Biomedical subjects

A F Meintjes

Publications and source records attributed to A F Meintjes.

8 recordsLinked to original sources

PubMed1996

NMDA receptor blockade in cat dorsal horn blunts reflex pressor response to muscle contraction and stretch.

The role of N-methyl-D-aspartate (NMDA) receptors in the reflex pressor response to static muscle contraction and passive stretch was examined by microdialyzing the NMDA receptor antagonist DL-2-amino-5-phosphonovalerate (AP-5) into the L7 or L6 and S1 levels of the dorsal horn of anesthetized cats. Contraction, elicited by electrical stimulation of the cut L7 and S1 ventral roots, increased mean arterial pressure (MAP) and heart rate (HR). Passive stretch at tensions similar to those generated by contraction also increased these variables. These cardiovascular changes were unaffected by dialyzing AP-5 (10 mM) into the dorsal horn at L7. Increasing the syringe concentration of AP-5 to 100 mM attenuated the pressor and HR responses from 62 +/- 8 to 31 +/- 6 mmHg and 18 +/- 4 to 12 +/- 4 beats/min, respectively. AP-5 blunted the increase in MAP (59 +/- 10 vs. 41 +/- 10 mmHg) evoked by muscle stretch. Simultaneously microdialyzing AP-5 (10 or 100 mM) into the dorsal horn at the L6 and S1 spinal levels also blunted the MAP and HR responses to contraction and stretch. These results suggest that NMDA receptors play a role in mediating the MAP and HR responses to static muscle contraction at the spinal level of the central nervous system. Furthermore, these data demonstrate that collaterals from muscle afferents partially mediate the reflex cardiovascular responses evoked by muscle contraction and stretch.

2-Amino-5-phosphonovalerate↗

PubMed1995

Modulation of reflex pressor response to contraction and effect on substance P release by spinal 5-HT1A receptors.

This study investigated whether activation of serotonin1A [5-hydroxytryptamine (5-HT)1A] receptors in the dorsal horn of the spinal cord attenuates the reflex pressor response to static contraction and passive muscle stretch. In addition, we determined if the attenuation of the response to contraction is mediated by inhibiting substance P (SP) release in the dorsal horn. Static contractions of the triceps surae muscle of chloralose-anesthetized cats were induced by stimulating the cut L7 and S1 ventral roots. Microdialysis (10 mM) of a selective 5-HT1A agonist [8-hydroxy-2-(di-N-propylamino)tetralin (8-OH-DPAT)] into the L7 dorsal horn region produced a reversible attenuation of the reflex pressor response to a 1-min contraction (in mmHg: control = 36 +/- 3; 8-OH-DPAT = 17 +/- 3; recovery = 31 +/- 8; P = 0.013; n = 6) or passive stretch (in mmHg: control = 36 +/- 6; 8-OH-DPAT = 15 +/- 2; recovery = 32 +/- 6; P = 0.002; n = 6). However, a 5-HT1B agonist, 1-[3-(trifluoromethyl)-phenyl]piperazine, had no effect on the reflex pressor response. During 5-min contractions (n = 8), 8-OH-DPAT (10 mM) also blunted the pressor response but had no effect on the levels of SP-like immunoreactivity (in fmol/100 microliters: control = 0.492 +/- 0.026; 8-OH-DPAT = 0.501 +/- 0.034). These results suggest that activation of 5-HT1A receptors in the dorsal horn attenuates the reflex pressor response to contraction through a mechanism other than inhibition of SP release.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1995

Attenuation of the exercise pressor reflex. Effect of opioid agonist on substance P release in L-7 dorsal horn of cats.

