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P Kempler

Publications and source records attributed to P Kempler.

At least 37 records · Page 2Linked to original sources
PubMed1998

Neuropathy as an extrahepatic manifestation of chronic liver diseases.

Gastrointestinal motor disturbances and various cardiovascular symptoms are the characteristic features of autonomic neuropathy. Autonomic and sensory neuropathy has been described in chronic alcoholic liver diseases. Cardiovascular autonomic reflex tests as the gold standard for autonomic neuropathy and measuring of thresholds for constant current electric sine wave stimulation by neurometer were used for measuring sensory neuropathy in patients with chronic liver diseases of different etiology. Autonomic and sensory neuropathy was also observed in non-alcoholic liver diseases. We proved that there is a correlation between autonomic neuropathy and prolongation of corrected QT interval in chronic liver diseases. We claim that autonomic neuropathy may have a role to play in the development of hyperdynamic circulation and portal hypertension in chronic liver diseases.

Autonomic Nervous System Diseases↗
PubMed1997

[Gallbladder hypomotility in diabetic polyneuropathy].

A study was made of the pathogenic role of gallbladder hypomotility, which is presumably responsible for the high incidence of gallstone disease in long-standing diabetes mellitus. The gallbladder motility of diabetic patients (n = 10) was measured by means of quantitative hepatobiliary scintigraphy, and the severity of concomitant autonomic and sensory polyneuropathy was determined. The presence of marked gallbladder hypomotility was proven, and a positive correlation was observed between the severity of autonomic neuropathy and the contractile disorder. In this group of diabetic patients, a hypaesthetic sensory polyneuropathy too was recognized, the degree of which exhibited a positive correlation with the autonomic neuropathy score. This study underlines the important role of the autonomic neural dysfunction in the development of gallbladder hypomotility accompanying long-term diabetes mellitus.

Diabetes Mellitus, Type 1↗
PubMed1996

Is autonomic neuropathy a risk factor for severe hypoglycaemia? The EURODIAB IDDM Complications Study.

The hypothesis that diabetic patients with autonomic neuropathy are at increased risk of severe hypoglycaemia was examined in an epidemiological study of over 3000 IDDM patients in Europe (EURODIAB IDDM Complications Study). Autonomic function was assessed by two standard cardiovascular tests: change in heart rate and systolic blood pressure on standing. Severe hypoglycaemia was defined as an attack serious enough to require the help of another person. Compared to patients (68%) reporting no attacks in the last year, those reporting one or more attacks were older (34.0 +/- 10.7 vs 32.1 +/- 9.9 years, mean +/- SD, p < 0.0001), had had diabetes for a longer period (16.6 +/- 9.5 vs 13.8 +/- 9.1 years, p < 0.0001), had better glycaemic control (HbA1c 6.4 +/- 1.8 vs 6.9 +/- 1.9%, p < 0.0001) and were more likely (p = 0.002) to have abnormal responses to both autonomic tests (13.0 vs 7.7%). A single abnormal autonomic response was not associated with an increased risk of severe hypoglycaemia. The odds ratio for severe hypoglycaemia in people with abnormal responses to both autonomic tests, compared to those with normal responses, was 1.7 (95% confidence interval 1.3, 2.2) after controlling for age, duration of diabetes, glycaemic control and study centre. In conclusion, a combined autonomic deficit in heart rate and blood pressure responses to standing is associated with only a modest increase in the risk of severe spontaneous hypoglycaemia. Although the increase in risk is not large, severe hypoglycaemia was a frequently reported event in this study. IDDM patients with deficient autonomic responses who strive for tight glycaemic control may therefore be at particular risk of severe hypoglycaemia.

Adult↗
PubMed1994

Aminophylline fails to improve the outcome of cardiopulmonary resuscitation from prolonged ventricular fibrillation: a placebo-controlled, randomized, blinded experimental study.

