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  • 1990-1994  (3)
  • 1955-1959
  • 1950-1954
  • ketanserin  (3)
  • 1
    ISSN: 0942-0940
    Keywords: Carbon dioxide ; cerebral blood flow ; cerebral oxygen metabolism ; cerebral vascular reactivity ; ketanserin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of the anti-hypertensive agent ketanserin on the cerebral blood flow (CBF) and the cerebrovascular CO2 reactivity was examined in 10 healthy volunteers. Ketanserin was administered as an intravenous bolus of 10 mg followed by an infusion of 6mg/h. Before administration CBF was measured by single photon emission computerized tomography (SPECT) of inhaled133 Xenon. Then arterial CO2 tension was subsequently decreased by voluntary hyperventilation and increased by breathing an air/CO2 mixture. The relative changes in CBF induced by the changes in arterial CO2 tension were estimated by the cerebral arterio-venous oxygen content difference method. One hour following the start of ketanserin infusion the SPECT measurement and CO2 manipulations were repeated. The CO2 reactivity (expressed as the slope of the regression line of the linear relation between CBF and PaCO2), was unchanged, i.e. 3.2%/0.1 kPa before ketanserin and 4. 1%/0.1 kPa during ketanserin, respectively. Using regression lines from a semi-logarithmic plot the CO2 reactivity was also unchanged 3.4%/0.1 kPa and 3.5%/0.1 kPa, respectively. Ketanserin did not change CBF. The cerebral oxygen metabolism (CMRO2) was decreased 19% one hour after the start of infusion of ketanserin. In conclusion administration of ketanserin in a clinically relevant dose to healthy volunteers does not change the regional CBF not the cerebrovascular CO2 reactivity, but a decrease in CMRO2 was observed. However further studies are needed to clarify whether ketanserin in fact has a depressing effect on CMRO2 or whether the different results are caused by methodological errors or stocastic variation.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 0942-0940
    Keywords: Cerebral blood flow ; cerebral oxygen metabolism ; blood pressure ; ketanserin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of the anti-hypertensive agent ketanserin on average global cerebral blood flow (CBF) and average global cerebral oxygen metabolism (CMRO2) was examined in 8 healthy volunteers. CBF and CMRO2 were measured with the Kety-Schmidt technique before ketanserin administration (baseline) and after administration of 2 different doses of ketanserin intravenously (dose I: 10 mg bolus and an infusion of 6 mg/h; dose II: 20 mg bolus and an ifusion of 20 mg/ h). Baseline CBF and CMRO2 were 60 and 3.6 ml/100 g/min, respectively, and were not changed by administration of ketanserin dose I. During administration of dose II, however, CBF fell to 52 ml/ 100 g/min (p=0.05) and CMRO2 was reduced to 3.2 ml/100 g/min (p 〈 0.05). We conclude that when administered in a high dose, ketanserin has the ability to depress cerebral oxygen metabolism, but when administered in a clinically relevant dose ketanserin does not influence average global CBF or average global CMRO2. Ketanserin could be a safe antihypertensive drug in neuroanaesthesia or in the neuro-intesive care unit.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0942-0940
    Keywords: Cerebral blood flow ; autoregulation ; arterial blood pressure ; ketanserin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of a clinically relevant dose of ketanserin (10 mg as a bolus followed by an infusion of 6mg/h) on cerebral blood flow (CBF) and CBF autoregulation was examined in 12 healthy volunteers. Changes in CBF were estimated by the cerebral arteriovenous-oxygen saturation difference method, while mean arterial blood pressure (MABP) was increased by norepinephrine and decreased by ganglionic blockade (trimethaphan camphosulphonate) combined with lower body negative pressure one hour after the infusion of ketanserin. During ketanserin infusion, MABP fell insignificantly by 2.5 mmHg (6 to −2), while CBF rose insignificantly by 5 ml/100 g/min. Autoregulation was preserved in all volunteers. CO2-correction factors from 0 to 4.6% CBF/0.1 kPa were used. The lower limit of CBF autoregulation was 82 mmHg (80–86) with an SE of 3 mmHg (1–5) similar to a previous control group of healthy volunteers. Aside from a major decrease in MABP in one subject, no adverse side effects were observed. The present study shows that CBF autoregulation is maintained during ketanserin infusion.
    Type of Medium: Electronic Resource
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