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Biomedical subjects

B Koley

Publications and source records attributed to B Koley.

12 recordsLinked to original sources
PubMed1998

Cardiac nociception induced rectal response: relation with haemodynamic changes.

Epicardial application of nicotine (200 micrograms/ml) over the left ventricle or occlusion of the left anterior descending coronary artery (LAD) in lightly anaesthetised cats resulted a biphasic change in rectal motility-initial relaxation followed by contraction along with biphasic changes of blood pressure (B.P.) with epicardial nicotine and only hypotension with LAD occlusion. Desensitisation of ventricular receptors by epicardial application of 2% lignocaine abolished the rectal response and the biphasic blood pressure response but not the LAD occlusion induced hypotension. Sectioning of left inferior cardiac nerve (LICN) abolished such cardiorectal reflex but not the B.P. changes. Stimulation of central cut end of LICN elicited similar cardiorectal reflex keeping the B.P. unaltered. Atropinization (1 mg/kg) abolished only the contractile phase of the cardiorectal reflex and also the hypotension induced by epicardial nicotine. Intra-arterial NG-nitro-L-Arginine (LNNA) at a dose of 2 mg/kg abolished the relaxation phase of such cardiorectal reflex keeping the B.P. changes unaltered. LAD occlusion induced hypotension was neither counteracted by atropine nor by LNNA pretreatment. These indicate that though the cardio-rectal reflexes are associated with B.P. changes, they do not have any direct correlation.

Animals↗
PubMed1997

Rectal response of cardiac origin in the cat: involvement of nitric oxide and acetylcholine.

Local application of nicotine over the surface of the left ventricle and also occlusion of the left anterior descending coronary artery in the lightly anaesthetised, open-chested, artificially ventilated cat resulted a biphasic rectal movement--initial relaxation followed by sustained contraction. However, distension of the atrial appendage did not evoke any change in rectal motility, indicating the non-involvement of atrial volume receptors in initiating this rectal response of cardiac origin. The relaxation phase of this response was not abolished by pretreatment with atropine or with phentolamine or propranolol but was abolished by the nitric oxide inhibitor, N(G)-nitro-L-arginine (LNNA), and this blockade of the relaxation phase by LNNA was reversed by L-arginine. The contraction phase, however, was abolished by atropine. From these observations it is clear that the relaxation phase of the rectal response to coronary occlusion or epicardial nicotine is mediated through neither cholinergic nor adrenergic pathways but through the release of nitric oxide whereas the contraction phase of such a cardio-rectal response is mediated through the release of the neurotransmitter, acetylcholine.

Acetylcholine↗
PubMed1996

Sympathoadrenal activity in the visceral (viscerovascular) reflexes to distension of the urinary bladder.

Distension of the urinary bladder can cause reflex pressor responses, which appear to be mediated by increased sympathetic activity. We correlated the involvement of the adrenal gland (medulla) itself and adrenosympathetic nerve activities with the viscerovascular reflexes and their role in controlling the reflex response following distension of the urinary bladder. The experiments were performed in 37 chloralose anesthetized cats. It was observed that reflex rise of blood pressure was not affected by intravenous administration of propranolol, indicating that the beta-adrenoceptors (inhibitory effect) were not involved in such reflex. Phentolamine, hexamethonium and guanethidine sulfate completely prevented the reflex action, and comparison of the magnitudes of responses and this inhibitory effect suggests the participation of alpha-adrenoceptors (excitatory effect) as a result of the vasoconstriction that develops during bladder distension. In the present study, we determined that adrenalectomy significantly (p < 0.0001) altered the magnitudes of reflex response during bladder distension. The 10.4% (systolic, p < 0.001) and 10.6% (diastolic, p < 0.01) change in reflex response was mediated directly through adrenomedullary catecholamines, and the 14.8% (systolic, p < 0.001) and 23.8% (diastolic, p < 0.0001) change in vasopressor response was mediated by adrenosympathetic ganglionic activity. The single unit activity from the central cut end of the adrenal sympathetic nerve was recorded for direct evidence. An increase in electrical activity (1-3 to 7-10 spikes/s; p < 0.001) of the adrenal sympathetic nerve with the rise of blood pressure during bladder distension was observed. We concluded that, like other sympathetic nerves, the adrenal sympathetic nerve contributed to the enhancement of blood pressure during bladder distension. This result also explains the partial inhibition of reflex hypertension during bladder distension after adrenalectomy. These studies also conclude that the adrenal gland and adrenosympathetic nerve act as facilitatory modulators in maintaining catecholamine secretion under conditions of stress (urinary bladder distension).

Animals↗
PubMed1995

Cardiovascular and respiratory changes following exposure to a synthetic toxin of Ptychodiscus brevis.

