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Biomedical subjects

F Sterz

Publications and source records attributed to F Sterz.

106 records · Page 6Linked to original sources
PubMed1990

Moderate hypothermia after cardiac arrest of 17 minutes in dogs. Effect on cerebral and cardiac outcome.

Moderate hypothermia (30 degrees C) induced before circulatory arrest is known to improve neurologic outcome. We explored, for the first time in a reproducible dog outcome model, moderate hypothermia induced during reperfusion after cardiac arrest (resuscitation). In three groups of six dogs each (N = 18), normothermic ventricular fibrillation cardiac arrest (no blood flow) of 17 minutes was reversed by cardiopulmonary bypass--normothermic in control group I (37.5 degrees C) and hypothermic to 3 hours in groups II (32 degrees C) and III (28 degrees C). Defibrillation was achieved in less than or equal to 5 minutes and partial bypass was continued to 4 hours, controlled ventilation to 20 hours, and intensive care to 96 hours. All 18 dogs survived. Electroencephalographic activity returned significantly earlier in groups II and III. Mean +/- SD best neurologic deficit between 48 and 96 hours was 44 +/- 8% in group I, 38 +/- 12% in group II, and 35 +/- 7% in group III (differences not significant). Best overall performance category 2 (good outcome) between 48 and 96 hours was achieved in none of the six dogs in group I and in four of the 12 dogs in the combined hypothermic groups II and III (difference not significant). Mean +/- SD brain total histologic damage score was 130 +/- 22 in group I, 93 +/- 28 in group II (p = 0.05), and 80 +/- 26 in group III (p = 0.03). Gross myocardial damage was greater in groups II and III than in group I--numerically higher overall and significantly higher in group III for the right ventricle alone (p = 0.02). Moderate hypothermia after prolonged cardiac arrest may or may not improve cerebral outcome slightly and can worsen myocardial damage.

Animals↗
PubMed1990

Hypertension with or without hemodilution after cardiac arrest in dogs.

We studied blood flow-promoting therapies after cardiac arrest in 18 dogs. Our model consisted of ventricular fibrillation (no blood flow) lasting 12.5 minutes, controlled reperfusion with cardiopulmonary bypass and defibrillation within 5 minutes, controlled intermittent positive-pressure ventilation to 20 hours, and intensive care to 96 hours. Group I (control, n = 6) dogs were reperfused under conditions of normotension (mean arterial blood pressure 100 mm Hg) and normal hematocrit (greater than or equal to 35%). Group II (n = 6) and III (n = 6) dogs were treated with norepinephrine at the beginning of reperfusion to induce hypertension for 4 hours. In addition, group III dogs received hypervolemic hemodilution to a hematocrit of 20% using dextran 40. There were no differences in the time to recovery of electroencephalographic activity among groups. All six group I dogs remained severely disabled; in groups II and III combined, six of the 12 dogs achieved good outcome (p less than 0.01). Some regional histopathologic damage scores at 96 hours were better in groups II and/or III than in group I (neocortex: p less than 0.05 group II different from group I; hippocampus: p less than 0.01 both groups II and III different from group I). Total histopathologic damage scores were similar among the groups. A hypertensive bout with a peak mean arterial blood pressure of greater than or equal to 200 mm Hg beginning 1-5 minutes after the start of reperfusion was correlated with good outcome (p less than 0.01). Our results support the use of an initial bout of severe hypertension, but not the use of delayed hemodilution.

Animals↗
PubMed1990

Therapeutic deep hypothermic circulatory arrest in dogs: a resuscitation modality for hemorrhagic shock with 'irreparable' injury.

