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Biomedical subjects

D Heuser

Publications and source records attributed to D Heuser.

At least 37 records · Page 2Linked to original sources
PubMed1983

Cerebral cortical extracellular fluid H+ and K+ activities during hypotension in cats.

Cerebral cortical blood flow, electrical activity, and extracellular fluid (ECF) pH and K+ ion activities were measured in anesthetized cats (0.7% halothane 65% N2O in O2) subjected to hypotension (mean BP 30-32 and 26-28 mmHg), induced by either practolol and trimetaphan (TMP) or practolol and nitroprusside (NTP). Limited blood withdrawal was also necessary to achieve these blood pressure (BP) levels. Cerebral cortical blood flow during hypotension was greater with NTP than with TMP, and hyperemia occurred in the recovery phase after NTP but not TMP. Electrical activity also was maintained better with NTP. ECF K+ increased in five of six TMP experiments but in only one of six NTP experiments. Values of K+ greater than 15 mM were only seen in the TMP group. Release of K+ into the ECF space occurred at values of cerebral cortical oxygen delivery below 3 ml 100 g-1 min-1. ECF K+ partially recovered after the end of hypotension in all except the experiment with the highest value. A progressive and severe cerebral acidosis was seen in all experiments during induced hypotension, and values below pH 6.50 were present at the stage of K+ increase in the ECF space. It is concluded that the ability of cell membranes in the cat's cortex to maintain normal ionic gradients is depressed by hypotension to these levels with TMP, but not with NTP, and that this difference is related to better-maintained oxygen supply values during NTP hypotension.

Animals↗
PubMed1979

Relationship between cerebral blood flow changes and cortical extracellular fluid pH during cerebral metabolic depression induced by althesin.

Baboons anaesthetized with halothane and nitrous oxide in oxygen were given Althesin 0.05 ml kg-1 i.v. Cerebral blood flow (c.b.f.) was measured by an electromagnetic flowmeter and by xenon clearance whilst extracellular fluid (e.c.f.) pH of the parietal cortex was measured with a micro pH electrode. Carotid blood flow (carBF) began to decrease and carotid vascular resistance (carVR) to increase 2.0 s (SEM 0.3) after the slowing of the e.e.g. produced by Althesin, while e.c.f. pH began to change to alkaline 10.5 s (SEM 1.0) after the e.e.g. change. The first statistically significant increase in mean e.c.f. pH occurred 25 s after the Althesin-induced change in the e.e.g. The duration of the changes in carVR and e.c.f. pH were 7 and 5 min respectively. It is concluded that the change in e.c.f. pH cannot have initiated the increase in carVR which followed the cerebral matabolic depression produced by Althesin. The later alkaline shift in e.c.f. pH may, however, have maintained the increased carVR during the duration of cerebral metabolic depression produced by Althesin.

Alfaxalone Alfadolone Mixture↗
PubMed1978

Control of cerebral vascular smooth muscle during general anaesthesia.

The effects of some general anaesthetics, for example thiopentone, Althesin (alphaxalone + alphadolone) and ketamine, on cerebral vascular smooth muscle are those which would be expected from their metabolic actions. With other anaesthetics, mainly those administered by inhalation, and especially the volatile agents, cerebral blood flow increases in excess of the metabolic activity, which is usually depressed to varying degrees. During general anaesthesia with any of these agents, responses to changes in arterial Pco2 or blood pressure are maintained. Furthermore, when seizure activity occurs during enflurane administration, there is a flow response to the associated metabolic stimulation. The time course of the flow response to the metabolically depressant drug Althesin has been measured in baboons and shown to be very rapid. Wtih this drug cerebrovascular resistance begins to increase within 2 s of its arrival in the brain. This rapid flow change occurs also after sympathetic denervation. Extracellular fluid pH of the cortex does not alter until after the initiation of the vascular smooth muscle response.

Alfaxalone Alfadolone Mixture↗
PubMed1975

Brain carbonic acid acidosis after acetazolamide.

In cats in barbiturate anesthesia extracellular pH and potassium were continously recorded from brian cortex by implanted microelectrodes. Implantation of the electrodes preserved the low permeability of the blood-brain-barrier to HCO3-minus and H+ions as indicated by the development of brain acidosis by I.V. injection of HCO3-minus. Acetazolamide (25 mg/kg) i.v. was followed by a marked brain acidosis which after 10 min had progressed to a drop in pH of 0.203 plus or minus 0.046 (x bar plus or minus S.D., n equals 8). The slowness ofthe development of acidosis points to a direct effect of the carbonic anhydrase inhibition on the brain tissue. As a further support for this conclusion was considered the finding of a prolonged response time of brain pH to HCO3-minus i.v. to CO2-minus inhalation, and to hyperventilation after the acetazolamide inhibtion. No changes in brain extracelllular potassium were found.

Acetazolamide↗