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Biomedical subjects

Jani Penttilä

Publications and source records attributed to Jani Penttilä.

8 recordsLinked to original sources
PubMed2006

Delirium in an adolescent patient during treatment with cephalexin.

Although cephalosporins are generally safe, they have been reported to cause neurotoxic effects in some subjects. We report on a 16-year-old boy with no previous history of psychiatric illness, who developed symptoms of delirium during treatment of paronychia infection with cephalexin. Possible reasons for our patient's particular vulnerability to adverse drug effects in the central nervous system include his young age, a developmental delay, and an earlier head injury.

Adolescent↗
PubMed2006

Estimation of cardiac output in a pharmacological trial using a simple method based on arterial blood pressure signal waveform: a comparison with pulmonary thermodilution and echocardiographic methods.

OBJECTIVE: Cardiac output (CO) has traditionally been measured using invasive techniques, which involve an element of risk. Thus, a reliable less-invasive method for determining CO would be very valuable for research use. We tested whether simple analysis of the arterial pulse waveform, not requiring large-vessel catheterisation or expensive equipment, could provide an estimate of CO that is accurate enough for pharmacological studies. METHODS: We measured CO in 11 healthy male subjects who received low and high doses of dexmedetomidine (alpha2-adrenoceptor agonist), using pulse contour analysis, echocardiography and pulmonary thermodilution techniques. RESULTS: At baseline, these methods gave the following mean (SD) values of CO: 6.18 (1.59), 5.22 (1.35) and 7.03 (1.54) l/min, respectively. High-dose dexmedetomidine reduced CO to 4.50 (0.68), 3.65 (0.65) and 4.80 (0.89) l/min, corresponding to -25 (14) %, -28 (12) % and -30 (14) % reductions from baseline, respectively. The pulse contour method described these dexmedetomidine-induced changes in CO very similarly to the thermodilution and echocardiographic methods. The limits of agreement [bias (2SD)] were 0.55 (2.55) and -0.10 (2.04) l/min, respectively. CONCLUSION: The minimally invasive pulse contour analysis technique might be suitable for pharmacological studies for the detection of major drug-induced reductions in CO.

Adrenergic alpha-Agonists↗
PubMed2006

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Journal Article↗
PubMed2005

Analysis of rapid heart rate variability in the assessment of anticholinergic drug effects in humans.

Anticholinergic agents have widespread therapeutic indications in clinical medicine. In addition, certain other drug groups-such as neuroleptics, antidepressants and antihistamines-possess distinct anticholinergic properties that reduce tolerance and compliance. Especially in patients with heart disease, attention should be paid to cardiac anticholinergic drug effects. The analysis of short-term heart rate variability (HRV) provides a noninvasive tool to estimate vagal cholinergic outflow. In this review article, we present the basic principles of the most relevant techniques to study rapid HRV: the time domain analysis methods RMSSD and pNN50, and the high-frequency (HF) spectral component of HRV. We provide examples of previously reported effects of anticholinergic agents on these measures and also describe how adrenergic drugs may influence them. We have the following recommendations for a clinical pharmacologist investigating anticholinergic agents. (1) If the breathing rate of the study subject can be controlled during the assessment and the electrocardiogram recordings contain good-quality, stationary segments that are at least a few minutes long, then the HF power of HRV should be the method of choice. (2) During uncontrolled conditions, RMSSD should be included in the analyses, because it is less affected by changes in the respiratory pattern and it can be measured from shorter segments of electrocardiogram data. (3) Reduced short-term HRV suggests an anticholinergic, but not necessarily an antimuscarinic drug effect, since the inhibition of cholinergic vagal efferent activity may also originate from central or peripheral adrenergic influences.

Adrenergic Agents↗
PubMed2004

Effects of fluoxetine on dopamine D2 receptors in the human brain: a positron emission tomography study with [11C]raclopride.

We have previously reported that repeated dosing with the selective serotonin reuptake inhibitor (SSRI) citalopram decreases striatal [11C]raclopride binding in healthy volunteers. As the SSRI-class antidepressant drugs are believed to have a similar mechanism of action, we wanted to explore whether the prototype SSRI drug, fluoxetine, shares the effects of citalopram on subcortical dopamine neurotransmission. Eight healthy male volunteers were studied using a randomized double-blind placebo-controlled study design. Striatal and thalamic D2-receptor binding was measured at baseline, after a single oral dose (20 mg) of fluoxetine, and after repeated dosing (2 wk, 20 mg/d). The D2-receptor binding potential (BP) was assessed using [11C]raclopride and 3D positron emission tomography. Repeated dosing of fluoxetine decreased BP in the right medial thalamus (p=0.022). Fluoxetine did not decrease striatal BP, but there was a trend (p=0.090) towards increased BP in the left putamen after repeated dosing. A single dose of fluoxetine did not affect BP in the thalamus or striatum. Fluoxetine appears to have a regionally selective effect on the dopaminergic neurotransmission in various areas of the brain. The current results after fluoxetine together with our previous data on citalopram suggest that the modulatory effects of these drugs on striatal dopaminergic neurotransmission are different upon repeated dosing and further substantiates pharmacological differences between SSRI-class drugs.

Adult↗
PubMed2004

Cardiovascular and parasympathetic effects of dexmedetomidine in healthy subjects.

We evaluated the cardiovascular effects of intravenously (i.v.) and buccally administered dexmedetomidine, a selective alpha2-adrenoceptor agonist. Six healthy male subjects were studied unmedicated and after 2 micro g/kg i.v. or buccal doses of dexmedetomidine, using repeated recordings of ECG and blood pressure. Cardiac parasympathetic activity was estimated by measurements of high-frequency (HF) heart rate variability. Intravenous, but not buccal, dexmedetomidine raised systolic blood pressure by 11 +/- 5 mmHg (mean +/- SEM) and diastolic by 16 +/- 3 mmHg (maxima at 10 min). Later on, both i.v., and buccal dexmedetomidine produced a very similar hypotensive effect: on average, >or=10 mmHg reductions in systolic and diastolic pressure at 3 h. Intravenous dosing was followed by a decline in heart rate (-11 +/- 2 beats/min) accompanied by a trend toward enhanced HF variability (maximal effect at 10 min), which probably reflected baroreflex-mediated parasympathetic efferent neuronal activation. Buccal dexmedetomidine increased significantly the HF variability (maximum at 45 min) without influencing heart rate. We conclude that dexmedetomidine, when administered by a method that avoids concentration peaks, e.g., buccal dosing, can be used to produce a prolonged augmentation of cardiac parasympathetic efferent neuronal activity.

Administration, Buccal↗
PubMed2003

Bioavailability of dexmedetomidine after extravascular doses in healthy subjects.

AIM: To determine the absolute bioavailability of extravascularly administered dexmedetomidine, a novel a2-adrenoceptor agonist, in healthy subjects. METHODS: Single 2 microg x kg-1 doses of dexmedetomidine were given intravenously, intramuscularly, perorally and buccally (where the solution is not swallowed) to 12 healthy male subjects. The drug concentration-time data were analysed using linear one-compartment (buccal and peroral data), or two-compartment modelling (intravenous data), or noncompartmental methods (intramuscular data). RESULTS: Mean (95% CI) absolute bioavailability after peroral, buccal and intramuscular administration was 16% (12-20%), 82% (73-92%) and 104% (96-112%), respectively. CONCLUSION: Dexmedetomidine is well absorbed systemically through the oral mucosa, and therefore buccal dosing may provide an effective, noninvasive route to administer the drug.

Adrenergic alpha-Agonists↗