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Biomedical subjects

D Bose

Publications and source records attributed to D Bose.

At least 73 records · Page 4Linked to original sources
PubMed1987

Progesterone derivatives that bind to the digitalis receptor: synthesis of 14 beta-hydroxyprogesterone. A novel steroid with positive inotropic activity.

The synthesis of 14-hydroxy-14 beta-pregn-4-ene-3,20-dione (14 beta-hydroxyprogesterone) is described. This novel steroid is about 10 times more potent than progesterone and one-tenth as potent as ouabagenin in an [3H]ouabain radioligand binding assay and is the first in a series of progesterone congeners that interact at the cardiac glycoside receptor both to possess the C/D cis ring junction and to enhance contractility of isolated cardiac tissue.

Animals↗
PubMed1987

Alteration of pial vessel responses to blood pressure changes in rats after hypoxia.

Previous studies in newborn lamb have shown impairment of cerebral blood flow autoregulation after hypoxia followed by reoxygenation. The present study was done to see if such a phenomenon existed in the adult rat and if it could be demonstrated at the level of the pial arterioles. Using an open cranial window preparation, we assessed the changes in pial vessel diameter during blood pressure alterations induced by hemorrhage and reinfusion of blood, before and after 30 s of hypoxia, in 15 male Sprague-Dawley rats. Mean diameters of pial arteries in the study group of rats were 128 +/- 54 microns before hypoxia and 141 +/- 61 microns after normoxia following hypoxia. The corresponding diameters in rats serving as time controls were 136 +/- 52 and 138 +/- 52 microns. Slopes of pial vessel diameters as a function of mean arterial blood pressures decreased significantly (p less than 0.05) after hypoxia from -0.86 +/- 0.45 to 0.03 +/- 0.66 (mean +/- SD). In the control rats not subjected to hypoxia, the slopes remained unchanged over a similar time period (-0.60 +/- 0.16 and -0.42 +/- 0.19). The negative slopes indicate that pial vessels dilate during hypotension and constrict during hypertension. Such vascular responses may play a role in autoregulation of cerebral blood flow. We found that a relatively brief period of hypoxia can cause a long-lasting impairment of vascular responses even after restoration of normoxia. These findings are consistent with a previous report of persistent impairment of cerebral blood flow autoregulation after a brief period of hypoxia.

Animals↗
PubMed1987

Role of sarcoplasmic reticulum in digitalis-induced electrical and mechanical oscillations in the heart.

The mechanism of cardiac oscillatory activity induced by digitalis was studied in the canine ventricular muscle. We determined the role of sarcoplasmic reticulum in the phenomenon of oscillatory afterpotential and mechanical aftercontractions. Additionally we wished to study the interaction between changes in stimulus interval, which are known to affect sarcoplasmic reticulum function and these oscillatory phenomena. Aftercontraction was induced by ouabagenin but it required previous stimulation of the heart. The production of aftercontraction depended on short stimulus interval and bore no relation with the size of the releasable pool of Ca in the sarcoplasmic reticulum as indicated by the size of the driven contraction. Aftercontraction was often seen without an accompanying action potential. When a depolarization was present during aftercontraction, its temporal relation with the contraction often did not show the usual delay, suggesting that electrical activity may not necessarily initiate contraction. This was supported by the finding that Mn, a Ca channel blocker, blocked normal contractions more than aftercontraction. However, inhibition of Ca release from the sarcoplasmic reticulum by ryanodine or of Ca reuptake by caffeine were effective in blocking aftercontraction and when present, oscillatory afterpotential. Abolition of aftercontraction was not due to slowing of relaxation. These studies confirm the role of sarcoplasmic reticulum in causing aftercontraction and oscillatory afterpotential during ouabagenin toxicity and also suggest that there is a relationship between the 'repriming' ability of the sarcoplasmic reticulum and the oscillatory phenomena.

Animals↗
PubMed1986

Acidemia impairs autoregulation of cerebral blood flow in newborn lambs.

Cerebral blood flow (CBF) and autoregulation of cerebral blood flow were assessed in newborn lambs before and after inducing metabolic acidemia. CBF was measured by xenon washout and autoregulation by the change in CBF after increasing mean arterial pressure (MAP) 30 per cent with 0.02 per cent phenylephrine hydrochloride. After surgical preparation, stabilization, and demonstration of the presence of autoregulation, six lambs received 10 mg X kg-1 of lactic acid intravenously over 30 minutes. Arterial pH decreased from 7.35 +/- 0.01 (mean +/- SEM) during the control period to 6.96 +/- 0.02 (p less than 0.01) at the end of the lactic acid infusion. Arterial blood gases, MAP's, and heart rates did not change. Prior to lactic acid infusion, CBF before and after raising MAP were 53 +/- 3 ml/100 g/min and 56 +/- 4 ml/100 g/min respectively. After lactic acid infusion, CBF increased from 54 +/- 2 ml/100 g/min to 62 +/- 3 ml/100 g/min (p less than 0.05) following phenylephrine induced rise in MAP. Five control lambs showed no significant change in any of these variables, including CBF, over the same time periods. These data indicate that metabolic acidosis per se does not alter CBF, but that metabolic acidosis impairs cerebral vascular autoregulation in hyperoxic lambs. Similar changes in human neonates might result in intracranial haemorrhage.