Early deaths from trauma are often caused by exsanguinating hemorrhage from injuries that appear "irreparable." We explored the limits of deep hypothermic circulatory arrest induced during hemorrhagic shock to enable repair of these injuries in a bloodless field. In 15 dogs, after 30 minutes of hemorrhagic shock (mean arterial pressure, 40 mm Hg), cardiopulmonary bypass (CPB) was used to cool to 15 degrees C in 13-37 minutes. After circulatory arrest of 60 (Group 1), 90 (Group 2), or 120 (Group 3) minutes, reperfusion and rewarming were accomplished by CPB. All dogs survived greater than 72 hours. Best neurologic deficit scores (ND) (0% = normal, 100% = brain death) were 0 +/- 0% (normal) in Group 1, 10 +/- 8% (mild disability) in Group 2, and 27 +/- 24% in Group 3. Outcome in Group 3 dogs ranged from near-normal to comatose. After perfusion-fixation sacrifice, brain histopathologic damage scores correlated with insult time, as did ND scores. Deep hypothermia can allow 60-90 min of circulatory arrest with good neurologic recovery, even after a period of severe hemorrhagic shock. This technique may allow repair of otherwise lethal injuries and survival without brain damage.

Animals↗
PubMed1989

Effect of excitatory amino acid receptor blocker MK-801 on overall, neurologic, and morphologic outcome after prolonged cardiac arrest in dogs.

Excitatory amino acids accumulating in the brain during ischemia may cause selective neuronal damage postischemia. This hypothesis was tested in a series of studies using MK-801, an N-methyl-D-aspartate (NMDA) receptor blocker, in a reproducible outcome model of prolonged cardiac arrest in dogs. After normothermic ventricular fibrillation cardiac arrest, the dogs were resuscitated with closed-chest femoral veno-arterial cardiopulmonary bypass. At 4 h they were separated from bypass, ventilation was controlled for 20 h, and intensive care was continued to 96 h. In Study I, ventricular fibrilation cardiac arrest (no-flow) was 17 min; starting immediately with reperfusion, MK-801 1200 mg/kg (n = 5) or an equal volume of placebo (n = 5) was infused over 12 h in blinded, randomized fashion. In Study II, the duration of the no-flow period was reduced to 15 min, and MK-801 2400 mg.kg-1 (n = 4) or placebo (n = 4) was infused. In Study III, no-flow lasted for 15 min, and MK-801 2400 mg/kg was started 30 min before ventricular fibrillation (n = 4); comparison was with Study II controls. In all three studies, MK-801 plasma concentrations peaked at greater than 50 ng/ml and were 15-30 ng/ml over 12 h. All 22 dogs of experiments within protocol survived with severe brain damage. MK-801 delayed return of pupillary reactivity, EEG activity, consciousness, and respiration, necessitating longer periods of controlled ventilation. Neurologic deficit scores, overall performance categories, and brain and heart morphologic damage scores at 96 h did not differ between placebo and MK-801 pretreatment or post-treatment groups. These negative outcome results after prolonged cardiac arrest do not negate the hyperexcitability hypothesis of selective vulnerability, but suggest the existance of additional mechanisms of secondary brain damage.

Animals↗
PubMed1987

[Trimethoprim as a monosubstance and cotrimoxazole in infections of the efferent urinary tract].

In a randomized single blind study the efficiency of Trimethoprim as a monosubstance used in the therapy of urinary tract infections was compared to that of Cotrimoxazole. There was a total of 40 patients available 20 of whom were given 2 X 200 mg Trimethoprim throughout 10 days whereas the other 20 patients were given 2 X 160 mg Trimethoprim + 800 mg Sulphamethoxazole in the same period. All patients were hospitalized during treatment. The urine was bacteriologically checked at the beginning of the treatment and after 7, 14 and 28 days respectively. The therapy was equally successful in both groups, both from the clinical and the bacteriological point of view (Trimethoprim 17, Cotrimoxazole 18); a statistically significant difference was not to be proved. In the Trimethoprim group there was one relapse, in the Cotrimoxazole group there were two. Undesirable side effects occurred in both groups with a larger number of them occurring in the Cotrimoxazole group. Cotrimoxazole and Trimethoprim proved equally efficient from a clinical point of view. The proportion of side effects is more favourable for Trimethoprim alone; the cost of therapy is almost 50% lower than that of Cotrimoxazole.

Adult↗
PubMed1986

[Pharmacologic modification of diastolic ventricular function in patients with coronary heart disease].