Using alpha-chloralose-anesthetized cats, we studied blood pressure and heart rate responses to static contraction and passive stretch of the triceps surae muscle before and after microdialyzing the mu-opioid agonist [D-Ala2]-methionine enkephalinamide (DAME, 200 mumol/L) into the L-7 dorsal horn of the spinal cord. In addition, we measured contraction-induced substance P release in the dorsal horn before and after drug delivery. After 92 +/- 3 minutes of dialyzing the opioid agonist, contraction-induced increases in mean arterial pressure and heart rate were attenuated from control values of 58 +/- 7 mm Hg and 17 +/- 3 beats per minute to postdrug values of 27 +/- 7 mm Hg and 10 +/- 2 beats per minute, respectively. A similar attenuation was observed for the passive muscle stretches after 97 +/- 5 minutes of dialysis (control, 38 +/- 4 mm Hg and 8 +/- 2 beats per minute; after drug, 23 +/- 4 mm Hg and 5 +/- 1 beats per minute). Prior microdialysis of naloxone (300 mumol/L), a mu-antagonist, blocked this effect, suggesting that the opioid agonist has a specific receptor action. Naloxone alone had no effect on the pressor or tachycardiac responses. The contraction-induced increase in substance P-like immunoreactivity was reduced from a control value of 0.119 +/- 0.024 to 0.047 +/- 0.010 fmol/100 microL by DAME. Time-control experiments revealed no decrease in the release of substance P-like immunoreactivity. Thus, activation of opioid receptors modulates the transmission of group III and IV muscle afferent nerve activity through the L-7 dorsal horn.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1994

Central cholinergic modulation of the exercise pressor reflex in anesthetized cats.

Effects of central administration of a cholinesterase inhibitor, physostigmine, on cardiovascular responses to static contraction and passive stretch of the triceps surae were studied using anesthetized cats. Contraction increased mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA) by 44 +/- 5 mmHg, 18 +/- 1 beats/min, and 86 +/- 6%, respectively. MAP, HR, and RSNA increased during stretch by 44 +/- 5 mmHg, 15 +/- 1 beats/min, and 61 +/- 4%, respectively. Administration of physostigmine (100 micrograms; 5 microliters) into the third ventricle decreased resting MAP by 22 +/- 3 mmHg and RSNA by 32 +/- 4%, with no effect on HR. Physostigmine attenuated the contraction-evoked responses as MAP, HR, and RSNA increased by 17 +/- 2 mmHg, 3 +/- 1 beats/min, and 31 +/- 6%, respectively. Also, physostigmine blunted MAP, HR, and RSNA responses to stretch (16 +/- 2 mmHg, 4 +/- 1 beats/min, and 9 +/- 6%, respectively). Posterior hypothalamic stimulation increased MAP by 39 +/- 3 mmHg, which was unaffected by physostigmine, despite a lower baseline. Cardiovascular and RSNA responses to contraction and stretch returned to control 90-120 min after physostigmine. Preadministration of the muscarinic antagonist, atropine sulfate (100 micrograms; 5 microliters), blocked the effects of physostigmine. Results suggest central cholinergic stimulation can inhibit the exercise pressor reflex in anesthetized cats.

Anesthesia↗

PubMed1994

Effects of clonidine on the reflex cardiovascular responses and release of substance P during muscle contraction.

The effects of microdialyzing clonidine into the L-7 dorsal horn on the cardiovascular responses, renal sympathetic nerve activity (RSNA), and release of substance P (SP) evoked by static contraction of the triceps surae muscle were studied using anesthetized cats. A microdialysis probe was inserted into the spinal cord ipsilateral to the muscle being contracted or stretched. Contraction, evoked by stimulation of the distal ends of the cut L-7 and S-1 ventral roots for 1 minute, increased mean arterial pressure (MAP), heart rate (HR), and RSNA by 48 +/- 6 mm Hg, 18 +/- 2 beats per minute, and 66 +/- 5%, respectively. Passive stretch of the same muscle for 1 minute also increased MAP, HR, and RSNA by 51 +/- 6 mm Hg, 17 +/- 2 beats per minute, and 50 +/- 3%, respectively. Microdialysis of clonidine (380 mumol/L) blunted the contraction-evoked responses: MAP, HR, and RSNA increased by 19 +/- 4 mm Hg, 7 +/- 1 beats per minute, and 24 +/- 5%, respectively. The increases elicited by passive stretch were also attenuated (MAP, 22 +/- 4 mm Hg; HR, 6 +/- 1 beats per minute; and RSNA, 15 +/- 4%). This attenuation by clonidine was dose dependent (3.8 mumol/L, 38 mumol/L, 380 mumol/L, and 3.8 mmol/L). Preadministration of the alpha 2-adrenergic antagonist yohimbine (3 mmol/L) blocked the effect of clonidine (380 mumol/L) on the cardiovascular and RSNA responses to muscle contraction. Clonidine (380 mumol/L) did not alter the release of SP in the dorsal horn during contraction (before clonidine, 0.380 +/- 0.018 fmol/100 microL; after clonidine, 0.356 +/- 0.012 fmol/100 microL).(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of Variance↗