Acidosis↗
PubMed1986

Comparison of two methods of altering blood pressures for assessing neonatal cerebral blood flow autoregulation.

The cerebral blood flow of newborn lambs at reduced and elevated arterial blood pressures, induced by intravenous infusion of sodium nitroprusside and phenylephrine hydrochloride as well as blood withdrawal and reinfusion, were compared. Both blood withdrawal and sodium nitroprusside infusion reduced mean arterial pressure from 83 to 60 mmHg (1 mmHg = 133 Pa). Reinfusion of blood increased arterial pressure to 94 mmHg. Phenylephrine hydrochloride infusion increased arterial pressure to 102 mmHg. The cerebral blood flows at corresponding arterial pressures were similar (coefficient of correlation = 0.88, P less than 0.01). Cerebral blood flow before and after infusion of phenylephrine hydrochloride and sodium nitroprusside into the brain via the carotid artery did not change. The results indicate that blood-borne phenylephrine hydrochloride and sodium nitroprusside, in concentrations that would alter arterial blood pressure significantly from its resting level, do not change cerebral blood flow directly.

Animals↗
PubMed1984

A versatile computer-controlled biological stimulus sequencer.

A computer-controlled stimulus sequencer has been developed. This device can be controlled by several commonly available, inexpensive 8-bit microcomputers in which the address, data, and control lines are externally accessible. Although the Apple implementation has been described, a similar interface has also been devised for the Radio Shack Color Computer. The hardware relies on the Rockwell Versatile Interface Adapter (VIA) chip (which has two 16-bit timers capable of functioning as frequency dividers, event counters, or one-shots) and a 12-bit digital-to-analog converter (DAC) chip. This hardware combination, along with software written in Basic and machine language (stored in an EPROM for turn-key operation), allows creation of a large number of unique trains that can be chained together in any sequence. This is aided by storing the train characteristics economically in the computer memory and chaining different train parameters in a link-list. Several train parameters can be incremented or decremented manually by a pair of keys. The amplitude of the train can be changed manually or under program control. Once created, the trains can be edited on the run or deleted from the sequence. The device also generates a trigger pulse that can be referenced to any pulse in a train and can be used to pretrigger an oscilloscope. The software has provision for detecting an external signal, and this information can be used to modify train parameters. The interface is interrupt driven and therefore does not require continuous use of the Basic interpreter.(ABSTRACT TRUNCATED AT 250 WORDS)

Computers↗
PubMed1983

Mechanism of biphasic contractions in strontium-treated ventricular muscle.

Biphasic contractions were produced in dog trabeculae by replacing 90-95% of the calcium in the bathing solution with strontium. These conditions produced prolonged action potentials accompanied by contractions with two distinct phasic components. The early component disappeared slowly when the remaining Ca++ was removed, whereas the late component was eliminated quickly when Sr++ was removed. Manganese ion (0.25 mM) preferentially decreased the late component without changing the action potential, whereas caffeine and ryanodine decreased or eliminated the early component. Ryanodine did not alter the action potential. Isoproterenol rapidly increased the early component and, more slowly and to a lesser degree, increased the late component. The results suggest that the early component is caused by intracellular release of activator cation, probably from the sarcoplasmic reticulum, whereas the late component is the result of Sr++ entry across the sarcolemma, possibly by way of the slow inward current.

Animals↗
PubMed1982

A simple microcomputer-controlled device for automated measurement of refractory period of excitable tissue.

A computer-controlled tissue stimulator interface will be described. This device can generate a basic train at a predetermined rate. An extra pulse is introduced after a selected number of pulses. The initial latency of this extra pulse is shorter than the tissue refractory period. The latency is increased, automatically, until the tissue produces a conducted response. This is made possible by the computer checking the tissue response. The device is inexpensive and can be readily controlled by any 8 bit microcomputer, such as the Commodore PET or VIC-20. The use of a signal conditioner has been discussed. Such a circuit facilitates detection of the often slowly occurring action potential of the premature beat riding on the repolarization phase of the normal action potential.

Electronics↗
PubMed1981

Adriamycin induced alterations in canine Purkinje fiber action potential.

To study the electrophysiologic effects of adriamycin, transmembrane action potential characteristics of canine purkinje fibers were analyzed. Adriamycin significantly (p less than 0.05) prolonged action potential duration and refractory period but did not significantly alter resting membrane potential, action potential amplitude, dV/dt max and threshold for stimulation. Furthermore adriamycin effects were not reversible 20 minutes after the drug had been 'washed out'. These data indicate that adriamycin has significant cardiac electrophysiology effects that may account for its toxicity in man and that these effects are not quickly reversible.

Action Potentials↗
PubMed1977

Sodium in smooth muscle relaxation.

