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J J Pandit

Publications and source records attributed to J J Pandit.

At least 19 recordsLinked to original sources
PubMed1997

KTP laser-resistant properties of the reinforced laryngeal mask airway.

We have assessed, in vitro, the effect of KTP laser strike on the reinforced laryngeal mask airway (RLMA) under a variety of conditions. At power densities normally encountered in clinical practice, using a divergent KTP laser beam, the RLMA could not be penetrated and did not ignite with laser strike. The RLMA was penetrated at a high power density of 6.94 W mm-2 after 45-60 s. A flame appeared over the RLMA shaft at this power density after 12-35 s. The black marker line on the RLMA shaft was somewhat more vulnerable to the effects of laser strike. The flow of oxygen and nitrous oxide within the shaft did not appreciably alter the laser-resistant properties of the RLMA. The RLMA cuff was more vulnerable to laser strike than was the shaft and was penetrated at very low power densities. Filling the cuff with saline had a protective effect and penetration did not occur at power densities which caused penetration of air-filled cuffs (0.37 W mm-2).

Air↗
PubMed1997

The effect of exercise on the development of respiratory depression during sustained isocapnic hypoxia in humans.

The purpose of this study was to examine whether sustained hypoxia during exercise attenuates the degree of decline in hypoxic ventilatory sensitivity which occurs during sustained hypoxia at rest. The acute ventilatory response to hypoxia (AHVR) was used as a measure of the hypoxic ventilatory chemoreflex sensitivity. Seven subjects undertook three protocols. Protocol A was designed to assess the reduction in AHVR as a result of 20 min of isocapnic hypoxia (end-tidal PO2 50 mm Hg) at rest. The first AHVR (control) was measured on exposure to the hypoxia, and the second AHVR (test) measured 6 min after the end of the hypoxic period. Protocols B and C were designed to assess the reduction in AHVR as a result of 20 min of isocapnic hypoxic exercise (70 W). In protocol B, the AHVR (test) was measured at rest, 6 min after the end of 20 min of isocapnic hypoxic (end-tidal PO2 55 mm Hg) exercise. In protocol C, the AHVR (control) as measured at rest, 6 min after the end of 20 min of euoxic (end-tidal PO2 100 mm Hg) isocapnic exercise. There was a 30 +/- 5% decline (mean +/- SEM) in the magnitude of the AHVR after the period of sustained hypoxia at rest. There was an 11 +/- 7% decline in the magnitude of the resting AHVR after the period of sustained hypoxic exercise. The percentage change in AHVR following hypoxic exercise was significantly less than following hypoxia at rest (p < 0.05; paired t test). We conclude that the decline in hypoxic chemoreflex sensitivity which occurs during sustained hypoxia at rest is genuinely attenuated as a result of exercise.

Adult↗
PubMed1996

Ventilatory chemoreflexes at rest following a brief period of heavy exercise in man.

1. Ventilatory chemoreflex responses have been studied at rest during the recovery from a brief period of heavy exercise. 2. Six young, healthy male subjects each undertook four experimental studies. In each study measurements were made at rest during recovery from an exhaustive 1-2 min sprint on a bicycle ergometer with a workload of 400 W. Three levels of end-tidal O2 pressure (Po2) were employed. Continuous ventilatory measurements were made during euoxia (end-tidal Po2, 100 Torr), hypoxia (end-tidal Po2, 50 Torr) and hyperoxia (end-tidal Po2, 300 Torr). Arterialized venous blood samples were drawn during each of the measurement periods for the estimation of arterial pH. In two of the studies, end-tidal CO2 pressure (Pco2) was maintained throughout at 1-2 Torr above the eucapnic level that existed prior to exercise (isocapnic post-exercise protocol, IPE). In the other two studies, end-tidal Pco2 was allowed to vary (poikilocapnic post-exercise protocol, PPE). Data from a previously published study on the same subjects involving an infusion of hydrochloric acid were used to provide control data with a varying level of metabolic acidosis, but with no prior exercise. 3. Ventilation-pH slopes in the IPE protocol were no different from control. Ventilation-pH slopes in the PPE protocol were significantly lower than in the IPE and control protocols (P < 0.05, ANOVA). This difference may be due to the progressive change in end-tidal Pco2 in the PPE protocol compared with the constant end-tidal Pco2 in the IPE and control protocols. 4. An arterial pH value of 7.35 was attained 30.4 +/- 2.7 min (mean +/- S.E.M.) after the end of exercise in the IPE protocol and 17.1 +/- 1.4 min after the end of exercise in the PPE protocol. 5. Hypoxic sensitivities at an arterial pH of 7.35 were not significantly different between the IPE, PPE and control protocols (ANOVA). 6. Euoxic ventilation at an arterial pH 7.35 was significantly greater than control for the IPE protocol (P < 0.001, Student's paired t test) and no different from control for the PPE protocol. 7. The results suggest that 30 min after heavy exercise, ventilation remains stimulated by processes other than the post-exercise metabolic acidosis, and that changes in peripheral chemoreflex sensitivity to hypoxia and acid are not implicated in this.