OBJECTIVES: The purpose of this study was to evaluate systematically the effects of the adenosine antagonist aminophylline on resuscitation outcome in a canine model of postcardioversion nonperfusing rhythm. BACKGROUND: Theoretic considerations and experimental studies indicate that myocardial adenosine accumulation during prolonged ventricular fibrillation might play a significant role in postcardioversion asystole and electromechanical dissociation. A recent uncontrolled clinical trial has suggested that the adenosine antagonist aminophylline might improve the outcome of cardiopulmonary resuscitation from refractory bradyasystolic cardiac arrest. METHODS: Two placebo-controlled, randomized, blinded experimental studies were performed. In protocol 1 (20 dogs), ventricular fibrillation was induced and maintained for 7.5 min. Sixty seconds before cardioversion, dogs received 1 mg of epinephrine followed by 250 mg of aminophylline or placebo. In protocol 2 (20 dogs), dogs were cardioverted to electromechanical dissociation after 5 min of unsupported ventricular fibrillation. Sixty seconds later, all dogs received 1 mg of epinephrine followed by 250 mg of aminophylline or placebo. In both experiments, resuscitation efforts were continued until return of spontaneous circulation, or up to 30 min. The primary end point was survival to 1 h. RESULTS: In protocol 1, 4 of 10 dogs survived in the aminophylline group, whereas 7 of 10 dogs survived in the placebo group, a nonsignificant trend toward unfavorable outcome from aminophylline. Pretreatment with aminophylline increased the number of cardioversion applications required to terminate ventricular fibrillation. In protocol 2, 5 of 10 and 6 of 10 dogs survived in the aminophylline and placebo groups, respectively. CONCLUSIONS: The results of this study suggest that aminophylline fails to improve the outcome of resuscitation from prolonged ventricular fibrillation. It does not reverse established electromechanical dissociation and may in fact increase the number of cardioversion applications required to terminate ventricular fibrillation. The rationale for conducting clinical trials with aminophylline during cardiopulmonary resuscitation is questionable.

Aminophylline↗
PubMed1993

[Autonomic neuropathy in chronic liver diseases].

Autonomic neuropathy has been evaluated by various cardiovascular bedside tests in 172 patients with chronic alcoholism (36 alcoholics without liver disease, 50 patients with fatty liver and 86 with cirrhosis), in 21 patients with HBsAg-positive chronic liver disease, in 14 patients with primary biliary cirrhosis, in 14 patients with cirrhosis of other origin and in 86 healthy controls. Parasympathetic integrity was evaluated by beat-to-beat variation during deep breathing, Valsalva manoeuvre and standing up, sympathetic function by blood pressure response to standing and to sustained handgrip test. Autonomic reflex damage was found in all groups examined. Patients with alcoholic cirrhosis exhibited the most severe alterations. Our results suggest, that chronic hepatopathy itself presents a pathogenetic factor of autonomic neuropathy. Autonomic failure has to be considered as a possible cause of symptoms in liver diseases with all its prognostic consequences.

Adult↗
PubMed1993

Neodymium:YAG contact laser photocoagulation of the in vivo canine epicardium: dosimetry, effects of various lasing modes, and histology.

UNLABELLED: Neodymium:YAG laser photocoagulation (LPC) is an investigational technique for the treatment of drug-resistant postinfarction ventricular tachycardia that requires cardiopulmonary bypass and open heart surgery. The purpose of this experimental study was to evaluate the feasibility of contact epicardial LPC to reach subepicardial, deep myocardial, and subendocardial regions without ventriculotomy and to analyze the dose-response relationships of this new technology. In 24 open-chest, closed heart dogs, a total of 219 epicardial laser lesions were generated under sterile conditions. Laser source was a continuous wave 1064 nm Nd:YAG; the delivery system consisted of a 400 mu bare quartz fiber fed into an 8F electrode catheter in direct contact with the epicardial surface. Laser variables were power at 10-15-20 W; lasing time, 6-12-18-24 s; lasing mode, continuous and pulse-pause; fiber mode, optical fiber tip inside and extending out from the electrode catheter. Hearts were harvested at 1 week. Histologic measurements included lesion surface diameter, internal diameter, and depth. RESULTS: Significant linear correlation was found between the total delivered energy and all measured lesion parameters. Transmural lesions were found at energy levels of 270-480 J. Maximum depth measured up to 1.68 cm; at high energies, it was limited by myocardial thickness only. At constant energy levels, power and lasing time did not independently affect lesion dimensions; lasing mode and fiber mode had statistically significant but minor effects. Laser lesions were homogeneous and sharply demarcated without epicardial crater or endocardial thrombus formation. Endocardial surface cooling by circulating blood and the presence of epicardial vessels resulted in modifications in lesion morphology. In 29 out of 74 grossly transmural lesions, there was a 0.082 +/- 0.127 cm thin surviving subendocardium. Forty-five coagulation lesions were truly transmural with no surviving myocardial strands. In conclusion, contact epicardial LPC can result in deep, transmural myocardial coagulation lesions. Lesion dimensions can be adequately controlled by total delivered energy. Closed heart epicardial Nd:YAG laser photocoagulation could become a new, less invasive surgical technique for the treatment of drug-resistant ventricular tachycardia.

Aluminum Silicates↗
PubMed1993

Selective elimination of retrograde conduction by intraoperative neodymium: YAG laser photocoagulation in dogs.

