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C F Cartheuser

Publications and source records attributed to C F Cartheuser.

8 recordsLinked to original sources
PubMed1994

Effects of dotarizine on peripheral and pulmonary circulation and cardiac dynamics in dogs.

The cardiovascular effects of dotarizine in 10-min intravenous infusions were studied in thiopental-anesthetized dogs. The effects of dotarizine 0.024 mg/kg/min almost paralleled those of saline controls; 0.079 mg/kg/min dotarizine significantly raised the stroke index and ejection fraction, and, at a rate of 0.25 mg/kg/min, further effects appeared and were dose-dependent. Dotarizine produced arterial dilation in both systemic and pulmonary circulation: the total peripheral resistance dropped, and femoral artery flow rose; aortic and pulmonary artery mean and diastolic pressures declined, and systolic pressures remained almost stable. A trend of bradycardia and pulmonary artery pressure reduction persisted for 30 min. As compared with the reduced total peripheral resistance, aortic pressure fell only moderately because of rising cardiac output due to a higher ejection fraction and stroke volume. Cardiac preload tended to decline; contractility tended to increase. Cardiac performance remained stable while myocardial oxygen consumption tended to fall, as did the pressure-rate product and the tension time index. Dotarizine exerted direct cardiovascular effects similar to those of the 5-HT2-receptor antagonist ketanserin and, more generally, to calcium channel blockers rather than to alpha-adrenoceptor blockers.

Animals↗
PubMed1993

Standard and pH-affected hemoglobin-O2 binding curves of Sprague-Dawley rats under normal and shifted P50 conditions.

1. The oxygen saturation (SO2) was determined of Sprague-Dawley rat blood having increased hemoglobin (Hb)-O2 affinity (P50 < 37 mmHg) or capacity (Cmax) over a range of pH's. 2. Rats were untreated (K), or had passed 14 d drinking 0.5% saline (C; ctrl) or NaOCN (N; chronically low P50, high Cmax), 5000 m altitude acclimatization (H; high Cmax), or exchange transfusion with OCN(-)-Hb red cell blood (X; acutely low P50). 3. The P50 [mmHg], Hill's "n", and Cmax [ml O2/100 ml], measured after tonometry, were 36.0, 2.60 and 20.6 (K), 32.6, 2.50 and 21.8 (C), 18.3, 2.35 and 23.9 (N), 36.0, 2.60 and 29.4 (H), and 24.9, 2.73 and 22.3 (X). 4. Oxygen dissociation curves (ODC's), derived from simultaneous SO2 and PO2 measurements during deoxygenation (PO2: 100-0 mmHg) of blood (normal and acidified with CO2 or lactic acid), delivered Bohr coefficients (BCCO2, BCLac) each differing between groups (C vs N) above SO2 50%; within groups BCCO2 vs BCLac differed at SO2 10-90% (P < 0.05). 5. Group-specific ODC's and pH-shifted curves (+/- 0.05, +/- 0.10 and +/- 0.15 units from 7.4, relying on BCCO2) are plotted for direct reading of SO2 and, with Cmax, accurate data on blood O2 content are obtained; corrections for lactic acidosis are discussed.

Acclimatization↗
PubMed1988

Slow channel inhibitor effects on brain function: tolerance to severe hypoxia in the rat.

1. The protective effects of ten slow channel inhibitor drugs against severe progressive hypoxia were investigated in rats breathing spontaneously during light anaesthesia. Respiration, heart rate, electrocorticogram (ECoG) and/or electroencephalogram (EEG) were recorded. 2. Tolerance times were monitored from hypoxia onset until cessation of respiration, ECoG, EEG synchronization, and 'background-EEG'. Drugs were administered i.v. 5 min before the onset of hypoxia. 3. Verapamil, gallopamil, and nimodipine resulted in a significant increase of tolerance times; fendiline and bepridil showed a small increase (not significant); bencyclan and prenylamine were ineffective; cinnarizine and diltiazem slightly reduced tolerance times as did flunarizine at low doses. 4. At protective doses, verapamil, gallopamil, and nimodipine significantly raised the respiration rate but had little or no cardiac depressor effects. Bencyclan showed ventilatory drive but cardiocirculatory depression. A clear-cut ventilatory drive did not occur with the other ineffective slow channel inhibitors. 5. It is suggested that the protective actions observed were not due to slow channel inhibition per se, nor to spasmolytic potency or increased cerebral blood flow. Ventilatory drive associated with other cardiopulmonary actions which secondarily raise the brain oxygen supply are likely to be responsible for this effect.

