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Biomedical subjects

P A Robbins

Publications and source records attributed to P A Robbins.

At least 37 records · Page 2Linked to original sources
PubMed1999

Ventilatory responses to hypercapnia and hypoxia after 6 h passive hyperventilation in humans.

1. Acute exposure to hypoxia stimulates ventilation and induces hypocapnia. Long-term exposure to hypoxia generates changes in respiratory control known as ventilatory acclimatization to hypoxia. The object of this study was to investigate the degree to which the hyperventilation and hypocapnia can induce the changes known as ventilatory acclimatization to hypoxia, in the absence of the primary hypoxic stimulus itself. 2. Three 6 h protocols were each performed on twelve healthy volunteers: (1) passive hypocapnic hyperventilation, with end-tidal CO2 pressure (PET,CO2) held 10 Torr below the eupnoeic value; (2) passive eucapnic hyperventilation, with PET,CO2 maintained eucapnic; (3) control. 3. Ventilatory responses to acute hypercapnia and hypoxia were assessed before and half an hour after each protocol. 4. The presence of prior hypocapnia, but not prior hyperventilation, caused a reduction in air-breathing PET,CO2 (P < 0.05, ANOVA), and a leftwards shift of the ventilatory response to hypercapnia (P < 0.05). The presence of prior hyperventilation, but not prior hypocapnia, caused an increase in the ventilatory sensitivity to CO2 (P < 0.05). No significant effects of any protocol were detected on the ventilatory sensitivity to hypoxia. 5. We conclude that following 6 h of passive hyperventilation: (i) the left shift of the VE-PET,CO2 relationship is due to alkalosis and not to hyperventilation; (ii) the increase in slope of the VE-PET,CO2 relationship is due to the hyperventilation and not the alkalosis; and (iii) ventilatory sensitivity to hypoxia is unaltered.

Acclimatization↗
PubMed1999

Effects of subanaesthetic sevoflurane on ventilation. 1: Response to acute and sustained hypercapnia in humans.

We have determined the influence of 0.1 minimum alveolar concentration (MAC) of sevoflurane on ventilation, the acute ventilatory response to a step change in end-tidal carbon dioxide and the ventilatory response to sustained hypercapnia in 10 healthy adult volunteers. Subjects undertook a preliminary 10-min period of breathing air without sevoflurane to determine their normal ventilation and natural end-tidal PCO2. This 10-min period was repeated while breathing 0.1 MAC of sevoflurane. Subjects then undertook two procedures: end-tidal PO2 was maintained at 13.3 kPa and end-tidal PCO2 at 1.3 kPa above the subject's normal value for 30 min of data collection, first with and then without 0.1 MAC of sevoflurane. A dynamic end-tidal forcing system was used to generate these gas profiles. Sevoflurane did not significantly change ventilation: 10.1 (SEM 1.0) litre min-1 without sevoflurane, 9.6 (0.9) litre min-1 with sevoflurane. The response to acute hypercapnia was also unchanged: mean carbon dioxide response slopes were 20.2 (2.7) litre min-1 kPa-1 without sevoflurane and 18.8 (2.7) litre min-1 kPa-1 with sevoflurane. Sustained hypercapnia caused a significant gradual increase in ventilation and tidal volume over time and significant gradual reduction in inspiratory and expiratory times. Sevoflurane did not affect these trends during sustained hypercapnia. These results suggest that 0.1 MAC of sevoflurane does not significantly affect the acute ventilatory response to hypercapnia and does not modify the progressive changes in ventilation and pattern of breathing that occur with sustained hypercapnia.

Acute Disease↗
PubMed1999

Effects of subanaesthetic sevoflurane on ventilation. 2: Response to acute and sustained hypoxia in humans.

We have determined the influence of 0.1 minimum alveolar concentration (MAC) of sevoflurane on the acute ventilatory response to hypoxia (AHVR), hypoxic ventilatory decline (HVD) and the magnitude of the rapid decline in ventilation on relief of sustained hypoxia (the off-response) in eight healthy adult volunteers. The following design was used with and without 0.1 MAC of sevoflurane: end-tidal PO2 was maintained at 13.3 kPa for 5 min, at 7.9 kPa for 20 min and at 13.3 kPa for 5 min. End-tidal PCO2 was held constant throughout at 1.3 kPa above the subject's normal value. A dynamic end-tidal forcing system was used to generate these gas changes. Sevoflurane reduced AHVR from 14.5 (SEM 1.2) to 11.6 (1.6) litre min-1, and the off-response at cessation of hypoxia from 7.1 (1.1) to 6.3 (1.4) litre min-1. The magnitude of HVD was slightly increased by sevoflurane from 8.2 (1.1) to 10.6 (2.8) litre min-1. None of these changes was significant (ANOVA). These results suggest that 0.1 MAC of sevoflurane had very little effect on the AHVR, and that it did not markedly alter the processes underlying HVD during sustained hypoxia.