PubMed1989

Improved physical fitness failed to alter the EEG patterns of sleep in young women.

We investigated the effect of a 12-week physical training programme on the sleep of nine unfit women. Data were collected at 0, 4, 8 and 12 weeks of the training programme. Changes in fitness were assessed by changes in maximal oxygen consumption (VO2max) and onset of blood lactate turn point (LTP). Lean body mass (LBM) was calculated from total body potassium measurements. The all-night sleep recordings were made following days during which the subjects carried out their normal daily routines and did no extra exercise. Although cardiorespiratory fitness improved significantly as indicated by an increase in both VO2max and LTP, there was no change in LBM. The improvement in cardiorespiratory fitness did not result in any changes in the sleep parameters measured. Other workers have reported an improvement in sleep quality in eight army recruits during their basic training. The male recruits showed improved cardiorespiratory fitness and an increase in muscle bulk. These results suggest that increased fitness only facilitates sleep when there is an associated increase in LBM. Alternatively it may be that the response of sleep to improved fitness is sex-linked.

Adult↗

PubMed1988

Daily exposure to forty percent oxygen causes a decrease in platelet count.

A study was undertaken to evaluate a previous observation made in this laboratory that hyperoxic treadmill training is associated with a decrease in the circulating platelet count (PLT). The subjects studied breathed air containing 40% oxygen for 30 min/day, 5 days/week, for 6 weeks, while at rest in the seated position. Such exposure resulted in a consistent fall in PLT between day 1 and day 5 of each week (P less than .01). In addition, there was a progressive decline in PLT over the 6 weeks of exposure to the hyperoxic air, PLT being inversely correlated with the duration of hyperoxic exposure (rs = -0.886, P less than .02). The total decrease in PLT over the 6 weeks was 56 +/- 46 x 10(9) l(-1) (P less than .025). Not surprisingly, these changes were mirrored in the plateletcrit (Pct). The decrease in PLT did not appear to be secondary to either hemodilution or reduced erythropoietic stimulation. The mechanism of production and the biological significance of these changes remain to be elucidated.

Administration, Inhalation↗

PubMed1988

Submaximal exercise effects on sleep patterns in young women before and after an aerobic training programme.

We studied the sleep patterns of nine young women when sedentary (untrained) and following a 12 week physical fitness training programme. A comparison of baseline sleep patterns and of sleep patterns following one hour of submaximal exercise performed in the evening was carried out at 0 and 12 weeks. The submaximal exercise task was for each subject to cycle for one hour at 70% of her maximal oxygen consumption (VO2 max) as measured when untrained and on completion of the training programme respectively. Changes in fitness were assessed by changes in VO2 max and anaerobic threshold (AT). On the day leading to the all night baseline sleep recordings the subjects carried out their normal daily routines and did no specific exercise. Lean body mass (LBM) was calculated from total body potassium measurements before and after training. A significant improvement in cardiorespiratory fitness did not result in any changes in baseline sleep parameters. The response to the submaximal exercise was an increase in stage 2 NREM sleep and a decrease in slow-wave sleep (SWS, stages 3 & 4) which is possibly indicative of a stress effect. However, in the trained compared to the untrained state, SWS was significantly higher after an exercise load.

Adult↗