The influence of 2 different cardiac pharmaceutics on the diastolic ventricular function (VF) in patients with ischaemic heart disease was examined. Diltiazem, a calcium antagonist, and k-strophanthine led to a reduction of time constant T of the isovolumic relaxation from 49 +/- 9 to 39 +/- 7 msec (p less than 0.005), to an increase of the quotient dt/T from 2.4 +/- 0.5 to 3.0 +/- 0.6 msec (p less than 0.01), to an increase of the peak filling rate (PFR) from 2.08 +/- 0.65 EDV/sec to 2.34 +/- 0.67 EDV/sec (p less than 0.001), to an increase of the filling fraction (FF) from 30 +/- 12% to 33 +/- 15% (p less than 0.001). The ejection fraction (EF) and the maximum rise of pressure dp/dt did not change significantly. After k-strophanthine T was reduced from 49 +/- 7 to 46 +/- 11 msec (p less than 0.05). The increase of dt/T from 2.5 +/- 0.4 to 2.7 +/- 0.4 msec was not significant. The PFR with 2.16 +/- 0.7 and 2.08 +/- 0.8 EDV/sec and the FF with 32 +/- 14 and 34 +/- 18% did not show any significant changes. The EF rose from 52 +/- 15 to 55 +/- 16 (p less than 0.05) and dp/dt rose from 1855 +/- 468 to 2124 +/- 591 (p less than 0.05). Diltiazem improves the diastolic VF without deteriorating the systolic VF in patients with ischaemic heart disease. K-strophanthine improves the systolic VF and the velocity of the isovolumic relaxation. The other variables of the diastolic VF did not show any directed changes.

Adult↗
PubMed1986

[Acute kidney failure].

The etiology of acute renal failure is quite complex, in contradistinction to the monotonous appearance of the corresponding renal pathomorphology (tubular necrosis, intracapillary coagulation). A basic prerequisite for the successful prevention of acute renal failure is the knowledge of the responsible atiopathogenetic factors and their early recognition. Once kidney damage has occurred, therapeutic measures shift to concentrate on the symptomatic treatment of renal failure and the prevention of accompanying complications such as a hemorrhagic tendency, susceptibility to infections, hyperkalemia, hyperhydration, catabolism etc. In addition to the proper choice of the detoxification procedure (hemodialysis, hemofiltration, peritoneal dialysis, continuous a.v. hemofiltration) precise fluid and electrolyte balance, optimal nutrition, and the adjustment of drug dosages to the degree of renal insufficiency all play an important rule. The therapeutic principles and the differential therapy of the various detoxification procedures are discussed on the basis of concrete recommendations.

Acute Kidney Injury↗
PubMed1985

Phosphorus kinetics during haemodialysis and haemofiltration.

Phosphorus excretion during haemodialysis positively correlates with the plasma inorganic phosphorus (Pi) concentration and the dialyser Pi clearance. Therefore, by using highly efficient dialysers or haemofilters, disciplined patients may achieve a well regulated P-balance. The plasma Pi concentration time curve during haemodialysis or haemofiltration must be seen as the result of passive diffusion combined with an active mobilisation of Pi from a rapidly exchangeable P-pool. The plasma Pi concentration hardly falls below the normal range in dialysis patients, regardless of the quantity of Pi removed by haemodialysis or haemofiltration. The stability of plasma Pi demonstrates the existence of a mechanism for phosphate regulation in body fluids, independent of the calcium homeostasis.

Blood↗
PubMed1984

[Endogenous creatinine clearing during cytostatic therapy].

25 patients with a malign neoplasia were treated with cytostatics. The endogenous creatinine clearance as a parameter of the kidney function was checked. Patients who had no side-effects, did not show important changes in kidney function immediately and 10 days after the treatment. Patients who had hyperemesis and diarrhoea showed an impairment, patients with a hyperkinetic reaction improvement of kidney function. General hyperhydration during a cytostatic treatment is not necessary, it can even be dangerous for patients with a hyperkinetic reaction.

