subunits was unaltered. Whole-cell current measurements did not reveal an increase of current density in heart failure. CONCLUSIONS: Individual L-type calcium channels are fundamentally affected in severe human heart failure. This is probably important for the impairment of cardiac excitation-contraction coupling.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1998

Simulation study of cellular electric properties in heart failure.

Patients with severe heart failure are at high risk of sudden cardiac death. In the majority of these patients, sudden cardiac death is thought to be due to ventricular tachyarrhythmias. Alterations of the electric properties of single myocytes in heart failure may favor the occurrence of ventricular arrhythmias in these patients by inducing early or delayed afterdepolarizations. Mathematical models of the cellular action potential and its underlying ionic currents could help to elucidate possible arrhythmogenic mechanisms on a cellular level. In the present study, selected ionic currents based on human data are incorporated into a model of the ventricular action potential for the purpose of studying the cellular electrophysiological consequences of heart failure. Ionic currents that are not yet sufficiently characterized in human ventricular myocytes are adopted from the action potential model developed by Luo and Rudy (LR model). The main results obtained from this model are as follows: The action potential in ventricular myocytes from failing hearts is longer than in nonfailing control hearts. The major underlying mechanisms for this prolongation are the enhanced activity of the Na+-Ca2+ exchanger, the slowed diastolic decay of the [Ca2+]i transient, and the reduction of the inwardly rectifying K+ current and the Na+-K+ pump current in myocytes of failing hearts. Furthermore, the fast and slow components of the delayed rectifier K+ current (I(Kr) and I(Ks), respectively) are of utmost importance in determining repolarization of the human ventricular action potential. In contrast, the influence of the transient outward K+ current on APD is only small in both cell groups. Inhibition of I(Kr) promotes the development of early afterdepolarizations in failing, but not nonfailing, myocytes. Furthermore, spontaneous Ca2+ release from the sarcoplasmic reticulum triggers a premature action potential only in failing myocytes. This model of the ventricular action potential and its alterations in heart failure is intended to serve as a tool for investigating the effects of therapeutic interventions on the electric excitability of the human ventricular myocardium.

Action Potentials↗
PubMed1998

Cell swelling causes the action potential duration to shorten in guinea-pig ventricular myocytes by activating IKATP.

In guinea-pig ventricular myocytes, cell swelling by incubation in hypotonic solution caused a pronounced shortening of the action potential duration (APD90: 15.5+/-14.6% compared to control; mean +/- SD) after a latency of 12 min when the intracellular ATP concentration was 2 mM. This shortening was partially reversible within 10 min after reperfusion with isotonic solution (APD90: 80. 5+/-12.1% compared to control). With 5 mM intracellular ATP in the pipette electrode, the effect of cell swelling on the action potential was significantly reduced. Incubation with 1 microM glibenclamide, a blocker of the ATP-dependent K+ current (IKATP), abolished the swelling-induced shortening of the action potential duration, whereas incubation with 0.5 mM 4, 4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS), a blocker of the swelling-induced Cl- current (ICl,swell), had no effect on the action potential duration in hypotonic solution. Simultaneous measurements of membrane currents substantiate that IKATP is the current that underlies this effect. These results suggest that in the ischaemic myocardium IKATP may be partially activated by cell swelling, resulting in a shortening of the action potential duration before the intracellular ATP concentration has fallen below 2 mM.

Action Potentials↗
PubMed1998

An overview of Medicaid managed care litigation.

Since the enactment of Medicaid in 1965, states have had the option of offering beneficiaries enrollment in managed care arrangements. With the advent of mandatory managed care reaching millions of beneficiaries (including a growing proportion of disabled recipients), the amount and scope of litigation involving Medicaid managed care plans can be expected to grow. A review of the current litigation regarding Medicaid managed care reveals two basic types of lawsuits: (1) those that challenge the practices of managed care companies under various federal and state laws that safeguard consumer rights, protect health care quality, and prohibit discrimination; and (2) suits that assert claims arising directly under the Medicaid statute and implementing regulations, as well as claims related to Constitutional safeguards that undergird the program. Lawsuits asserting claims arising under Medicaid tend to raise two basic questions: (1) the extent to which enrollment in a Medicaid managed care plan alters existing Medicaid beneficiary rights and state agency duties under federal or state Medicaid law; and (2) the extent to which managed care companies, as agents of the state, act under "color of law" (i.e., undertaking to perform official duties or acting with the imprimatur of state authority). Additionally, states might see an increase in litigation brought by prospective and current contractors who assert that they have been wrongfully denied contracts or improperly penalized for poor performance. These assertions may involve claims that are grounded in federal and state law, the Medicaid statute, and the Constitution. Moreover, in light of the consumer protection elements of the managed care reforms contained in the Balanced Budget Act, future managed care litigation may focus on the manner in which companies carry out states' obligations toward managed care enrollees. Resolution of Medicaid managed care cases involves the application of general principles of administrative and regulatory law. Thus, Medicaid managed care cases have implications for other public purchasers of managed care arrangements, including state mental health and alcohol and substance abuse agencies.

