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J P Jantzen

Publications and source records attributed to J P Jantzen.

At least 19 recordsLinked to original sources
PubMed1999

[Hemodynamic effects of a ventriculo-cisternal perfusion of bupivacaine].

OBJECTIVES: The cardiotoxic properties of bupivacain have been well documented under in-vitro, as well as under in-vivo conditions. A further mechanism of cardiovascular impairment by bupivacaine via the central nervous system gained investigational interest in animal studies. The aim of our study was to demonstrate the effect of a ventriculocisternal perfusion of bupivacain on systemic hemodynamic variables and their reversibility by wash-out with mock-CSF. METHODS: After obtaining animal investional committee consent, nine anaesthetized and relaxed pigs were prepared for a ventriculocisternal perfusion (VCP). Hemodynamic data were obtained by invasive blood pressure measurements in the high and low pressure system as well as cardiac output (thermodilution technique), intracranial pressure and electrocardiogram. Systemic vascular resistance and stroke volume were calculated using standard formulas. A second group of three animals were exposed to an intravenous infusion of the same dose of bupivacain over the same period of time to rule out direct cardiac effects. After instrumentation baseline data were obtained (K0 1) under VCP with mock-CSF for 30 minutes. The mock-CSF was replaced by 0.05% bupivacaine in mock-CSF and VCP was continued with 3 ml.h-1 for 20 minutes. After administration of 500 micrograms bupivacaine data were collected (BU). The bupivacaine solution was replaced by mock-CSF and after twenty minutes hemodynamic measurement were repeated (K02). RESULTS: The intravenous administration of 500 micrograms bupivacaine had no effect on all measured variables. VCP of the same dose resulted in significant increase in heart rate, systolic, diastolic and mean arterial blood pressures. Left and right heart filling pressures as well as systemic vascular resistance were not affected while the stroke volume decreased. After continuation of VCP with mock-CSF hemodynamic changes were reversed. DISCUSSION: Our results demonstrate that bupivacaine initiates an indirect cardiovascular stimulating effect of a VCP with 500 micrograms of bupivacaine via the central nervous system. The intravenous administration of the same dose had no effect. The centrally mediated cardiovascular effect of bupivacaine was reversed by wash-out with mock-CSF. The cardiovascular stimulation observed in this animal experiment may be of clinical relevance as a potential sign of toxic effects of bupivacaine on the CNS.

Anesthetics, Local↗
PubMed1999

Local brain surface temperature compared to temperatures measured at standard extracranial monitoring sites during posterior fossa surgery.

Mild hypothermia is assumed to protect against secondary brain injury. However, the accuracy of brain temperature estimation remains debatable if direct measurement in the target area is to be avoided or is impossible. Furthermore, intracerebral temperature gradients exist, especially under intraoperative conditions. We aimed to establish how brain surface temperatures (TBrain) relate to temperatures taken at standard sites in posterior fossa surgery. Ten patients undergoing cerebellopontine angle tumor removal were monitored for TBrain, esophageal temperature (TEso), bladder temperature (TBlad), ipsi- and contralateral tympanic membrane (TTymp-I, TTymp-C), and scalp temperatures (TScalp). During monitoring, TEso increased from 35.3+/-0.2 degrees C to 36.0+/-0.3 degrees C. After dura opening, TBrain was -0.14+/-0.1 degrees C below TEso. At the end of tumor removal, this difference increased to -0.43+/-0.31 degrees C (P < 0.05). TTymp-C was -0.29+/-0.18 degrees C below TBrain at dura opening. TTymp-C reflected the behavior of TEso adequately (r = 0.938), however, with a mean difference of -0.39+/-0.04 degrees C. In contrast, TTymp-I readings closely followed temperature changes in the area of surgery. TBlad reflected TEso except in periods of rapid temperature changes. In posterior fossa (PF) surgery, local TBrain is most accurately reflected by TEso. For clinical use TBlad and TTymp-C are also sufficient to assess brain surface temperature in the PF. Intraoperative surface cooling of the brainstem is less than the previously described cooling rate of exposed cerebral cortex.

Adult↗
PubMed1998

[Regional distribution of predisposition to maligant hyperthermia in Germany: tate in 1997].

Malignant hyperthermia (MH) is a rare autosomally dominantly hereditary and potentially life-threatening disease. The prevalence of the genetic MH predisposition is estimated as 1:10,000 to 1:20,000. In Germany no data on the regional distribution are available. Therefore, the purpose of this investigation is to summarise and present the epidemiological data of all German MH laboratories. Nine German hospitals offer the specific in vitro contracture test to diagnose the MH predisposition. All German MH laboratories carry out the examination in accordance with the standardised protocol of the European Malignant Hyperthermia Group. The laboratories were asked to provide the number of all patients investigated, excluding those suffering from other neuromuscular diseases, separated according to diagnostic groups and their places of residence, the number of the identified MH-families as well as the number of the clinically suspected and investigated MH cases with their places of residence. Eight MH laboratories provided the requested data. Until September 1997 a total of 2620 patients were investigated. In 865 patients (34%) MH suspicion was confirmed (diagnosis: MHS). 1494 patients (56%) were released by investigation from MH-suspicion (diagnosis: MHN). In 261 patients (10%) the MH-predisposition remained unsolved (diagnosis: MHE). 580 MH families were identified. Among 2620 patients 757 were clinically suspected MH cases. 35% of these suspected MH cases were classified as MHS, 10% as MHE and 55% as MHN. The documentation of the patients places of residence classified as MHS and MHE into a map of Germany demonstrates an exhaustive distribution with an increased regional prevalence in the areas of the MH laboratories. This concentration in the area of the MH laboratories becomes even more evident, when the places of residence of the MH suspected cases are demonstrated. In conclusion, the distribution of the MH predisposition is uniform and exhaustive in Germany. The presented regional concentration of clinically suspected MH cases among the MH laboratories is mainly interpreted as an expression of effective regional education and information. Considering the overall incidence of the MH predisposition as described above only 15-20% of the MH patients have so far been identified. The MH laboratories have already released about 10,000 patients from the suspicion of MH predisposition. A preliminary prevalence of at least 1:60,000 to 1:80,000 in Germany can be estimated according to the presented data.