Acute Disease↗
PubMed1999

Effects of dopamine and domperidone on ventilatory sensitivity to hypoxia after 8 h of isocapnic hypoxia.

Acclimatization to altitude involves an increase in the acute hypoxic ventilatory response (AHVR). Because low-dose dopamine decreases AHVR and domperidone increases AHVR, the increase in AHVR at altitude may be generated by a decrease in peripheral dopaminergic activity. The AHVR of nine subjects was determined with and without a prior period of 8 h of isocapnic hypoxia under each of three pharmacological conditions: 1) control, with no drug administered; 2) dopamine (3 microg. min-1. kg-1); and 3) domperidone (Motilin, 40 mg). AHVR increased after hypoxia (P </= 0. 001). Dopamine decreased (P </= 0.01), and domperidone increased (P </= 0.005) AHVR. The effect of both drugs on AHVR appeared larger after hypoxia, an observation supported by a significant interaction between prior hypoxia and drug in the analysis of variance (P </= 0. 05). Although the increased effect of domperidone after hypoxia of 0. 40 l. min-1. %saturation-1 [95% confidence interval (CI) -0.11 to 0. 92 l. min-1. %-1] did not reach significance, the lower limit for this confidence interval suggests that little of the increase in AHVR after sustained hypoxia was brought about by a decrease in peripheral dopaminergic inhibition.

Acclimatization↗
PubMed1999

Assessments of flow by transcranial Doppler ultrasound in the middle cerebral artery during exercise in humans.

This study examined the consistency between three indexes of cerebral blood flow (CBF) obtained by using transcranial Doppler ultrasound in eight human volunteers. Each subject undertook three sessions of graded exercise, consisting of 6 min of rest, 6 min at 20% of maximal oxygen uptake (VO2 max), 6 min at 40% VO2 max, and 6 min of recovery. Values were obtained every 10 ms for the velocity associated with the maximal frequency of the Doppler shift (VP), the intensity-weighted mean velocity (VIWM), and total signal power (P). Beat-by-beat averages for three indexes (P, IWM, provided significantly different results for the percent changes in CBF with exercise. At 20% of VO2 max, P and IWM showed significant (P < 0.05) increases of 8 and 6%, respectively, whereas showed a nonsignificant increase of 3%. At 40% of VO2 max, P and IWM showed significant (P < 0.05) increases of 14 and 8%, respectively, whereas showed a nonsignificant increase of 4%. Our results suggest that the increase in CBF with exercise that has been reported with transcranial Doppler ultrasound needs to be treated with caution, as much of the response could arise as an artifact from the increase in amplitude and frequency of the arterial pressure waveform.

Adult↗
PubMed1999

Ventilatory effects of 8 h of isocapnic hypoxia with and without beta-blockade in humans.

This study investigated whether changing sympathetic activity, acting via beta-receptors, might induce the progressive ventilatory changes observed in response to prolonged hypoxia. The responses of 10 human subjects to four 8-h protocols were compared: 1) isocapnic hypoxia (end-tidal PO2 = 50 Torr) plus 80-mg doses of oral propranolol; 2) isocapnic hypoxia, as in protocol 1, with oral placebo; 3) air breathing with propranolol; and 4) air breathing with placebo. Exposures were conducted in a chamber designed to maintain end-tidal gases constant by computer control. Ventilation (VE) was measured at regular intervals throughout. Additionally, the subjects' ventilatory hypoxic sensitivity and their residual VE during hyperoxia (5 min) were assessed at 0, 4, and 8 h by using a dynamic end-tidal forcing technique. beta-Blockade did not significantly alter either the rise in VE seen during 8 h of isocapnic hypoxia or the changes observed in the acute hypoxic ventilatory response and residual VE in hyperoxia over that period. The results do not provide evidence that changes in sympathetic activity acting via beta-receptors play a role in the mediation of ventilatory changes observed during 8 h of isocapnic hypoxia.

Adrenergic beta-Antagonists↗
PubMed1999

Exercise-induced hyperkalemia and concentration of Na,K-pumps in skeletal muscle in mitral stenosis: effect of balloon mitral valvotomy.

