Search PubMed⌕ Search

Biomedical subjects

P Reinstrup

Publications and source records attributed to P Reinstrup.

31 records · Page 2Linked to original sources
PubMed1997

Weight gain during pregnancy does not influence the spread of spinal analgesia in the term parturient.

BACKGROUND: It is still controversial whether the spread of spinal anaesthesia in pregnancy is influenced by particular physique. Investigation was based on a clinical observation that parturients with a pronounced "pregnant" physique, e.g. generalised oedema and heavy abdomen, tended to develop more cephalad sensory blockades than parturients without these physical signs. Using weight gain during pregnancy as a measure for the physique at term, we aimed to determine whether this parameter influences the distribution of analgesia after subarachnoidal injection of plain bupivacaine. METHODS: Thirty women presenting for elective Caesarean section were studied. All the women received 13.5 mg plain bupivacaine via subarachnoid injection at the L2-3 interspace. Thirty minutes after the injection, while the women were in the supine position with a left lateral tilt on a horizontal operating table, the maximum cephalad extent of sensory analgesia (loss of sensation to sharpness of pinprick) was determined. RESULTS: Neither weight gain during pregnancy (6-22 kg, range), height (152-185 cm), weight (56-98 kg) nor body-mass index (20.2-31.8 kg/m2) correlated with the cephalad spread of sensory blockade. CONCLUSION: In parturients, weight gain during pregnancy, height, weight and body-mass index did not influence the extent of sensory analgesia after subarachnoidal administration of plain bupivacaine.

Analgesia, Obstetrical↗
PubMed1995

Distribution of cerebral blood flow during anesthesia with isoflurane or halothane in humans.

BACKGROUND: Halothane and isoflurane have been shown to induce disparate effects on different brain structures in animals. In humans, various methods for measuring cerebral blood flow (CBF) have produced results compatible with a redistribution of CBF toward deep brain structures during isoflurane anesthesia in humans. This study was undertaken to examine the effects of halothane and isoflurance on the distribution of CBF. METHODS: Twenty ASA physical status patients (four groups, five in each) anesthetized with either isoflurane or halothane (1 MAC) during normo- or hypocapnia (PaCO2 5.6 or 4.2 kPa (42 or 32 mmHg)) were investigated with a two-dimensional CBF measurement (CBFxenon, intravenous 133xenon washout technique) and a three-dimensional method for measurement of the regional CBF (rCBF) distribution with single photon emission computer-aided tomography (SPECT; 99mTc-HMPAO). In the presentation of SPECT data, the mean CBF of the brain was defined as 100%, and all relative flow values are related to this value. RESULTS: The mean CBFxenon level was significantly influenced by the PaCO2 as well as by the anesthetic used. At normocapnia, patients anesthetized with halothane had a mean CBFxenon of 40 +/- 3 (SE) ISI units. With isoflurane, the flow was significantly (P < 0.01, 33 +/- 3 ISI units) less than with halothane. Hypocapnia decreased mean CBFxenon (P < 0.0001) during both anesthetics (halothane 24 +/- 3, isoflurane 13 +/- 2 ISI units). The effects on CBFxenon, between the anesthetics, differed significantly (P < 0.01) also during hypocapnia. There were significant differences in rCBF distribution measured between the two anesthetics (P < 0.05). During isoflurane anesthesia, there was a relative increase in flow values in subcortical regions (thalamus and basal ganglia) to 10-15%, and in pons to 7-10% above average. Halothane, in contrast, induced the highest relative flow levels in the occipital lobes, which increased by approximately 10% above average. The rCBF level was increased approximately 10% in cerebellum with both anesthetics. Changes in PaCO2 did not alter the rCBF distribution significantly. CONCLUSIONS: There is a difference in the human rCBF distribution between halothane and isoflurane with higher relative flows in subcortical regions during isoflurane anesthesia. However, despite this redistribution, isoflurane anesthesia resulted in a lower mean CBFxenon than did anesthesia with halothane.

Anesthesia↗
PubMed1994

[Acute acalculous cholecystitis].