The contraction of guinea-pig taenia coli due to high K+ could not be reversed by washing when Na+ was absent from the medium. Reintroduction of Na+ (7 mM or more) caused relaxation. Similar results were obtained with rat uterus. The effect of sodium replacement was not due to change in ionic strength because equal or higher osmoles of choline, Ca++, K+, Mn++, or Mg++ had little or no effect. Persistence of contraction in the Na+-free medium was not due to a "catch state" of the contractile apparatus. Impairment of Ca+ removal from the cytoplasm rather than persistent increase in Ca+ influx seemed to sustain the mechanical response. This was because D600 (a calcium influx blocker) failed to completely relax K+-induced contraction in the absence of Na+ and also because the ability of EGTA to produce relaxation was reduced in the absence of Na+. Measurement of tissue calcium content using the lanthanum method revealed coincident decrease in tissue calcium and tension to control level during Na+-mediated relaxation. The results suggest a role for transmembrane Na+-Ca++ exchange in causing the Na+-mediated relaxation of taenia undergoing Na+-free contracture.

Animals↗
PubMed1977

Excitation-contraction coupling in multiunit tracheal smooth muscle during metabolic depletion: induction of rhythmicity.

Multiunit canine tracheal smooth muscle responded to carbachol with graded depolarization and tonic contraction. The same concentration of carbachol, after metabolic depletion by substrate removal, produced rhythmic contractions and action potentials. Similar mechanical effects were also observed with acetylcholine or histamine. These effects were reversed by reintroducing glucose or beta-hydroxybutyrate, but not by 3-O-methylglucose, which is not metabolized; hence, the structural requirements for glucose, per se, or any osmotic effect were ruled out. Sensitivity to extracellular Ca2+ was increased. A Ca2+-influx blocker, D-600, in low concentration (2 X 10(-8) M) abolished the rhythmic contractions without affecting the tonic contraction. Progressive metabolic depletion in presence of carbachol led to fluctuations in membrane potential with a crest of depolarization and appearance of action potentials, each of which resulted in a small contraction. Many of the small contractions partially fused to form the major rhythmic contractions which appeared at a frequency of one per minute. Rhythmicity could not be produced by increasing extracellular K+ concentration (20-120 mM) in presence of atropine (13(-7) M), but instead a tonic contraction occurred. These results suggest changes in excitation-contraction coupling mechanism with agonists like acetylcholine, carbachol, or histamine during substrate deprivation.

Acetylcholine↗
PubMed1976

Potassium and the recovery of splenic capsular smooth muscle after cold storage.

Cat spleen capsular smooth muscle, depleted of potassium and enriched with sodium by cold storage in a potassium free medium, relaxed and underwent transient reduction in responsiveness to noradrenaline when potassium was introduced into the bathing medium. Both these effects could be blocked by ouabain, lithium substitution for sodium or low ambient temperature, suggesting possible involvement of the sodium pump. In the continued presence of potassium, relaxation was maintained but sensitivity to noradrenaline increased, possibly due to restoration of normal intracellular sodium and potassium concentrations.

Animals↗
PubMed1976

Increase in resting tension of tracheal muscle due to rigor during metabolic inhibition.

Resting tension of canine tracheal smooth muscle increased when glucose and oxygen were withdrawn from the bathing medium. Similar treatment of muscle stimulated with carbachol caused first a relaxation and then a secondary increase in tension. The increase in tension due t0 metabolic inhibition, unlike normal tracheal contractions, was insensitive to calcium depletion, was not associated with an active state, and was accompanied by marked reduction of tissue adenosine triphosphate, creatine phosphate, and glycogen content. Because muscle stiffness was also increased we concluded that hypoxic glucose-free contracture is due to rigor and not to an increased tissue calcium level as has been previously suggested. Rigor shortening during lightly loaded isotonic conditions is better maintained than rigor tension during isometric conditions. Our results also indicate that rigor tension is reduced irreversibly on imposition of a load and, therefore, the load-extension relationship during rigor in smooth muscle should be studied by making only small load changes.

Adenosine Triphosphate↗
PubMed1975

Mechanism of mechanical inhibition of smooth muscle by ouabain.

1 Ouabain (10 mug/ml) caused an initial increase followed by a decrease in tension in guinea-pig taenia coli bathed in normal sodium and potassium containing medium. 2 The excitatory effect of ouabain was prevented by the elevation of extracellular potassium while the inhibitory effect was abolished in the absence of sodium in the bathing medium. 3 In the presence of sodium, the inhibitory effect of ouabain disappeared when the drug was washed out, but in the presence of lithium (which is not extruded by the Na-K pump) the inhibition was not abolished. 4 The inhibitory effect of ouabain was accompanied by an increase in tissue Na and a decrease in tissue K concentration. The increase in intracellular [45Ca] which occurred when extracellular [k] was varied, was also reduced by ouabain. 5 It is concluded that a high intracellular level of sodium inhibits contractions in visceral smooth muscle probably by a mechanism involving decreased Ca influx.

Animals↗