Consumer Advocacy↗
PubMed1996

Functional interaction between K(ATP) channels and the Na(+)-K(+) pump in metabolically inhibited heart cells of the guinea-pig.

1. Transmembrane current through ATP-regulated K(+) channels (IK(ATP)) was measured in ventricular heart cells of the guinea-pig in the whole-cell and cell-attached patch configurations under conditions of metabolic poisoning with the mitochondrial uncoupler 2,4-dinitrophenol (DNP). 2. Maintained exposure of the cells to DNP resulted in a transient appearance of whole-cell IK(ATP) When IK(ATP) had reached several nanoamps, blocking the forward-running Na(+)-K(+) pump with 0.5 mM strophanthidin decreased IK(ATP) after a delay. The time course of this decrease could be described by a single exponential function, which yielded a time constant(T)of 4.51+/- 1.89 s (n=8). 3. Hyperpolarization from 0 mV to -100 or -150 mV for 2 s caused IK(ATP) (measured at 0 mV) to decrease by 34.2 +/- 14.1 % (n = 8) and 37.6 +/- 9.4% (n = 8), respectively. After the hyperpolarizing pulse, IK(ATP) returned to its higher initial level within a couple of seconds. 4. Driving the pump backwards by removing the extracellular K(+) ions caused the permanent disappearance of DNP-induced IK(ATP). 5. Application of 0.5 mM strophanthidin in the absence of external K(+) ions induced a transient increase in IK(ATP), as did washing out the glycoside (n = 5). 6. When pump action was inhibited by using Na(+), K(+)-free Tyrode solution (see Methods) in the bath, strophanthidin did not have a comparable direct effect on IK(ATP). 7. In cell-attached patches, strophanthidin applied via the bath caused a reduction in IK(ATP) with a similar time course to that in whole-cell experiments. This suggests that the interaction between the pump molecules and the K(ATP) channels is not restricted to closely neighbouring molecules. 8. The data support the hypothesis that [ATP] at the cytosolic face of the membrane may drop to practically zero, thereby passing an 'ATP window' in which the channels first open and then close, and that the submembrane [ATP] is readily controlled by the cytosolic [ATP].

2,4-Dinitrophenol↗
PubMed1983

[Semiquantitative determination of the cutaneous blood flow].

A semiquantitative determination of the cutaneous blood flow is possible by a simple thermic method using a heat conduction probe. There is a quantitative uncertainty because of the possible existence of relatively big vessels which do not participate in the blood supply of the examined tissular region but in the determination of the convection within the temperature field of the thermal conduction probe. The values of blood circulation derived from the stationary temperature field will therefore always be higher than the values of the real blood supply. This procedure necessitates a determination of the tissular heat conductivity. This will not be possible in all cutaneous regions. A relative method can be useful here inserting a binding lambda G value which lies below the thermal transport value lambda for normal blood circulation.

Humans↗
PubMed1979

[Optimal measurement technic for the vasoconstrictor effect of corticosteroids. Comparative studies with reflection photometry and flow measurement].

In 20 healthy male test subjects, a non-specific ointment base was applied to the back of the hand over 16 hours. Two days later, the same ointment base with 0.25% triamcinolone acetonide was once more applied to the back of the hand over 16 hours. The light reflection of the skin was measured by reflection photometry and the heat transport coefficient was measured fluvographically under the condition of the tourniquet test. The results show that the vasoconstrictor effect of triamcinolone acetonide is best detected by the reflection photometric measurements. In fluvographic measurement, the heat transport coefficient is most affected in maximal reactive hyperemia when the tourniquet has been removed. Application of the base led to a reduction of the blood flow and the water content of the skin after 16 hours, whereas the water content of the skin was unaffected in the presence of triamcinolone acetonide.

Adrenal Cortex Hormones↗
PubMed1975

Methods of thermal blood flow measurement.

All techniques for measuring thermal blood flow have in common a small heat source and two temperature difference sensors placed in or on the tissue. The measured temperature difference can be quasistationary, nonstationary or constant, depending upon the heating pattern. Its extent and course, respectively the heating output in the case of pulse fluvography, are dependent upon blood flow. Conversion of the heat transport coefficient into specific blood flow is possible only if the vessels in the temperature field are predominantly capillaries. Both the sink and the pore theory make it possible to draw conclusions about specific blood flow from the measurement values obtained.

Animals↗