Adolescent↗
PubMedDate not supplied

Effects of adenosine on electrical activity of isolated guinea pig hearts.

Negative chronotropic and dromotropic effects of adenosine seem to be responsible for its antiarrhythmic action on supraventricular tachyarrhythmias. To further characterize the effects of adenosine on supraventricular arrhythmias heart rate, conduction, refractoriness, the time to steady-state of AV-nodal conduction slowing and of sinus rate reduction were evaluated. Changes of heart rate, conduction intervals and effective refractory periods were determined by the use of a high-resolution ECG recording technique in isolated guinea pig hearts perfused by the method of Langendorff. Adenosine in concentrations of 3 and 10 microM reduced sinus rate and prolonged AV-nodal conduction significantly, while intraventricular and His bundle conduction were not altered. The maximal effect of adenosine on the sinus node and AV nodal conduction occurred after 636 +/- 109 and 111 +/- 35 (mean +/- SE) beats, respectively. During programmed stimulation at a cycle length of 250 ms, adenosine reduced atrial ERP in a dose-dependent manner. At cycle lengths of 170 and 200 ms, adenosine increased the atrial ERP at 3 microM, and then progressively shortened the ERP at higher doses. At all adenosine concentrations used, the usual rate-dependent adaption in ERP was suppressed. These observations explain the efficacy of adenosine against supraventricular tachyarrhythmias where the AV-node forms a part of a reentrant circuit. Adenosine shortened the atrial ERP, but at high pacing rates also led to a relative prolongation of the atrial ERP as the rate-dependent adaption was suppressed. These opposite effects of adenosine may explain earlier contradictory findings of its action on atrial arrhythmias.

Adenosine↗
PubMedDate not supplied

Multifocal cerebral blood flow by Xe-CT and global cerebral metabolism after prolonged cardiac arrest in dogs. Reperfusion with open-chest CPR or cardiopulmonary bypass.

Using the stable xenon-enhanced computed tomography (Xe-CT) method in dogs, we studied local, regional and global cerebral blood flow (LCBF, rCBF and gCBF) in two sham experiments and nine cardiac arrest experiments. Within the same experiments without arrest, gCBF and rCBF values were reproducible and stable. LCBF values varied over time. In group I (n = 4), ventricular fibrillation cardiac arrest (no blood flow) of 10 min was reversed by open-chest cardiopulmonary resuscitation (CPR). In group II (n = 5), ventricular fibrillation cardiac arrest of 12.5 min was reversed by brief closed-chest cardiopulmonary bypass. This was followed by controlled ventilation, normotension, normoxia, normocarbia and normothermia to 4 h (n = 7) or 20 h (n = 2) postarrest. The postarrest CBF patterns were similar in both groups. Open-chest CPR during ventricular fibrillation generated near-baseline gCBF and lower LCBF ranges. During postarrest spontaneous circulation, transient diffuse hyperemia was without low-flow regions, longer in brain stem and basal ganglia than in neocortex. During delayed hypoperfusion at 1-4 h postarrest (n = 9), mean gCBF was 44-60% baseline, rCBF in primarily gray matter regions was 15-49 ml/100 cm3 per min and LCBF voxels with trickle-flow and low-flow values, in percent of CT cut area, were increased over baseline. Global CMRO2 (n = 3 of group II) recovered to near baseline values between 1 and 4 h postarrest, while gCBF and O2 delivery were about 50% baseline (mismatching of O2 uptake and O2 delivery).

Animals↗
PubMedDate not supplied

Successful automatic external defibrillator operation by people trained only in basic life support in a simulated cardiac arrest situation.