Animals↗
PubMed1988

Progressive hypoxia until brain electrical silence: a useful model for studying protective interventions.

Anesthetized spontaneously breathing rats, fitted with epicortical electrodes and catheters for sampling arterial, venous, and cerebral venous blood, were exposed to standardized progressive hypoxia. Three minutes of hypoxia sequentially caused hyperpnea, hypopnea, apnea, and cessation of electrocorticogram "spiking," of synchronization, and of background in electroencephalogram (EEG). Blood data and cerebral blood flow and metabolism were measured throughout and at "insults," i.e., at apnea and cessation events, to clarify their interdependence. Arterial and brain venous PO2 fell linearly with inspired oxygen (final value of 2% at 280 s). Hyperpnea induced arterial alkalosis; subsequent hypopnea led to near-normal PCO2 and pH when EEG ceased. Hypercapnia was more pronounced in cerebral than in systemic venous blood; time courses of pH changes were similar. Sagittal sinus blood pressure and outflow were linearly related and resembled the time course of local cerebral blood flow. Blood flow increased by 25% at apnea and only 60% at EEG silence. Cerebral metabolic rate of O2 rose during the hyperpnea phase and fell exponentially thereafter. Cerebral glucose uptake and lactate release increased within the first 3 min but fell abruptly when cortico-electric spiking ceased. Time courses of cerebral O2 consumption and spike rate were linearly related; both showed inverse linear relations to cerebral perfusion. The hypoxic insults were well defined by blood data; critical PO2 values were lower than previously assumed. This model is proving to be a useful, controlled method by which mechanisms of cerebral hypoxia tolerance may be studied in vivo.

Animals↗
PubMed1987

Verapamil enhances brain function tolerance against severe hypoxia without enhancing cerebral blood flow in the rat.

In spontaneously breathing, lightly anesthetized rats with chronically implanted epicortical electrodes, tolerance times were measured from onset of progressive hypoxia, anoxia or decapitation, until ultimate apnea and subsequent cessation of brain electrical activities. Arterial and cerebrovenous blood was collected initially and during progressive hypoxia, starting 5 min after intravenous verapamil or NaCl (controls). Verapamil induced significant hyperpnea, arterial alkalosis, slight bradycardia and brain venous acidosis. During progressive hypoxia, hyperpnea persisted and heart rate remained stable for a longer period than in controls. Tolerance times were significantly prolonged. Time courses of arterial PO2 and PCO2 and of cerebrovenous PO2 were hardly influenced. However, arterial alkalosis and brain venous acidosis became highly significant versus control courses. This raised the O2 saturation in arterial and O2 extraction in cerebral venous blood. Sinus sagittalis puncture needle outflow (as a measure of CBF) tended to be below the control rat courses throughout. This led to a higher O2 supply to the brain in verapamil rats only during severe hypoxia. Verapamil did not prolong tolerance times in anoxia or ischemia. It is concluded that the verapamil-induced increase of tolerance to hypoxia is primarily due to the acid-base (Bohr) effects observed in response to hyperpnea and prolonged cerebral metabolic activity.

Animals↗
PubMed1977

[Dihydralazin versus prazosin. The hemodynamic effect of the modul substances (author's transl)].

The hemodynamic effects of dihydralazine and prazosin (0.1 and 1.0 mg/kg i.v.) on the circulatory system and left ventricular dynamics and contractility has been performed in 10 purebred beagle dogs (15.5 +- 1.4 kg) under pentobarbital sodium (35-40 mg/kg i.p.) anaesthesia by means of thermodilution and catheter technics. The changes of cardiovascular values were: 1. Either dihydralazine and prazosin decreased mean arterial blood pressure in the dose of 0.1 mg/kg i.v. Following application of 1.0 mg/kg intravenously, the arterial pressure abruptly decreased after prazosin. 2. Both pharmaca caused tachycardia. Being slowly introduced but continued by dihydralazine, the increase of pulse rate after prazosin was only initial. 3. The cardiac dynamics were differently influenced by dihydralazine and prazosin. In the estimated dose range prazosin led to an increase of cardiac output directly after application while dihydralazine induced a gradual enhancing of cardiac output. 4. The stroke volume was decreased by prazosin and slightly increased by dihydralazine. 5. While distinctly decreasing initially after prazosin, peripheral total resistance was slowly reduced by dihydralazine. 6. The contractility of the left ventricle, estimated as dp/dtmax and VCE, showed a distinct increase of the myocardial inotropy after both compounds. The maximal effect after prazosin, however, was to be seen immediately post applicationem. Dihydralazine led to a deferred enhancing of the measured contractility parameter.

Animals↗