Acidosis↗
PubMed1996

Statistical properties of breath-to-breath variations in ventilation at constant PETCO2 and PETO2 in humans.

The purpose of this study was to provide a statistical description of the breath-to-breath variations in ventilation during steady breathing in both rest and during light exercise, with the end-tidal gases controlled by using an end-tidal forcing system. Sixty data sets were studied, only one of which was white (i.e., did not show autocorrelation). Three simple autoregressive moving average (ARMA) models, i.e., AR1, AR2, and AR1MA1, and one simple state-space model were fitted to the data and resulted in white residuals in 15, 31, 46, and 48 out of 60 occasions, respectively. Evolutionary spectral analysis revealed that only 13 data sets had a constant power spectrum, although 50 were uniformly modulated. An autoregressive estimate of variance could be used to "demodulate" the data in most cases, but the results were not significantly affected by fitting the model to the demodulated data. The results indicate that 1) both simple ARMA models and a simple state-space model can describe the autocorrelation present; 2) variations in spectral power were present in the data that cannot be described by these models; and 3) these variations were often due to a uniform modulation and did not significantly affect the coefficients for the models. For these kinds of data, a heteroscedastic form of state-space model provides an attractive theoretical structure for the noise processes.

Air Pressure↗
PubMed1995

An assessment of central-peripheral ventilatory chemoreflex interaction using acid and bicarbonate infusions in humans.

1. The object of this study was to investigate the effect of central chemoreceptor stimulation on the ventilatory responses to peripheral chemoreceptor stimulation. 2. The level of central chemoreceptor stimulation was varied by performing experiments at two different levels of end-tidal CO2 pressure (PCO2). Variations in peripheral chemoreceptor stimulus were achieved by varying arterial pH (at constant end-tidal PCO2) and by varying end-tidal O2 pressure (PO2). 3. Two protocols were each performed on six human subjects. In one protocol ventilatory measurements were made during eucapnia, when the arterial pH was lowered from 7.4 to 7.3. The variation in pH was achieved by the progressive infusion of acid (0.1 M HCl). In the other protocol ventilatory measurements were made during hypercapnia, when the arterial pH was increased from 7.3 to 7.4. The variation in pH was achieved by the progressive infusion of 1.26% NaHCO3. In each protocol ventilatory responses were measured during euoxia (end-tidal PO2, 100 Torr), hypoxia (end-tidal PO2, 50 Torr) and hyperoxia (end-tidal PO2, 300 Torr), with end-tidal PCO2 held constant. 4. The increase in ventilatory sensitivity to arterial pH induced by hypoxia (50 Torr) was not significantly different between protocols (acid protocol, -104 +/- 31 l min-1 (pH unit)-1 vs. bicarbonate protocol, -60 +/- 44 l min-1 (pH unit)-1; mean +/- S.E.M.; not significant (n.s.)). The ventilatory sensitivity to hypoxia at an arterial pH of 7.35 was not significantly different between protocols (acid protocol, 14.7 +/- 3.3 l min-1 vs. bicarbonate protocol, 15.6 +/- 2.4 l min-1; mean +/- S.E.M.; n.s.). The results provide no evidence to suggest that peripheral chemoreflex ventilatory responses are modulated by central chemoreceptor stimulation.

Adolescent↗
PubMed1994

Acute ventilatory responses to hypoxia during voluntary and electrically induced leg exercise in man.