Acute acalculous cholecystitis (AC) is an inflammatory process of the gallbladder, often caused by other severe diseases. The etiology is multifactorial, but the pathogenesis is in all cases a reduction in the gallbladder's emptying capacity. The mortality of AC reaches 85% without treatment. This fact makes it important to consider AC as a possible complication to major surgery, multi-trauma, and artificial ventilation. Symptoms resemble "normal" cholecystitis, but may be masked by the underlying severe disease. Fever without known focus may be the only symptom. Ultrasound, CT-scanning or cholangiography are used to verify the diagnosis, supplemented by laboratory investigations. Treatment is cholecystectomy. Percutaneous ultrasonic guided cholecystotomy is a good alternative if the diagnosis made in an early stage. The mortality is considerably reduced by early intervention.

Acute Disease↗
PubMed1994

Influence of halothane and isoflurane on the contractile responses to potassium and prostaglandin F2 alpha in isolated human pial arteries.

Volatile anaesthetics may modulate cerebrovascular resistance, but their direct actions on human cerebral arteries are unknown. In the present study, we have evaluated the effects of halothane and isoflurane at different MAC (0.4, 1.0 and 2.0) on contractions induced by depolarization (potassium) or receptor stimulation (prostaglandin F2 alpha) in isolated ring segments of human pial arteries. Neither halothane nor isoflurane had significant effects on potency (unaffected EC50 value) or the maximum response (Emax) in potassium-contracted arteries, even though there was a general tendency to attenuation of Emax. Similarly, the potency of prostaglandin F2 alpha was unchanged (unaffected EC50 value). However, the Emax value for prostaglandin F2 alpha at normocapnia (mean PCO2 4.3 (SEM 0.1) kPa, pH 7.41 (0.01)) and addition of halothane (0.4, 1.0 and 2.0 MAC) was significantly attenuated to 96 (2)%, 91 (3)% and 84 (4)% at the respective MAC concentrations. Isoflurane at 2 MAC and normocapnia also reduced Emax to 94 (3)%. During hypocapnia (PCO2 2.7 (0.1) kPa, pH 7.64 (0.01)), the vasodilator effect of halothane was reduced, whereas isoflurane at 0.4 and 1.0 MAC enhanced the contraction induced by prostaglandin F2 alpha.

Adult↗
PubMed1994

Effects of nitrous oxide on human regional cerebral blood flow and isolated pial arteries.

BACKGROUND: Results from previous studies on the effect of nitrous oxide (N2O) on the cerebral circulation are conflicting. Early reports claim N2O to have no effect whereas recent findings demonstrate a cerebral cortical vasodilatation during N2O inhalation, but the regional cerebral blood flow (CBF) in the subcortical structures is unknown. METHODS: Regional CBF was measured three-dimensionally with single photon emission computer-aided tomography after injection of xenon 133 in 8 spontaneously breathing men (mean age 29.6 yr) during normocapnia and hypocapnia with and without inhalation of 50% N2O. 8 isolated human pial arterial segments were mounted in organ baths. The segments were contracted with prostaglandin F2 alpha and subjected to 30% oxygen and 5.6% carbon dioxide in nitrogen or N2O. RESULTS: Normocapnic young men had a global CBF of 55 +/- 4 ml.100 g-1.min-1. Decreasing end-tidal CO2 tension by 1.3 kPa (9.3 mmHg) reduced CBF uniformly, with a decrease in global CBF to 45 +/- 2 ml.100 g-1.min-1 (P < 0.0001). During normocapnia, inhalation of 50% N2O increased mean CBF to 67 +/- 7 ml.100 g-1.min-1 (P < 0.0001). Inhalation of 50% N2O during hypocapnia increased mean CBF to 63 +/- 5 ml.100 g-1.min-1 (P < 0.0001). During N2O inhalation there was no significant difference in mean CBF between normo- and hypocapnia. However, during hypocapnia, but not during normocapnia, N2O inhalation significantly changed the distribution of regional CBF (P < 0.0001). Compared with hypocapnia without N2O, flow increased through the frontal (143%), parietal (140%) and temporal (133%) regions as well as through insula (151%), basal ganglia (145%) and thalamus (133%). In isolated human pial arteries, addition of N2O changed neither basal tension, nor the contraction elicited by prostaglandin F2 alpha. CONCLUSIONS: Inhalation of 50% N2O increased global CBF mainly by augmenting flow in frontal brain structures. In contrast, changes in carbon dioxide without N2O affected CBF uniformly in the brain. The uneven change in distribution of the CBF when N2O was added during hypocapnia, the reduced carbon dioxide response, and the lack of effect of N2O on isolated human pial arteries suggest that N2O may increase metabolism in selected brain areas.

Adult↗
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↗