OBJECTIVES: The purpose of this study was to test the feasibility of selective elimination of ventriculoatrial (VA) conduction by limited laser photocoagulation of the atrioventricular (AV) node, and to analyze the histologic substrate of unidirectional retrograde block. BACKGROUND: Atrioventricular node reentry requires intact retrograde conduction. METHODS: Neodymium:yttrium-aluminum-garnet laser photocoagulation was performed during cardiopulmonary bypass through a right atriotomy in 15 dogs that had intact retrograde conduction before operation. Short laser pulses were delivered to an area between the coronary sinus orifice and the proximal His bundle. The end point of lasing was second-degree AV node block at a paced atrial cycle length of 250 ms. RESULTS: Complete retrograde block developed immediately in 11 of the 15 dogs (group I), while AV conduction persisted in all 11. In 4 of the 15 dogs (group II), both AV and VA conduction remained intact. During a 3-month follow-up period, retrograde conduction remained absent in all group I dogs. Retrograde block was not reversed by isoproterenol. Anterograde AV node characteristics (Wenckebach cycle length, functional refractory period, ventricular rate during atrial fibrillation) were unchanged in five dogs and modified in six. Complete AV block did not develop. In four control dogs (group III, sham operation), anterograde and retrograde AV node characteristics were unchanged. The anterograde Wenckebach cycle lengths in groups I, II and III at 3 months measured 192 +/- 15 ms, 195 +/- 6 ms and 170 +/- 22 ms, respectively, whereas the retrograde Wenckebach cycle lengths in groups II and III measured 345 +/- 62 ms and 278 +/- 25 ms, respectively. Histologic study at 3 months in cases with unidirectional VA block showed the compact part of the AV node intact with destruction of the atrial approaches and the superficial layers of the proximal end of the node on the right side. CONCLUSIONS: 1) With limited laser photocoagulation of the proximal AV node area, VA conduction can be eliminated and anterograde AV node transmission maintained. 2) Destruction of the atrial approaches on the right side with preservation of the compact part of the AV node may result in unidirectional retrograde block.

Animals↗
PubMed1993

Catheterization technique for laser photoablation of atrioventricular conduction from the aortic root in dogs.

A simple catheterization technique for producing suppression or block of atrioventricular (AV) conduction in dogs by neodymium:YAG (Nd:YAG) laser photocoagulation from the aortic root is described. In 14 canines, electrode catheters were percutaneously advanced to the high right atrium, to the His bundle area at the tricuspid valve (right His [RH]), and the noncoronary cusp of the aortic valve (left His [LH]). A 400 microns optical fiber was fed into the lumen of the LH catheter. Continuous wave Nd:YAG lasing at lambda = 1,064 nm at 15-20 watts was performed at the site of the largest recorded LH deflection, opposite to the RH catheter, until complete AV block (CAVB, group I, eight dogs) or persistent A-H prolongation (AHPr, group II, four dogs) occurred; in two animals, laser photoablation was unsuccessful. CAVB and AHPr were achieved in < 140 seconds of lasing. Mean lasing time was 51 +/- 41 seconds, total energy delivered, 776 +/- 601 J. There were no complications. Dogs were followed for up to 120 days. In group I, 6/6 dogs followed for at least 1 week continued to have CAVB (three AV nodal, five infra-His). In group II, 1/4 dog progressed to infra-His CAVB; 3/4 had depressed AV nodal function. AV block was not reversed by isoproterenol. Aortic root angiograms revealed intact valve function in all. Histology showed various degrees of damage and repair of AV junctional tissue. There were no valvular perforations. Transcatheter Nd:YAG laser photocoagulation of the AV junction from the aortic root is a fast, simple, and safe method for creating AV conduction block in dogs.

Animals↗
PubMed1993

Prolongation of the QTc-interval reflects the severity of autonomic neuropathy in primary biliary cirrhosis and in other non-alcoholic liver diseases.

It was the aim of our study to prove a potential correlation (a) between laboratory findings of cholestasis and autonomic neuropathy (AN) and (b) between the severity of AN and the prolongation of the corrected QT-time (QTc). The five standard tests of autonomic cardiac neuropathy were investigated. QTc was calculated according to Bazett's formula. 12 out of 14 patients with primary biliary cirrhosis, 18 out of 21 patients with HBsAg positive liver diseases and 11 out of 14 patients with cirrhosis of other origin had AN. No significant correlation between the laboratory parameters of cholestasis and AN was found. Abnormal QTc values (> 440 m/sec) were observed significantly more often (p < 0.002) in patients with AN than in patients without AN. Significant linear regression (p < 0.01) could be confirmed between the prolongation of the QTc-time and the severity of AN. Besides the non-invasive investigation of the cardiovascular reflexes the evaluation of the QT-time might be an additional diagnostic means to identify patients with an increased cardiovascular risk in chronic non-alcoholic liver diseases.

Adult↗