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Biomedical subjects

P Reinstrup

Publications and source records attributed to P Reinstrup.

7 recordsLinked to original sources
PubMed1992

[Closed anesthetic systems].

Anaesthesia with closed anaesthetic systems demands knowledge of the physiology of the patients and of how the various anaesthetic gases behave in the organism as only the gases which the patients produces and absorbs are eliminated and replaced. The system is educational as it provides knowledge of the genuine absorption of oxygen and anaesthetic gases. The method is favourable to the environment as only the gases which are used are supplied and it is thus economical in use although investment in monitoring equipment is necessary. In practice, induction and waking of the patient are complicated with this system and it requires an anaesthetist who constantly adjusts the gases in the circuit.

Anesthesia, Closed-Circuit↗
PubMed1992

[Low-flow anesthesia systems].

At present, when economy and environment receive high priority, the ideal anaesthesia system with inhalation anaesthetics is a closed circle system in which only the gases which the patient consumes or produces are replaced or eliminated. Low-flow (LF) anaesthesia in which the fresh gas flow which is employed in a closed system, provides a stable system compares with closed anaesthesia systems. Compared with open systems and circler systems with considerable fresh gas flow, the LF system provides advantages as regards economy, environment and exposure of staff to inhalation anaesthetics. The special conditions involved in LF anaesthesia are described in detail with the hope that the method will obtain more widespread distribution than is the case in Denmark today. If greater safety under anaesthesia is desired, eg by monitoring the concentrations of CO2, O2 and inhalation anaesthetics which the patients inspire and expire, this monitoring equipment can be financed by introduction of LF anaesthesia.

Anesthesia, Closed-Circuit↗
PubMed1992

Oxygen modulates contractile responses to potassium and prostaglandin F2 alpha in human pial arteries.

Oxygen may modulate cerebrovascular resistance, but its direct influence on human pial arteries is unknown. We have investigated the effects of varying oxygen tension (73, 30 and 8 kPa) in depolarized (potassium) and receptor stimulated (prostaglandin F2 alpha) isolated human pial arteries. Control responses were obtained at an oxygen tension of 30 kPa. Contractions induced by prostaglandin F2 alpha and potassium showed no significant difference in potency (unaffected EC50 values) at the different oxygen concentrations. In contrast, the maximum contractions (Emax) were dependent on the oxygen tension. Potassium-induced contractions were enhanced (Emax = 107 (SE 3)% of control contractions (P less than or equal to 0.01)) at an oxygen tension of 73 kPa, whereas a reduction in tension to 8 kPa had no significant effect (97 (2)%). Prostaglandin F2 alpha-induced contractions were enhanced at 73 kPa (115 (6)%) (P = 0.02) and depressed at 8 kPa (96 (2)%) (P = 0.02). Reduction in oxygen tension induced a relaxation in depolarized and in receptor stimulated arteries, regardless of whether or not oxygen was replaced by nitrogen or by helium. Low oxygen tension relaxed arteries despite pretreatment with 2,4-dinitrophenol, an agent which blocks oxidative phosphorylation. It is concluded that a reduction in oxygen tension exerted a direct, although small, depressant effect on human pial arteries, and that this effect was not mediated exclusively by hyperpolarization or by inhibition of oxidative phosphorylation.

2,4-Dinitrophenol↗
PubMed1992

Modulation by carbon dioxide and pH of the contractile responses to potassium and prostaglandin F2 alpha in isolated human pial arteries.

Variation of PCO2 with concomitant changes in extracellular pH (pHo) may modulate cerebrovascular resistance, but the direct actions of carbon dioxide and pHo on human cerebral arteries are unknown. In this study, we have evaluated the effects of different carbon dioxide tensions (2.7, 4.2 and 7.2 kPa) with either fixed (pHo = 7.44) or concomitant changes in pHo, on contractions induced by depolarization (potassium) or receptor stimulation (prostaglandin F2 alpha) in isolated human pial arteries. Isolated changes in PCO2 had no significant effect on either potency (unchanged EC50 value) or the maximum response (Emax) in potassium-contracted arteries. Hypercapnia with uncompensated pHo significantly decreased both EC50 and Emax values, whereas uncompensated hypocapnia significantly increased the EC50 value without any effect on Emax. Concentration-response curves induced by prostaglandin (PG) F2 alpha were shifted significantly to the right (increased EC50 = decreased potency) during both hypo- and hypercapnia, independent of changes in pHo. The maximal responses were enhanced significantly during hypocapnia (Emax = 110 (SEM 2)%), but this enhancement was converted into a slight attenuation when pHo was compensated (Emax = 92 (4)%). Hypercapnia, with or without compensation of pHo, decreased the Emax values to 69 (16)% and 73 (9)%, respectively. We conclude that hypocapnia increases contractility in human pial arteries--an effect which is reversed by compensation of pHo. In contrast, the hypercapnic decrease of PGF2 alpha-induced contractions appears to be independent of pHo. The results confirm a relationship between contractility and pHo, but do not exclude a direct action of carbon dioxide in receptor-stimulated arteries.

Adult↗
PubMed1990

Actions of platelet-activating factor on isolated feline and human cerebral arteries.

The effects of platelet-activating factor (PAF) were studied on isolated feline basilar arteries (BAs) and human pial arteries (PAs). PAF contracted the BAs by 67% of the contraction induced by 124 mM K+ and the PAs by 80%. The contraction in BAs was unaffected by both indomethacin and the thromboxane receptor antagonist AH23848. PAF relaxed prostaglandin F2 alpha-contracted arteries. In BAs 10(-6) M PAF reduced the contraction by 17% and in PAs by 47%. The relaxant effects in both arteries were unaffected by indomethacin. In conclusion, PAF can act both as a constrictor and as a dilator of isolated feline and human cerebral arteries. The effects are seemingly unrelated to vascular prostanoid production.

Animals↗