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Biomedical subjects

S Lahiri

Publications and source records attributed to S Lahiri.

At least 73 records · Page 4Linked to original sources
PubMed1997

Effect of CO on VO2 of carotid body and chemoreception with and without Ca2+.

This study was done using high PCO (> 500 Torr at PO2 of 120 Torr) in the carotid body perfusate in vitro, and recording simultaneously the activity of the whole carotid sinus nerve (CSN) and VO2 of the carotid body. In the cascade of excitation of CSN by high PCO in the dark [light eliminated the excitation; S. Lahiri, News Physiol. Sci. 9 (1992) 161-165], Ca2+ effects occur at the level of neurosecretion after the level of oxygen consumption, according to the following scheme: CO-hypoxia-->VO2 decrease-->K+ conductance decrease-->cell depolarization-->cytosolic Ca2+ rise-->neurosecretion-->neural discharge. Thus, a part of the hypothesis was that [Ca2+] decrease, being a downstream event, may not affect VO2 of the carotid body. Also, to determine to what extent the intracellular calcium stores contribute to cystolic [Ca2+] and chemosensory discharge with high PCO, we tested the effect of interruption of perfusate flow with medium nominally free of [Ca2+] on CSN excitation and VO2 of the carotid body with and without high PCO. High PCO in the dark decreased carotid body VO2, independent of [Ca2+]o. CSN excitation was always enhanced by high PCO, and its sensitivity to perfusate flow interruption. Also, nominally Ca(2+)-free solution increased the latency and decreased the rate of rise and peak activity of CSN during interruption of perfusate flow, but CO augmented the responses. This reversal effect by CO suggests that Ca2+ is released from intracellular stores, because CO has no other way to excite the chemoreceptors than by acting on the intracellular stores.

Animals↗
PubMed1997

CO interact with intracellular [H+] with and without CO2-HCO3- in the cat carotid chemosensory discharge.

To test the hypothesis whether CO2-HCO3- buffer is essential for the expression of chemoreception and to distinguish between pHi and pHo interaction with pCO in the carotid chemosensory response, we superfused-perfused in vitro cat carotid bodies using HEPES-Tyrode's solution with and without CO2-HCO3-, and compared the responses at the same pHo in the absence and presence of light. In the absence of light, pCO (> 138 Torr) stimulated the carotid body chemoreceptors in CO2-HCO3- buffer at pHo of 7.40, whereas pCO (69-550 Torr) did not stimulate the neural discharge in HEPES buffer at the pHo of 7.4-7.1 but did so below pHo 7.1. In the presence of light, all the responses were diminished proportionately.

Animals↗
PubMed1997

Potential role of H2O2 in chemoreception in the cat carotid body.

The hypothesis that H2O2 plays a critical role in hypoxic chemoreception in the cat carotid body (CB) was tested using a perfused-superfused preparation in vitro, measuring chemosensory discharge and CB tissue PO2 (PtiO2). According to the hypothesis NADPH mediated, PO2 dependent increase in H2O2 production would hyperpolarize the glomus cell, decreasing the chemosensory discharge. Thus, lactate and aminotriazole which would increase H2O2 concentration, would decrease the chemosensory discharge during hypoxia. However, 2.5-5.0 mM lactate and 25 mM aminotriazole did not diminish the hypoxic response. But, 2.5 mM lactate decreased the chemosensory discharge during normoxia which can be explained by an increase of CB PtiO2. Diethyldithiocarbamic acid (5 mM), which blocks the conversion of superoxide to H2O2, also diminished the chemosensory discharge, presumably due to an increased CB PtiO2. Menadione (increasing H2O2) and t-butyl hydroperoxide irreversibly decreased the chemosensory discharge, and the data are not useful. H2O2 increased the PO2 of the perfusate, and therefore could not be tested against PO2. Thus, perturbation of endogenous or exogenous H2O2 did not provide any evidence for its critical role in O2 chemoreception.

Amitrole↗
PubMed1997

Cat carotid body chemosensory discharge (in vitro) is insensitive to charybdotoxin.

