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Biomedical subjects

P Varma

Publications and source records attributed to P Varma.

14 recordsLinked to original sources
PubMed2001

Gap junction blockers decrease defibrillation thresholds without changes in ventricular refractoriness in isolated rabbit hearts.

BACKGROUND: The maintenance and termination of reentry arrhythmias are determined by tissue properties such as refractoriness and conduction velocity. Although the effects of Na(+) and K(+) channel block on electrophysiological properties and defibrillation threshold (DFT) have been studied, little is known about the effect of gap junction blockers on defibrillation and tissue electrophysiological properties. METHODS AND RESULTS: Triplicate DFTs (volts) were obtained before and 15 minutes after 4 micromol/L 16-doxyl-stearic acid (16-DSA, n=8), 1 mmol/L 1-heptanol (n=12) (both gap junction blockers), 3 microg/mL lidocaine (a sodium channel blocker) (n=8), and respective controls (n=27) in isolated perfused rabbit hearts. DFT decreased after 16-DSA (23+/-14%, P<0.01) and 1-heptanol (21+/-16%, P<0.01) but increased after lidocaine (26+/-28%, P<0.05). Ventricular fibrillation cycle length (VFCL) and QRS duration increased after all 3 agents, by 36+/-19% and 44+/-16% (16-DSA), 87+/-42% and 49+/-15% (heptanol), and 57+/-20% and 43+/-26% (lidocaine), respectively (all P<0.01). Spatially averaged temporal VFCL dispersion decreased significantly after all 3 agents, by 47+/-42% (16-DSA, P<0.05), 74+/-19% (1-heptanol, P<0.01), and 82+/-13% (lidocaine, P<0.01), respectively. Ventricular effective refractory period and monophasic action potential duration at 90% repolarization were unchanged after 16-DSA and 1-heptanol (P=NS) but increased after lidocaine (16+/-13%, P<0.01, and 6+/-5%, P=NS, respectively). There were no significant changes in DFT or any other electrophysiological variable in control hearts. CONCLUSIONS: Electrical uncoupling by 16-DSA and 1-heptanol significantly lowers DFT and dispersion of VFCL without altering refractoriness; lidocaine, at doses resulting in similar slowing of conduction, increases DFT.

Animals↗
PubMed1998

Absence of an apolipoprotein E epsilon4 allele is associated with increased parietal regional cerebral blood flow asymmetry in Alzheimer disease.

BACKGROUND: The apolipoprotein E (Apo E) epsilon4 allele has been associated with parietal metabolic abnormalities and asymmetries in asymptomatic subjects at risk for Alzheimer disease (AD). However, previous research has shown minimal effect of the epsilon4 allele on regional cerebral blood flow (rCBF) and metabolism in patients with probable AD. OBJECTIVE: To determine whether the Apo E epsilon4 allele is associated with parietal rCBF abnormalities and asymmetries in patients with probable AD. PATIENTS AND METHODS: Thirty patients with AD with the epsilon4 allele (epsilon4+ AD), 22 patients with AD without the epsilon4 allele (epsilon4- AD), and 14 healthy control subjects underwent single-photon emission computed tomography (SPECT) scanning with 740 MBq technetium Tc 99m hexamethylpropyleneamine oxime. Ratios of parietal-unaffected regions and a left-right parietal asymmetry index were compared between both patient groups. RESULTS: The group with epsilon4- AD was younger (P = .005, Student t test) and had an earlier age of onset (P = .005) than the group with epsilon4+ AD. Analysis of covariance revealed no significant difference in the parietal rCBF ratio, controlling for age of onset and Mini-Mental State Examination score (F(1,48) = 0.06; P = .81). However, contrary to hypothesis, significantly greater parietal rCBF asymmetry was seen in patients with epsilon4- AD (mean +/- SD, 9.7% +/- 5.5%) than those with epsilon4+ AD (6.3% +/- 4.7%; F(1,50) = 5.89; P = .02; analysis of variance). When number of epsilon4 allele copies was considered, this effect appeared to accrue primarily from a difference between patients with 0 and with 2 epsilon4 allele copies. An exploratory analysis of multiple cortical structures suggested that this asymmetry extended to additional regions (superior temporal) and to combined association cortex. CONCLUSIONS: Greater parietal rCBF asymmetry is involved in epsilon4- AD than in epsilon4+ AD. Lack of the epsilon4 allele may be associated with other (as yet undiscovered) genetic or environmental risk factors, which confer greater neuropathological asymmetry.

