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Biomedical subjects

C Puchstein

Publications and source records attributed to C Puchstein.

At least 37 records · Page 2Linked to original sources
PubMed1984

Haemodynamic and cerebral effects of ATP-induced hypotension.

Controlled decreases in mean arterial pressure to 20%, 40% and 60% of baseline were produced by the administration of increasing concentrations of adenosine triphosphate (ATP) i.v. in five anaesthetized baboons. Indices of the systemic circulation (arterial pressure, right atrial pressure, pulmonary artery pressures, cardiac output) and of the cerebral circulation (cerebral blood flow, cerebral metabolic rate for oxygen, cerebrovascular reactivity) were obtained as arterial pressure was decreased, and following discontinuation of the infusion of ATP. A neuropathological investigation was undertaken at the end of the experimental procedure. The infusion of ATP produced dose-dependent decreases in systemic vascular resistance and mean arterial pressure (MAP). Cardiac output and stroke volume were maintained close to baseline values, or increased slightly. Cerebral blood flow (CBF) increased initially (48 +/- 4 ml min-1/100 g to 68 +/- 9 ml min-1/100 g) and then decreased progressively as MAP was decreased to 40% and 60% of baseline. Cerebrovascular reactivity was shown to be impaired during, and for up to 90 min following, the administration of ATP. However, there was no morphological evidence of ischaemic cell damage in any animal. Tachyphylaxis was not observed during, and there were no instances of rebound hypertension following, the infusion of ATP. The concentration of uric acid had increased significantly by the 40% decrement in MAP, and remained so 60 min after the restoration of the arterial pressure.

Adenosine Triphosphate↗
PubMed1984

Influence of ketanserin, an antihypertensive agent with specific 5-HT2-receptor blocking activity, on intracranial pressure.

During administration of ketanserin, a selective 5-HT2-receptor blocker, intracranial pressure (ICP) was measured in dogs without (group 1) and with (group 2) intracranial hypertension (ICP greater than 20 mm Hg). A bolus of 1 mg/kg body weight and subsequent infusion of 13.25 +/- 1.2 mg/kg of ketanserin decreased mean arterial pressure 35% +/- 18% in group 1 and 35% +/- 19% in group 2. In both groups, there was no change in ICP or in ventricular volume-pressure response curves (intracranial compliance [ICC]) after the administration of ketanserin. Ketanserin may be a safe antihypertensive drug for avoiding and treating hypertension in neurosurgical patients.

Animals↗
PubMed1984

[The use of urapidil in the postoperative period].

Increases in blood pressure and heart rate often seen with endotracheal intubation during induction of anaesthesia and with extubation during termination of anaesthesia are dangerous for many patients. In 20 patients pretreated with urapidil, a new antihypertensive agent, changes in blood pressure and heart rate were compared with the haemodynamic parameters of 20 untreated patients. 0.6 mg/kg urapidil are given before induction of anaesthesia and 0.4 mg/kg +/- 0.2 mg/kg urapidil before its termination. The results show that urapidil is a suitable drug to avoid dangerous increases in blood pressure during such situations, without producing hypotension. Therefore urapidil is recommended as a supplementary therapy in high risk patients.

Adult↗
PubMed1984

Changes in intracranial pressure and compliance during adenosine triphosphate-induced hypotension in dogs.

Intracranial pressure (ICP) was measured during induced hypotension with increasing doses of adenosine triphosphate (1-5 mg X kg-1 X min-1 ATP) in dogs without (group I) and with (group II) intracranial hypertension. After administration of 1 mg X kg-1 X min-1 ATP, ICP increased significantly from 11 +/- 4 mm Hg to 14 +/- 5 mm Hg (mean +/- SEM) (P less than 0.05; group I) and from 27 +/- 2 mm Hg to 38 +/- 6 mm Hg (P less than 0.05; group II), while mean arterial pressure (MAP) decreased from 103 +/- 10 mm Hg to 86 +/- 6 mm Hg (P less than 0.05; group I) and from 110 +/- 11 mm Hg to 90 +/- 11 mm Hg (P less than 0.05; group II). In both groups a slow decrease of ICP after the initial increase occurred with further lowering of MAP, but ICP remained significantly above control values even with a dose of 5 mg X kg-1 X min-1 ATP (P less than 0.05). Ventricular volume-pressure response curves (VPR) before and during intravenous infusion of 3 mg X kg-1 X min-1 ATP were constructed to determine changes in intracranial compliance (ICC). In both groups I and II ATP decreased ICC. On the basis of these results it is recommended that in the presence of intracranial mass lesions ATP should not be given to induce arterial hypotension before the dura is opened.

Adenosine Triphosphate↗
PubMed1983

Treatment of hypertension with labetalol in neurosurgical practice. Influence of labetalol on cerebral perfusion pressure in dogs without and with intracranial mass lesions.