Charybdotoxin (ChTX), a venom protein, suppresses Ca2+-activated K+ (K+(Ca)) currents in the glomus cell of neonatal rat carotid body. If it works similarly for cat carotid body chemoreceptors, charybdotoxin is expected to stimulate the chemosensory discharge during normoxia, and particularly hypoxia and hypercapnia. We studied the effects of charybdotoxin (20-40 nM) in vitro (perfused/superfused) on the cat carotid chemosensory discharge, and simultaneously tissue PO2 (PtiO2), as a measure of positive control. ChTX (20 nM) only increased PtiO2 and decreased carotid chemosensory discharge during hypoxia, indicating vasodilation. We conclude that K+(Ca) channels do not appear to play a significant role in chemotransduction in the cat carotid body.

Animals↗
PubMed1997

Superoxide radical production stimulates retroocular fibroblast proliferation in Graves' ophthalmopathy.

Retroocular fibroblast proliferation is believed to be a key component in the pathogenesis of Graves' ophthalmopathy. In the present study, we assessed the ability of superoxide radicals, generated using the xanthine oxidase/hypoxanthine system to induce cellular proliferation in cultured human retroocular fibroblasts obtained from two patients with severe Graves' ophthalmopathy and two control patients undergoing corrective eye surgery. In tissue obtained from patients with Graves' ophthalmopathy, fibroblast proliferation, as assessed by [3H]-thymidine incorporation, was induced by superoxide radicals in a dose-dependent manner. Xanthine oxidase or hypoxanthine alone had no proliferative effect, and control retroocular fibroblasts showed no proliferation in response to superoxide generation. Preincubation with the antithyroid drug methimazole, at concentrations ranging from 0-25 microM, prevented superoxide-induced fibroblast proliferation in a dose-response pattern. Preincubation with the xanthine oxidase inhibitor, allopurinol (1.0 mM) or the antioxidant nicotinamide (10 microM) also inhibited superoxide-induced fibroblast proliferation, whereas propylthiouracil (10 microM) had little effect. These studies suggest a pathway through which oxygen free radicals may contribute to the retroocular fibroblast proliferation observed in patients with Graves' ophthalmopathy.

Allopurinol↗
PubMed1997

Awareness and knowledge of AIDS among Indian women: evidence from 13 states.

Over 30,000 ever-married women in 13 (out of 25) Indian states where HIV is thought to be highly prevalent-Maharashtra, West Bengal, Tamil Nadu, and ten other less populous states-were surveyed about their awareness and knowledge of AIDS. Only one in six women had heard of AIDS. Among those, knowledge about transmission and prevention is poor. Multivariate analyses reveal that rural, poorly educated, and poor women are the least likely to be AIDS-aware and if aware, have the poorest understanding of the syndrome. Despite low levels of awareness and knowledge, we find a strong positive association between AIDS awareness and knowledge and condom use.

Adolescent↗
PubMed1996

Stimulus interaction between CO and CO2 in the cat carotid body chemoreception.

Since high PCO in the dark works like hypoxia in the carotid body chemoreceptors and since hypoxia shows a stimulus interaction with CO2, it is hypothesized that high PCO will show a similar interaction with PCO2 in the chemosensory excitation in the dark. We tested the hypothesis using cat carotid body perfused and superfused in vitro with Po2 of about 100 Torr. In one series, the chemosensory discharges were tested at three levels of PCO2 at high PCO of 500 Torr in the absence and presence of light. In the dark, normocapnia (PCO2 approximately 30 Torr) with high PCO promptly stimulated the sensory discharges to a peak, subsiding to a lower level. In hypocapnia (PCO2 approximately 18 Torr) with high PCO, all phases of activities were significantly lower than those of normocapnia, showing stimulus interaction. Hypercapnia saturated the activity with high PCO and seems to preclude a clear demonstration of stimulus interaction. In another series, an intermediate level of PCO (approximately 150 Torr), which showed a half-maximal activity in normoxia, showed a clear interaction with hypercapnia in the dark. With high PCO, bright light promptly reduced the activity to baseline at all PCO2 levels. This then increased somewhat to a steady-state. Withdrawal of the light was followed by a sharp rise in the activity to a peak which then fell to a somewhat lower level of steady-state. The peak discharge rate in the presence of light did not differ significantly from those of PCO2 alone.