BACKGROUND AND AIMS OF THE STUDY: The study aim was to examine the effects of balloon mitral valvotomy (BMV) on exercise-induced hyperkalemia, and on changes in the concentration of Na,K-pumps in skeletal muscle, as an exaggerated exercise-induced rise in potassium concentration ([K+]) may contribute to exertional fatigue and breathlessness. METHODS: Eight subjects were evaluated with mitral stenosis (mean age 34 +/- 5.2 years) before, and at two weeks and four months after BMV. Subjects underwent incremental exercise to exhaustion for exercise-induced rise in [K+] and vastus lateralis biopsy for concentration of Na,K-pumps. RESULTS: Mean (+/- SE) valve area increased from 0.89 +/- 0.03 cm2 before to 1.75 +/- 0.05 cm2 after BMV. There was a progressive increase in VO2,max (15.3 +/- 1.6, 17.2 +/- 1.4 and 19.9 +/- 1.9 l/kg/min) at baseline, early after and later after BMV, respectively (p < 0.01). The rise in [K+] with absolute workload fell progressively at early and late follow up post-BMV (p < 0.05), but was unchanged when plotted against percentage of VO2,max to match for relative workload. The concentration of Na,K-pumps was similar to baseline at early follow up (233 +/- 10 versus 228 +/- 15 pmol/g wet weight), but was significantly increased at late follow up after four months (265 +/- 17 pmol/g; p < 0.05). When the relationship between the concentration of Na,K-pumps and the exercise-induced rise in [K+] was studied, a negative correlation was found. However, correlation analysis for the effects of changes in Na,K-pumps on changes in exercise hyperkalemia after BMV was not significant. CONCLUSIONS: The progressive reduction in exercise-induced rise in [K+] after BMV may contribute to the progressive improvement in exercise performance. The increased concentration of Na,K-pumps in skeletal muscle may assist in this improvement, and emphasizes the importance of peripheral adaptations in clinical improvement after BMV.

Adult↗
PubMed1998

Human immunodeficiency virus type 1 infection of antigen-specific CD4 cytotoxic T lymphocytes.

The effect of macrophage (M)-tropic and T cell line (T)-tropic human immunodeficiency virus type 1 (HIV-1) infection on antigen-specific CD4 cytotoxic T lymphocytes (CTLs) has been studied using a CD4 CTL line specific for a peptide from influenza B virus hemagglutinin. In the absence of antigen presentation, the production of CC chemokines was low. Both the M-tropic HIV-1 strain (HIV-1AD) and the T-tropic HIV-1 strain (HIV-1LAI) established productive infections in the CD4 CTLs, decreasing antigen-specific cytotoxicity. Peptide presented to the CD4 CTLs increased their secretion of RANTES and MIP-1beta, suppressed M-tropic HIV-1 replication, downmodulated CCR5 expression, and preserved CTL recognition. The suppression of M-tropic HIV-1 replication and downmodulation of the CCR5 receptor likely resulted from CC chemokine secretion since antibodies to CC chemokines restored M-tropic HIV-1 replication. Antigen presentation did not protect CD4 CTLs from T-tropic HIV-1 infection or preserve their CTL recognition. Thus, these CD4 CTLs do not make suppressor factors that inhibit the T-tropic HIV-1LAI isolate. The results indicate that these CD4 CTLs can either harbor or suppress M-tropic HIV-1 infection, depending on whether antigen is present. CD4 CTLs might therefore provide some protection in the early stages of HIV-1 infection when M-tropic isolates are present.

B-Lymphocytes↗
PubMed1998

Leg blood flow and increased potassium release during exercise in chronic heart failure: effect of physical training.

BACKGROUND: Exercise-induced hyperkalemia, which may contribute to exercise hyperpnea and exertional fatigue, is increased in patients with chronic heart failure (CHF). This study examined whether differences in leg blood flow during exercise could be responsible for alterations in the level of hyperkalaemia, as well as the effect of physical training. METHODS AND RESULTS: We studied 10 subjects with CHF (ejection fraction 23 +/- 3.9%; mean +/- SD) and 10 subjects with normal left ventricular function (NLVF) who had undergone previous coronary bypass graft surgery (ejection fraction 64 +/- 8.0%; mean +/- SD). Subjects performed incremental cycle exercise to exhaustion before and after physical training. The rises in femoral venous potassium concentration ([K+]), heart rate, lactate, and ventilation (VI) with exercise were all greater in the subjects with CHF than in those with NLVF (P < .05). There was no difference between the groups in leg blood flow during submaximal exercise but peak leg flow was greater in the group with NLVF (P < .01). Physical training was well tolerated and both groups increased their peak VO2 (8 +/- 3.2% CHF (P < .05); 11 +/- 2.7% NLVF (P < .01); mean +/- SE). Training resulted in a reduced rise in femoral venous [K+] and VI (P < .05), but did not affect leg blood flow during submaximal exercise in either group. CONCLUSIONS: The rise in the femoral venous [K+] with exercise is increased in patients with CHF and can be reduced by physical training. These changes are not a consequence of different leg blood flows, either between groups or with training. The study also suggests that femoral venous [K+] is not a powerful regulator of leg blood flow during exercise.

Aged↗