In neurosurgical patients autoregulation of cerebral perfusion is often lost. Therefore, a sudden increase in blood pressure may lead to an increase in cerebral blood flow and cerebral oedema may follow. The influence of labetalol, a new alpha- and beta-adrenoceptor blocking agent, on intracranial pressure and cerebral perfusion pressure was investigated in dogs without and with mass lesions. During hypotension with labetalol the intracranial pressure remained unchanged and the cerebral perfusion pressure decreased to the same extent as mean arterial pressure (30%). Labetalol seems to be suitable to treat hypertension perioperatively in neurosurgical patients but it is not a suitable drug for induced hypotension.

Animals↗
PubMed1983

The influence of urapidil, a new antihypertensive agent, on cerebral perfusion pressure in dogs with and without intracranial hypertension.

The influence of urapidil, an arylpiperazinederivate, on intracranial pressure (ICP), mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) was investigated in dogs with (group II) and without (group I) intracranial hypertension. After i.v. administration of urapidil, intracranial pressure remained unchanged and cerebral perfusion pressure decreased to the same extent as mean arterial pressure (20%). As in neurosurgical patients, autoregulation of cerebral blood flow is often lost; a sudden increase in blood pressure may lead to an increase in cerebral blood flow and to a damage of the blood bain barrier with consequent cerebral edema. Urapidil seems to be suitable for treating hypertensive episodes perioperatively in neurosurgical patients.

Anesthesia, Conduction↗
PubMed1983

Influence of urapidil on intracranial pressure and intracranial compliance in dogs.

During induced hypotension with urapidil, measurements of intracranial pressure and of the ventricular volume-pressure response (intracranial compliance) were obtained in dogs with and without intracranial hypertension. A bolus of urapidil 50 mg plus an infusion of urapidil 8.2 +/- 1.2 mg min-1 decreased mean arterial pressure by 22 +/- 10% from control in group I (without intracranial hypertension) and by 24 +/- 8% in group II (with intracranial hypertension). In both groups there was no change in intracranial pressure or in intracranial compliance after the administration of urapidil.

Animals↗
PubMed1982

Effect of labetalol on intracranial pressure in dogs with and without intracranial hypertension.

Intracranial pressure measurements and ventricular volume pressure response curves were made during induced hypotension with labetalol, a combined alpha- and beta-adrenoceptor antagonist, in dogs without (group I) and with (group II) intracranial hypertension. The administration of 600 mg labetalol resulted in a percentage decrease of mean systemic arterial blood pressure (MAP) of 27% (+/- 10%) in group I, and 32% (+/- 9%) in group II from control values without changes in intracranial pressure and the ventricular volume pressure response curve. Larger decreases in MAP were not possible, even with a dose 3 times that clinically recommended. Labetalol may be a safe hypotensive agent to supplement neurolept analgesia, but it is not the drug of choice to induce deliberate hypotension.

Animals↗
PubMed1982

The use of labetalol in producing deliberate hypotension and its effects on intracranial pressure in dogs.

The use of effective and safe hypotensive agents in neuroanesthesia is a difficult and unanswered question. Most hypotensive agents produce an increase in intracranial pressure and as a result can not be used until the dura is opened. In experiments in dogs, Labetalol, a combined alpha and beta-adrenoceptor antagonist, showed no increase in intracranial pressure and no change in intracranial compliance by producing hypotension.

Anesthesia↗
PubMed1982

[Controlled hypotension with ATP. Animal experiment studies in dogs].

Reliable efficacy and short half-time, combined with the absence of tachyphylaxis and reactive hypertension during and after controlled hypotension should be considered important factors in the use of hypotensive drugs. The vasodilating action of adenosine triphosphate (ATP) was investigated for deliberate hypotension in anaesthesized dogs. During a continuous infusion, in which the dose of ATP was increased from 1 mg/kg . min ATP to 5 mg/kg . min ATP, a stepwise decrease in mean arterial pressure (MAP) and systemic vascular resistance (SVR) could be observed (55%; p less than 0.001). Cardiac output and heart rate increased (p less than 0.05). The physiological intrapulmonary shunt remained unchanged during ATP infusion. ATP acts within 30 sec. and after the end of the infusion haemodynamic parameters returned to control levels within two minutes.

Adenosine Triphosphate↗
PubMed1979

Specific binding of 3H-adenosine to rat brain membranes.

The binding of 3H-adenosine to rat brain membranes was studied by a microcentrifugation technique. Specific binding of 3H-adenosine was rapid, reversible, saturable and dependent on pH and temperature. Scatchard plots of equilibrium binding data were nonlinear suggesting the existence of two different binding sites for adenosine. The dissociation constants (Kd) were 1.7 muM and 13.6 muM and the maximal number of binding sites (Bmax) 31 and 165 pmol adenosine bound per mg of membrane protein. Ten adenosine derivatives were studied for their ability to compete with 3H-adenosine binding. The phosphorylated adenosine compounds 5'-AMP, cyclic AMP and ATP were most potent in displacing 3H-adenosine from its binding sites and the IC50-values ranged from 11--25 muM. N6-Phenylisopropyladenosine produced only partial inhibition (30%) of 3H-adenosine binding and no stereospecific difference between the (-)- and (+)isomer was observed. Several methylxanthines known as adenosine antagonists competed for the 3H-adenosine binding sites parallel with their pharmacological potency. The results offer a first approach for the study of adenosine binding sites in brain membranes.

Adenosine↗