Animals↗
PubMed1996

Thapsigargin enhances carotid body chemosensory discharge in response to hypoxia in zero [Ca2+]e: evidence for intracellular Ca2+ release.

To test the hypothesis that Ca2+ is released from intracellular store in the carotid body glomus cells during hypoxia, we stimultaneously measured chemosensory discharge and tissue PO2 of perfused-superfused cat carotid body before and during flow interruption in the presence and absence of extracellular [Ca2+] with and without thapsigargin (1-10 microM). Ca(2+)-free solution increased the latency of sensory response, and decreased the rate of rise and peak activity but thapsigargin significantly influenced these responses, without affecting oxygen consumption. Since thapsigargin depletes the intracellular Ca2+ store, and since Ca2+ is needed for the sensory discharge, these results suggest that intracellular release and influx of Ca2+ occur during hypoxia.

Animals↗
PubMed1996

Effects of hypoxia on carotid body dopamine content and release in developing rabbits.

Hypoxia induces dopamine (DA) release from the carotid body (CB), but the role of DA during hypoxia in the postnatal maturation of carotid chemosensory discharge remains controversial. The aim of this study was to evaluate changes in CB content and release of DA evoked by hypoxia at different stages of development in the rabbit. Five groups of rabbits aged < or = 24 h (n = 9), 5 days (n = 27), 15 days (n = 18), 25 days (n = 16), and > or = 1 yr (n = 11) were studied. CBs were surgically removed and immediately incubated at 37 degrees C for 1 h in a surviving medium equilibrated with 100% O2 or 8% O2 in N2. The content of DA in the CB ([DA]CB) and the DA released in the surviving medium ([DA]r) were measured by high-performance liquid chromatography. [DA]CB was significantly larger in adults than in all pup groups in both 100% O2 [385.5 +/- 74.1 (SE) pmol/CB in adults and 43.6 +/- 6.0 pmol/CB in pups; P < 0.01] and hypoxia (518.1 +/- 99.9 pmol/CB in adults and 24.7 +/- 3.2 pmol/CB in pups; P < 0.01), presumably because of the larger CB mass. [DA]r was significantly larger in hypoxia than in 100% O2 only in 25-day-old rabbits (19.8 +/- 4.2 and 3.6 +/- 1.1 pmol/h, respectively; P < 0.01) and in adults (183.9 +/- 57.7 and 7.9 +/- 1.7 pmol/h, respectively; P < 0.01). The average ratio of [DA]r in hypoxia to [DA]r in 100% O2 ranged from 1.3 to 2.2 in the three younger age groups and was 5.5 and 23.3 in 25-day-old and adult rabbits, respectively. We conclude that the release of DA evoked by hypoxia is weak at birth and develops during the first weeks of life in rabbits.

Aging↗
PubMed1996

Adaptation to hypercapnia vs. intracellular pH in cat carotid body: responses in vitro.

The hypotheses that the chemosensory discharge rate parallels the intracellular pH (pHi) during hypercapnia and that the initial change in pHi (delta pHi) is always more than the stead-state delta pHi were studied by using cat carotid bodies in vitro at 36.5 degrees C in the absence and presence of methazolamide (30-100 mg/l). Incremental acidic hypercapnia was followed by an incremental initial peak response and a greater adaptation. A given acidic hypercapnia elicited a rapid initial response followed by a slower adaptation; isohydric hypercapnia produced an equally rapid initial response but of smaller magnitude that returned to near-baseline level; alkaline hypercapnia induced a similar rapid initial response but one of still smaller magnitude that decreased rapidly to below the baseline. Methazolamide eliminated the initial overshoot, which also suggested involvement of the initial rapid pHi in the overshoot. These results show that the initial delta pHi is always greater than the steady-state delta pHi and during hypercapnia. Also, the steady-state chemoreceptor activity varied linearly with the extracellular pH, indicating a linear relationship between extracellular pH and pHi.