The present study demonstrated cardiorespiratory effects of a synthetic phosphorus-containing ichthyotoxic metabolite elaborated by the marine dinoflagellate Ptychodiscus brevis in anaesthetised cats. The metabolite at a dose of 0.25-1.5 mg/kg i.v., resulted in a dose-dependent fall in blood pressure and such vasodepressor effect was associated with bradycardia. There is initial respiratory apnoea followed by increased rate and depth of respiration (hyperapnoea) following the administration of the toxin. The hypotensive response was accompanied by a decrease in aortic baroreceptor activity. The ECG showed atrioventricular conduction block, arrhythmia and depression of S-T segment and T wave which indicated coronary insufficiency. Vasodepressive property of the toxin is presumably muscarinic in nature as atropine counteracted the vasodepression.

Animals↗
PubMed1995

Sympathetic efferent activity in the viscerovascular reflexes induced by urinary bladder distension.

In chloralose-anesthetized cats, rapid distension of the urinary bladder with warm (37 degrees C) normal saline (50-60 ml) causes an increase in blood pressure and contraction of the spleen. This response is due to peripheral vasoconstriction. In this experiment, the evidence of direct involvement of the spleen, as well as splenic and splanchnic sympathetic efferent activity on the viscerovascular reflexes, was investigated by pharmacological and electrophysiological (single unit preparation) means and analysis. The viscerovascular reflexes induced by urinary bladder distension remained unaffected by propranolol, but phentolamine, guanethidine sulfate, and hexamethonium completely antagonized the reflex vasopressor response. All these results with these blocking agents show that sympathetic nerves are actively involved in the reflex responses to distension of the urinary bladder with activation at the postganglionic level involving alpha-adrenoceptors and thereby the release of catecholamines. It is thus evident that the same mechanisms operate in the case of reflex elevation of blood pressure and contraction of the spleen. After bilateral denervation of the splanchnic sympathetic nerves, bladder distension failed to produce a reflex response. The efferent activity from the splanchnic and splenic sympathetic nerves in producing a reflex rise in blood pressure was recorded for direct evidence. The significant increase of asynchronous spontaneous discharge rate in the splanchnic and splenic sympathetic nerves was found along with a rise in blood pressure during bladder distension. On the basis of this study, it may be suggested that the spleen as well as splenic and splanchnic sympathetic nerves play an important role in the control of viscerovascular reflexes.

Animals↗
PubMed1990

Pharmacological and electrophysiological analysis of nicotine induced apnoea in the cat.

Intravenous nicotine (20-60 micrograms/kg) produced an initial brief apnoea followed by hyperventilation in anaesthetized cats. The apneic response to nicotine remained uneffected by atropine, by phentolamine or propranolol. Hexamethonium and guanethedine sulphate antagonized the apneic response. In bilateral vagotomized cats, nicotine failed to produce respiratory apnoea. Veratridine and phenyldiguanide produced apnoea similar to that produced by nicotine within 2-3 sec. administered intraartrially. Nicotine failed to stimulate pulmonary stretch receptors as did veratridine in artificially ventilated cats. The alpha and gamma motoneurone activity of inspiratory and expiratory muscles and the phrenic efferent activity were inhibited during apnoea. These inhibitions were absent in vagotomized cats. In conclusion, these results suggest that the nicotine induced apneic response is mediated through pulmonary vagal afferents, probably through J-receptors, which in turn inhibit the motoneurone activity involving the respiratory muscles.

Animals↗
PubMed1989

Cardiac nociceptors and ischemia: role of sympathetic afferents in cat.

In total, 86 units were recorded from T2 and T3 left thoracic rami of cat. These receptors were located on the circumflex coronary artery, anterior descending coronary artery, and its adjacent myocardial regions. The conduction velocity of these fibres was in the range of "C" (0.5 to 1.8 m/s) and "A delta" (5.96 to 17 m/s) fibres. Out of these 86 units, only 28 units were activated by coronary occlusion. The average resting frequency of the spontaneous unit was 0.8 +/- 0.06 impulses/s which increased to 35 +/- 4.8 impulses/s on mechanical probing. In order to examine whether the units sensitive to coronary occlusion were also responsive to algesic agents, some of these units were studied applying lactic acid, bradykinin, prostaglandins, and nicotine. It was observed that these ischemia-sensitive units are also sensitive to lactic acid (10 units), bradykinin (16 units), prostaglandins (12 units), and nicotine (15 units). These ischemia-sensitive units are presumably nociceptors and activated by algestic agents that cause cardiac ischemic pain.

Adrenergic Fibers↗
PubMed1989

High threshold aortic baroreceptors afferents in the sympathetic nerve of monkey.

A total of 25 afferent units were recorded in the thoracic sympathetic rami (T3-T4) localised at the base of the bracheocephalic trunk and the descending aorta. Two types of receptors, Type I and Type II, were found. Type I receptors, localised at the base of the bracheocaphalic trunk, were fast adapting and exhibited synchronous discharge with each systolic height of blood pressure and behaved like baroreceptors. There was no discharge at the diastolic phase of the cardiac cycle. These receptors also gave occasional single spike at each systolic height of pressure of about 90-120 mmHg. When the systemic pressure was increased from 120 to 180 mmHg due to occlusion of the descending aorta or intravenous administration of adrenaline, the frequency of discharge of Type I receptors increased and they behaved like the typical sino-aortic baroreceptors. Type II receptors, localised over the wall of the descending aorta, fired irregularly and they did not have any relation with heart beat and did not behave like baroreceptors. On the basis of the present observation it may be suggested that Type I receptors are high threshold baroreceptors which play a role in the homeostatic control during high blood pressure and that Type II receptors do not play such a role.