Epidemiologic Studies↗
PubMed1994

Effects of fenoldopam on intracranial pressure and hemodynamic variables at normal and elevated intracranial pressure in anesthetized pigs.

Fenoldopam (FE), a dopamine DA1-receptor agonist, has been introduced for treatment of arterial hypertension and heart failure and for preservation of renal function. Vasodilators are generally assumed to affect all vascular beds including the cerebral circulation. We have evaluated effects of FE-induced (4 micrograms.kg-1.min-1) arterial hypotension on intracranial pressure (ICP) and intraocular pressure (IOP) under conditions of normal and increased intracranial elastance. ICP and IOP responses to hypertension were tested by infusion of angiotensin II (15 micrograms.kg-1.min-1), and the response to hypercapnia was tested by elimination and reintegration of soda lime canisters in the breathing circuit. Intracranial elastance was increased by infusing mock cerebrospinal fluid (CSF) into the lateral ventricle (20 +/- 3 ml.h-1). Arterial hypotension induced with FE did not increase ICP. With increased intracranial elastance, the infusion rate of mock CSF had to be reduced while administering FE to avoid a rise in ICP (p < 0.05 compared with preinfusion value); this indicates a shift on the volume-pressure curve to the right. There were no indicators that cerebral autoregulation or CO2 reactivity of the cerebral vasculature were affected by FE in this anesthetized porcine model, as speculated from analysis of the time course of delta ICP. There are, however, indicators of increased intracranial elastance, most likely caused by vasodilation. Caution should hence be exercised when FE is administered to patients with increased intracranial elastance.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1994

[Cerebral neuroprotection and ketamine].

Ketamine is said to increase intracranial pressure (ICP), cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) and hence to be unsuitable for neuroanaesthesia. This may require reconsideration in the light of the neuroprotective properties mediated by the interaction of ketamine with the N-methyl-D-aspartate receptor (NMDA). Meta-analysis of published experimental rodent studies yields contradictory conclusions. Ketamine does not provide neuroprotection against hypoxic hypoxaemia or focal cerebral ischaemia. During complete forebrain ischaemia of 10 min duration, ketamine offers some degree of protection only if administered before (i.e. prophylactically) and after (i.e. therapeutically) a transient ischaemic episode. In experimental head injury, ketamine may be protective if administered therapeutically within 2 h after the trauma. In the case of incomplete forebrain ischaemia, ketamine provides neuroprotection if administered both before and during ischaemia. Clinical or primate studies are not available; extrapolation of results derived from rodent studies requires caution and has limitations. With respect to the pharmacodynamic action providing neuroprotection, NMDA-receptor antagonism may be just one of several mechanisms; others include scavenging of free radicals, a central sympatholytic effect and augmentation of dopamine metabolism in the caudate. The suitability of ketamine for neuroanaesthesia, which must also take account of its effects on ICP, CBF and CMRO2, is--for the time being--questionable.

Animals↗
PubMed1993

[Fiberoptic intubation of neurosurgical patients].

Patients with cervical spine injury presenting with respiratory distress require airway management that does not compromise integrity of the atlanto-occipital joint. Endotracheal intubation by means of direct laryngoscopy is not suitable. The method of choice is nasotracheal intubation of the awake patient, using a flexible fibre bronchoscope. If anatomy or surgical access render the nasal approach impossible, fibre optic intubation can be performed orotracheally, utilising specific technical aids. Flexible fibrescopes are available in different sizes (length and diameter): selection is base on the patient's anatomical requirements. Aids to orotracheal intubation are constructed with a bore wide enough to accommodate an endotracheal tube, and a face mask equipped with an extra intubation port allowing introduction of an endotracheal tube, slipped over a fibrescope. Premedication of the patients consists of an orally administered benzodiazepine. Topical anaesthesia and vasoconstriction of the nasal passages are achieved by cocaine (5-10%), or a local anaesthetic, combined with a vasoconstrictor. The selected nostril is prepared by means of introducing a nasopharyngeal airway, which--lubricated with xylocaine gel and left in place for few minutes--widens the nostril and facilitates passage of the endotracheal tube. Through the other nostril, oxygen is administered. Systemic analgo-sedation is strictly limited to fentanyl, 0.1 mg i.v. Topical anaesthesia of the larynx and cranial trachea is achieved by xylocaine, 2%, administered under direct vision through the instrumentation channel of the fibrescope.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