Adaptation, Physiological↗
PubMed1996

Public perceptions of brain tumours in Scotland: the need for access to appropriate information.

The aim of the study was to evaluate knowledge and perceptions of brain tumours in a heterogeneous, highly educated group of adults living in Edinburgh. Two hundred and forty four respondents answered a questionnaire about the causes, effects and treatments of brain tumours. There were misconceptions about several clinical and biological aspects of intracranial tumours although most respondents were aware of the bleak prognosis associated with many neoplasms. These results, from the intellectual elite of Scotland's capital, suggest that access to information about brain tumours should be readily available. Five leaflets, covering various aspects of brain tumours, that are available through the recently established Scottish charity Brain Tumour Action seem well formulated to address areas of concern and misconception.

Adult↗
PubMed1995

Nitric oxide synthase in autonomic innervation of the cat carotid body.

In the cat carotid body, nitric oxide synthase (NOS) immunoreactivity and NADPH diaphorase activity localize in nerve fibers mainly associated with blood vessels and occasionally lying close to glomus cells. The NOS-positive innervation originates in part from multipolar ganglion cells scattered in and around the carotid body and in the glossopharyngeal nerve. In the superior cervical ganglion, NOS and diaphorase staining localizes to many preganglionic axons and also to a small population of vasoactive intestinal peptide-positive, presumably cholinergic, ganglion cells. Positively stained ganglion cells are absent in the petrosal ganglion and very rare in the nodose ganglion, although both sensory ganglia display characteristic distributions of cells immunoreactive for calcitonin gene-related peptide, substance P and tyrosine hydroxylase. The NOS-positive innervation of the carotid body thus appears to be autonomic, originating mainly from a population of dispersed ganglion cells, and probably parasympathetic in nature. The superior cervical ganglion also may supply some pre- or postganglionic NOS-positive axons. Nitric oxide released from these nerves could affect glomus cell activity directly or indirectly by vasoregulation.

Animals↗
PubMed1995

Reciprocal photolabile O2 consumption and chemoreceptor excitation by carbon monoxide in the cat carotid body: evidence for cytochrome a3 as the primary O2 sensor.

High carbon monoxide (CO) gas tensions (> 500 Torr) at normoxic PO2 (125-140 Torr) stimulates carotid chemosensory discharge in the perfused carotid body (CB) in the absence but not in the presence of light. According to a metabolic hypothesis of O2 chemoreception, the increased chemosensory discharge should correspond to a photoreversible decrease of O2 consumption, unlike a non-respiratory hypothesis. We tested the respiratory vs. non-respiratory hypotheses of O2 chemoreception in the cat CB by measuring the effect of high CO. Experiments were conducted using CBs perfused and superfused in vitro with high CO in normoxic, normocapnic cell-free CO2-HCO3- buffer solution at 37 degrees C. Simultaneous measurements of the rate of O2 disappearance with recessed PO2 microelectrodes and chemosensory discharge were made after flow interruption with and without CO in the perfusate. The control O2 disappearance rate without CO was -3.66 +/- 0.43 (S.E.) Torr/s (100 measurements in 12 cat CBs). In the dark, high CO reduced the O2 disappearance rate to -2.35 +/- 0.33 Torr/s, or 64.2 +/- 9.0% of control (P < 0.005, 34 measurements). High CO was excitatory in the dark, with an increase in baseline neural discharge from 129.2 +/- 47.0 to 399.3 +/- 49.1 impulses per s (P < 0.0001), and maximum discharge rate of 659 +/- 76 impulses/s (N.S. compared to control) during flow interruption. During perfusion with high CO in the light, there were no significant differences in baseline neural discharge or in the maximum neural discharge after flow interruption, and little effect on O2 metabolism (88.8 +/- 11.5% of control, N.S., 29 measurements).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