Age of Onset↗
PubMed1992

Cervical status as a predictor of preterm labour.

A study was conducted on 140 pregnant women at and after 28 weeks of pregnancy for finding out the relationship of cervical length and position with onset of preterm labour. Incidence of preterm labour was significantly higher (p < 0.001) in women with central position of cervix (54.67%) than that with posterior position of cervix (10.77%). Onset of preterm delivery was closely related to cervical length of 2.5 cm or less irrespective of central (82.75%) or posterior (20%) position of cervix (p < 0.001).

Adult↗
PubMed1979

Mitosis in the haemocytes of Sarcophaga ruficornis (Diptera).

Among the haemocytes of Sarcophaga ruficornis, only the prohaemocytes divide. Injection of phytohaemagglutinin-P induces 100% prohaemocytes to undergo mitosis but does not induce mitosis in other cells. Mitotic stages other than the prophase are apparently very short lived.

Animals↗
PubMed1978

Intestinal laceration secondary to clamping of an occult omphalocele.

An omphalocele is a congenital defect of the abdominal wall, through which intestines and other intraabdominal organs protrude outside the abdominal cavity. The defect in the abdominal wall is covered by a translucent sac composed of peritoneum internally and amniotic membrane externally, through which the viscera can be seen. Such an anomaly is obvious and easily recognized at birth when the defect in the abdominal wall is large, but a small defect, also designated as umbilical cord hernia, is often unnoticed and may, when the cord is clamped, result in an iatrogenic laceration of the gut. We report such an encounter to alert the physician and suggest a method to prevent the iatrogenic misadventure. A careful follow-up of the child, including developmental evaluation, is presented and compared with her healthy twin. A review of the relevant literature shows that the anomaly is not rare and that there is often a delay of several days in establishing the correct diagnosis, leading to a fatal outcome in some cases.

Diseases in Twins↗
PubMed1977

Deuterolysis of amino acid precursors: evidence for hydrogen cyanide polymers as protein ancestors.

Deuterolysis experiments suggest that hydrogen cyanide polymers rather than aminoacetonitriles are major precursors of alpha-amino acids obtained from spark reactions and other studies on chemical evolution. These results are consistent with the hypothesis that the original heteropolypeptides on the earth were synthesized spontaneously from hydrogen cyanide and water without the intervening formation of alpha-amino acids.

Amino Acids↗
PubMed1975

Heteropolypeptides from poly-alpha-cyanoglycine and hydrogen cyanide: a model for the origin of proteins.

Poly-alpha-cyanoglycine, a homopolymer synthesized from the N-carboxyanhydride of alpha-cyanoglycine, is converted by cumulative reaction of hydrogen cyanide to heteropolypeptides that can be hydrolyzed to protein amino acids, including glycine, alanine, valine, aspartic acid, and glutamic acid. These results are consistent with the hypothesis that the original heteropolypeptides on the earth arose spontaneously from hydrogen cyanide and water without the intervening formation of alpha-amino acids.

Chemical Phenomena↗
PubMedDate not supplied

A mechanism of action of phenylephrine on heart.

Phenylephrine exerted a positive chronotropic and inotropic effect on isolated, spontaneously beating, atria of reserpinised rabbits. Addition of phenoxybenzamine and phentolamine resulted in a depression of control contractile amplitude. Practolol, however, was devoid of this effect. The positive inotropic response to phenylephrine was significantly antagonised by all the three blockers used, while positive chronotropic response was annulled by phentolamine and practolol, but not with phenoxybenzamine. It is, therefore, suggested that phenylephrine exerts its cardiostimulant effects through mediation of both alpha and beta-1 adrenoceptors. A probable mechanism of action could be, that phenylephrine acts on some specific chemical group, shared by alpha and beta1 receptors. This specific group is probably blocked by both alpha and betaceptor antagonists separately, so phenylephrine becomes ineffective in presence of these antagonists.

Animals↗