1. The acute ventilatory response to a brief period of hypoxia (AHVR) was measured in six subjects (a) at rest, (b) during electrically induced leg exercise (EEL), (c) during voluntary leg exercise at an external work rate matched to electrical exercise (EV1) and (d) during voluntary leg exercise at an internal work rate (i.e. metabolic rate) matched to electrical exercise (EV2). The end-tidal PO2 during hypoxia was 50 mmHg and the end-tidal PCO2 was held constant at 1-2 mmHg above resting values throughout each of these four protocols. 2. EEL was produced by surface electrode stimulation of the quadriceps muscles so as to cause the legs to extend at the knee and lift a set of weights via a pulley system. During EV1, each subject lifted the same weight through the same height and at the same frequency as during his EEL protocol. During EV2, the weight, the height through which it was lifted and the frequency of voluntary contractions were altered to produce a similar O2 consumption and CO2 production as during EEL. 3. In each subject, end-tidal PCO2 values showed no change between the four protocols, and in three subjects in whom they were measured, arterial PCO2 values were also similar between the protocols. Venous lactate levels did not increase after EEL or EV2. 4. The AHVR during EEL (14.1 +/- 1.42 l min-1; mean +/- S.E.M) was significantly increased (Student's paired t test) compared with rest (7.55 +/- 1.10 l min-1; P < 0.003).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Increased hypoxic ventilatory sensitivity during exercise in man: are neural afferents necessary?

1. The acute ventilatory response to 3 min periods of hypoxia (AHR) was examined in nine patients with clinically complete spinal cord transection (T4-T7) during (a) rest and (b) electrically induced leg exercise (EEL). 2. EEL was produced by surface electrode stimulation of the quadriceps muscles so as to cause the legs to extend at the knee against gravity. End-tidal PCO2 was held constant 1-2 mmHg above resting values throughout both protocols. 3. On exercise, the average increase in metabolic CO2 production (VCO2 +/- S.E.M.) was 41 +/- 5 ml min-1. Venous lactate levels did not rise with exercise. 4. Baseline euoxic ventilation did not increase significantly with EEL, but there was a consistent and highly significant increase in the ventilatory response to hypoxia during EEL (mean delta AHR +/- S.E.M. of 1.6 +/- 0.21 min-1). 5. We conclude that an increase in hypoxic sensitivity during exercise can occur in the absence of volitional control of exercise and in the absence of afferent neural input from the limbs.

Adult↗
PubMed1992

Effects of different levels of end-tidal PO2 on ventilation during isocapnia in humans.

The purpose of this investigation was to examine how the ventilatory decline observed during sustained, eucapnic hypoxia (HVD) is affected by different levels of hypoxia. Six subjects were each studied 3-6 times at each of 5 different levels of isocapnic hypoxia (end-tidal PO2 equal to 45, 50, 55, 65 and 75 Torr) in random order. The following variables were linearly related to saturation: (1) the rapid increase in ventilation at the onset of hypoxia; (2) the decline in ventilation over the period of hypoxia; and (3) the undershoot in ventilation below the pre-hypoxic control values at the relief of hypoxia. The rapid decrease in ventilation at the relief of hypoxia, however, was not linearly related to saturation. The mean time to peak ventilation was 2.13 +/- 0.07 min (+/- SE) at the onset of hypoxia, which was significantly longer (P less than 0.05) than the time to minimum ventilation at the relief of hypoxia of 1.23 +/- 0.18 min. The recovery from the undershoot in ventilation was 95% +/- 3% complete after 5 min, whereas the recovery in sensitivity to hypoxia was only 35% +/- 13% complete after 5 min of euoxia.

Adult↗
PubMed1991

The ventilatory effects of sustained isocapnic hypoxia during exercise in humans.

To investigate how the ventilatory response to isocapnic hypoxia is modified by steady-state exercise, five subjects were studied at rest and performing 70 W bicycle exercise. At rest, isocapnic hypoxia (end-tidal PO2 50 Torr) for 25 min resulted in a biphasic response: an initial increase in ventilation was followed by a subsequent decline (HVD). During exercise, an end-tidal PO2 of 55-60 Torr was used. The magnitude of the initial ventilatory response to isocapnic hypoxia was increased from a mean +/ SE of 1.43 +/- 0.323 L/min per % arterial desaturation at rest to 2.41 +/- 0.424 L/min per % during exercise (P less than 0.05), but the magnitude of the HVD was reduced from 0.851 +/- 0.149 L/min per % at rest to 0.497 +/- 0.082 L/min per % during exercise (P less than 0.05). The ratio of HVD to the acute hypoxia response was reduced from 0.696 +/- 0.124 at rest to 0.202 +/- 0.029 during exercise (P less than 0.01). We conclude that while exercise augments the ventilatory sensitivity to hypoxia, it also has a direct effect on the mechanisms by which sustained hypoxia depresses peripheral chemosensitivity.

Adult↗