OBJECTIVE: To show whether in an in-hospital cardiac arrest, early defibrillation can also be performed by hospital staff trained only in basic life support. BACKGROUND: The International Liaison Committee on Resuscitation (ILCOR) endorses the concept that in many settings non-medical individuals should be allowed and encouraged to use defibrillators. METHODS: Five different groups of hospital staff were evaluated whether they were able to correctly operate an automatic external defibrillator in a simulated sudden cardiac arrest situation without any prior instruction. The participants were assigned either to the 'basic life support-trained' group (BLS, n = 40, or to the 'advanced life support-trained' group (ALS, n = 40). RESULTS: All persons of the 'only BLS-trained' group delivered the three sequential ('stacked') shocks with the automatic external defibrillator when persistent ventricular fibrillation was simulated. The 'ALS-trained' persons successfully delivered the three shocks with the automatic external defibrillator in 98% of the cases. When this group used a conventional defibrillator, only 88% were able to deliver the three shocks, however they were able to do it significantly more quickly. CONCLUSION: Using an automatic defibrillator without any prior instruction, even persons trained only in BLS were able to deliver three sequential shocks in a simulated persistent ventricular fibrillation cardiac arrest.

Adult↗
PubMedDate not supplied

Measurement of myocardial contractility following successful resuscitation: quantitated left ventricular systolic function utilising non-invasive wall stress analysis.

After successful resuscitation from cardiac arrest, prolonged contractile failure has been demonstrated in animal experiments. No systematic evaluation of myocardial contractility following successful resuscitation after human cardiac arrest exists. The aim of this study was to assess left ventricular contractility following human cardiac arrest with successful resuscitation. In 20 adult patients after cardiac arrest and in four control patients, the relation between meridional wall stress (MWS) and rate-corrected mean velocity of circumferential fibre shortening (Vcf(c)), a load independent and rate corrected index of left ventricular contractility was measured within 4 h after return of spontaneous circulation and after 24 h by means of transoesophageal echocardiography. As the normal values of Vcf(c) depend on MWS, a normal deviate (z) was calculated. A normal z-score is defined as 0+/-2, < -2 indicates reduced contractility, > + 2 increased contractility. Data are presented as median and the interquartile range (IQR). For the comparison of related samples the Wilcoxon sign test was used. In most patients after cardiac arrest contractility was severely impaired within 4 h after successful resuscitation [z - 7.0 (IQR - 8.9 - (-2.5))]. Contractility did not significantly improve within the observational period [z after 24 h - 3.7 (IQR - 7.9 - (-1.8))] (P = 0.3). The four control patients had normal left ventricular contractility on arrival (z 0.0, range - 0.9-0.8) and after 24 h (z 0.7, range - 1.5-2.7). In conclusion non-invasive wall stress analysis can be applied to quantitate systolic left ventricular function, which was severely compromised in most patients within the first 24 h after successful resuscitation. Whether depression of left ventricular function is caused by cardiac arrest itself or by the underlying disease remains speculative.

Adult↗
PubMedDate not supplied

[Intravenous urapidil versus sublingual nifedipine in the treatment of hypertensive emergencies].

In a 6-month prospective study, the efficacy and safety of urapidil and nifedipine in an out-patient population with hypertensive urgencies (systolic blood pressure > 200 mmHg; diastolic blood pressure > 110 mmHg) was investigated. Response to treatment was defined as a stable reduction of systolic blood pressure below 180 mmHg and diastolic blood pressure below 100 mmHg 15 minutes after application of a single dose of either 25 mg urapidil intravenously (N = 26) or 10 mg nifedipine sublingually (N = 27). If the blood pressure was still elevated, a second dose of 10 mg nifedipine or 12.5 mg urapidil was given, and blood pressure response was evaluated 15 minutes after application of the second dose according to the aforementioned criterias. After the first application of nifedipine, 19 (70%) responders have been observed. Eight patients needed an additional 10 mg of nifedipine. In four of these patients, no reduction of blood pressure was observed after a second dose of nifedipine. In contrast, 24 (92%) patients responded well to the first application of 25 mg of urapidil. Two patients required a second dose of 12.5 mg of urapidil, but no nonresponder to urapidil was observed. No severe side-effects were noted in both groups. Intravenous urapidil is a highly effective drug in the treatment of hypertensive urgencies and is more effective than sublingual nifedipine, because the number of patients treated successfully was significantly higher.

Administration, Sublingual↗