Biomedical subjects

T Tähtinen

Publications and source records attributed to T Tähtinen.

3 recordsLinked to original sources

PubMed2000

Blood pressure responses to whole-body cold exposure: effect of carvedilol.

OBJECTIVE: The aim of this study was to test the effects of carvedilol on blood pressure (BP) and heart rate (HR) during whole-body cold exposure in hypertensive and normotensive subjects. METHODS: Ten hypertensive and twelve normotensive subjects were exposed to cold (-15 degrees C, wind 3.5 m/s) three times for 15 min with a 1-week interval between the exposures. The study design was made according to a randomised double-blind, crossover method. Before the cold exposures the subjects ingested carvedilol or placebo once a day (carvedilol 12.5 mg/day for 2 days and then 25 mg/day for 5 days) for 1 week. The systolic (SBP) and diastolic (DBP) blood pressure and HR were measured every 3 min during the test procedures using an indirect ambulatory blood pressure monitor device (ABPM-02, Meditech Co.). RESULTS: In the hypertensive group, the cold exposure increased SBP/DBP from 119/75 mmHg to 143/96 mmHg during carvedilol treatment (P<0.001) and from 132/85 mmHg to 159/106 mmHg during placebo (P<0.001). In the normotensive group the cold exposure increased SBP/DBP from 112/72 mmHg to 142/93 mmHg during carvedilol treatment (P<0.001) and from 121/75 mmHg to 147/98 mmHg during placebo (P<0.001). In the hypertensive group, the levels of SBP, DBP and MAP (mean arterial pressure) were significantly lower with carvedilol than with placebo during the cold exposure although carvedilol did not affect the cold-induced rise of the BP. The BPs were lower also with carvedilol in the normotensive group than the placebo during the cold exposure, but the differences were smaller than in the hypertensive group. Carvedilol decreased the BP more the higher the initial mean SBP/DBP was with placebo during the cold exposure. CONCLUSION: Carvedilol reduced the BP during the cold exposure, especially in the hypertensive subjects but also in normotensive ones, without effect on the cold-induced rise of the BP.

Adrenergic beta-Antagonists↗

PubMed1999

Effect of amlodipine on blood pressure responses in local and whole-body cooling in normotensive men.

The objective of this study was to determine the ability of amlodipine (CAS 88150-42-9, Norvasc) to affect the cold-induced rise of blood pressure and heart rate in normotensive men. Fourteen normotensive men underwent a one-hand cold pressor test (+10 degrees C, 5 min) and a whole-body cold air exposure test (+5 degrees C, 45 min) in a crossover study with and without amlodipine at a seven-day interval. Amlodipine decreased the levels of initial systolic and diastolic blood pressure before both tests, but it had no influence on heart rate. During the cold pressor test, amlodipine lowered the peak diastolic pressure from 96 +/- 10 mmHg (mean +/- SD) to 92 +/- 10 mmHg (p = 0.024). The rise of diastolic blood pressure was 13 +/- 7 mmHg with amlodipine and 16 +/- 8 mmHg without amlodipine (p = 0.138). During the whole-body cold air exposure test, amlodipine decreased the systolic pressure from 135 +/- 2 mmHg to 133 +/- 3 mmHg (p = 0.008) and the diastolic pressure from 88 +/- 2 mmHg to 86 +/- 1 mmHg (p = 0.005). However, the cold-induced rise of blood pressure in whole-body cooling was not affected by amlodipine, because it also decreased the initial values. Amlodipine did not affect the initial or cold-induced changes of heart rate in these tests. In conclusion, in normotensive men amlodipine lowers the peak of diastolic blood pressure in a cold pressor test. In whole-body cold air exposure, amlodipine slightly decreases the levels of both systolic and diastolic pressures, but has no effect on the cold-induced rise of blood pressure. Amlodipine does not prevent the cold-induced physiological responses of blood pressure or heart rate.

Adult↗

PubMed1983

Mouse IgG antibodies have subclass associated affinity differences.

Subclasses of IgG were separated from pools of mouse sera by letting immunoglobulins absorb on protein A-Sepharose and by eluting with buffers of decreasing pH. Most donor mice were immunized with a conjugate of a hapten (NIP) and chicken gamma globulin 20 days previously. The results indicate that concentrations of IgG varied from 5.1 to 8.6 mg/ml in the pools of immune sera and was 3.0 mg/ml in one normal serum tested. One half of this was IgG1, ca. 20% of IgG2a and IgG2b each, and 10% IgG3 in the pools of BALB/c sera. IgG2a and IgG3 could not be separated from C57BL sera (due to allotype b), but their combined share of IgG appears to be higher than in BALB/c. Immune sera contained 0.5-1.6 mg/ml of anti-NIP antibodies. Of this 90-98% was IgG1 and the remainder was split between the other subclasses. Up to one half of the protein in the IgG1 fraction was anti-NIP antibody. This surprising finding was confirmed by demonstrating that nearly 50% of the u.v.-light absorption was specifically removed by a NIP-immunosorbent. Subclass-associated affinity-differences were observed. IgG1 anti-NIP had a greater average affinity than IgG2a anti-NIP antibodies. The difference was ca. 1.5-fold when the equilibrium dialysis was focusing on the high-affinity bracket of the total population (concentration of free hapten 16-200 nM). At higher hapten concentrations the trend was the same but the data are fewer. Antibodies in subclasses IgG2b and IgG3 appear to share the lower affinity of IgG2a.

Animals↗