Animals↗
PubMed1987

The role of calcium channel in the effect of nicotine on contractility in isolated toad ventricle.

The mechanism of the positive inotropic effect produced by nicotine (6.2 X 10(-5) mol/l to 4.9 X 10(-4) mol/l) on electrically driven toad ventricles was investigated. The response to nicotine was not affected by 6-hydroxydopamine pretreatment, bretylium (2.4 X 10(-4) mol/l) exposure or tyramine tachyphylaxis. Following desensitisation by isoprenaline (4.2 X 10(-6) mol/l) of the beta-adrenoceptor in the ventricles, the response to nicotine was no affected. However, the response was antagonised by ethylene diamine tetraethyl acetate (2.3 X 10(-4) mol/l), verapamil (0.4 X 10(-5) mol/l) or calcium-free Ringer. Nicotine prolonged the action potential duration and enhanced the force of contraction. Nicotine induced slow action potentials in partially depolarized (in high potassium solution) ventricles and this was antagonised by verapamil (0.4 X 10(-5) mol/l). These results suggest that the effects of nicotine are mediated by a direct interaction with the Ca2+ channels at the cell surface.

Action Potentials↗
PubMed1985

High threshold aortic baroreceptor afferents in the sympathetic nerve.

In anaesthetized cats, 40 sympathetic sensory units in the bracheocephalic artery (30 units) and the descending aorta (10 units) were recorded by means of single-unit preparation. Direct evidence is available for the mechanosensitive nature of the receptors in the sympathetic afferents at the level of T3 and T4. Two distinct types of receptors were found (Type I and Type II). Type I receptors, which were fast adapting, gave a spike discharge at each systolic height of pressure (70-110 mmHg). However, they sometimes failed to appear even at such systolic pressure. When the systemic pressure was increased by occluding the descending aorta or by infusing adrenaline solution intravenously, the frequency of discharge of Type I receptors increased and they behaved much the same as the typical sinoaortic baroreceptors. Type II receptors were activated by mechanical probing and at high systemic pressure, though they did not fire always synchronously with heart beat. On the basis of the study it may be suggested that Type I receptors are high threshold baroreceptors and like other systemic baroreceptors, play a role in homeostatic control presumably in a state of high blood pressure, but on the other hand Type II receptors do not play such a role.

Animals↗
PubMed1984

The effects of nicotine on spontaneous contractions of cat urinary bladder in situ.

Nicotine and dimethyl-phenylpiperazinium (DMPP) increased intravesicular pressure and then transiently depressed the spontaneous activity of the urinary bladder in chloralose anaesthetized cats. Adrenaline (5-10 micrograms kg-1), noradrenaline (5-20 micrograms kg-1) and isoprenaline (40-50 micrograms kg-1) which depressed spontaneous urinary bladder activity, were antagonized by the beta-receptor blocking agent propranolol (1 mg kg-1). Phenylephrine (10-30 micrograms kg-1) was ineffective on the urinary bladder though it increased the systemic blood pressure. This latter effect was blocked by the alpha-receptor blocking agent phentolamine (2 mg kg-1). Acetylcholine (2-8 micrograms kg-1) caused a marked fall in systemic blood pressure, which was potentiated by physostigmine, but failed to produce any response on the intravesicular pressure even after physostigmine (50-100 micrograms kg-1) treatment. ATP (2 mg kg-1) produced an increase in intravesicular pressure accompanied by a fall in systemic blood pressure. The increased intravesicular pressure was antagonized by quinidine (20 mg kg-1); however, the fall in blood pressure remained unaltered. The increased intravesicular pressure induced by nicotine (20-40 micrograms kg-1) or DMPP (50-100 micrograms kg-1) was not affected by phentolamine (2 mg kg-1), propranolol (1 mg kg-1) or guanethidine (15-20 mg kg-1). Physostigmine (50-100 micrograms kg-1), hemicholinium 3 (2 mg kg-1) or atropine (1 mg kg-1) were also unable to affect the response to nicotine. Hexamethonium (1 mg kg-1), reduced the amplitude of spontaneous bladder contractions and quinidine (20 mg kg-1) abolished the effect of nicotine. 7 Bilateral sectioning of the cervical sympathetic or hypogastric nerves did not alter the effect of nicotine or DMPP. Higher spinal cord transection (Cl-C2) blocked the spontaneous, as well as the nicotine- and DMPP-induced, contractions of the bladder. 8 It is concluded that the increase in intravesicular pressure induced by nicotine is atropineresistant and is not mediated either through adrenergic or cholinergic mechanisms. It is probable that a purinergic mechanism is involved, via the activation of P2-receptors present in the urinary bladder.

Adenosine Triphosphate↗