Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: DrugBank:EXPT02427 (Atropine)
 3,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cerebral chemical vasomotor reactivity and autoregulation were tested in normal baboons before and after the intravenous or intravertebral infusion of atropine sulfate (0.02 mg/kg). Atropine did not appreciably effect autoregulatory response, but intravertebral injection suppressed the increase of cerebral blood flow (CBF) by inhalation of 5% CO2 and enhanced the decrease of CEF induced by hyperventilation. These changes produced by intravertebral injection of atropine were not observed after intravenous injection. Since the vertebrobasilar arterial system supplies the brain stem and diencephalon, this suggests that a central vasodilator tonus of the cerebral vessels is maintained by the innervation of the cerebral vessels by cholinegic neurons which have their central origin in the brain sterm and diencephalic area.
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PMID:Neurogenic control of cerebral blood flow in the baboon. 119 35

Periodic increases in blood pressure (BP) can occur in the sleep apnea syndrome (SAS) during recurrent apneas. To investigate the mechanisms causing this periodic hypertension, we simulated SAS by imposing a matching breathing pattern on seven healthy awake male volunteers. Continuous finger arterial BP, electrocardiogram, arterial O2 saturation (SaO2), end-tidal CO2, and tidal volume were measured. The role of hypoxia was studied by comparing apneas during depletion of O2 in the spirometer with those during 100% O2 breathing. In all subjects, BP periodically reached values greater than 150/95 mmHg in the hypoxic series. During the hyperoxic apnea series, however, BP remained stable. End-apneic mean BP was shown to be inversely correlated to SaO2 in six subjects in the SaO2 range from 60 to 100%. Although the hypoxic BP pattern closely mimicked that in SAS, the heart rate pattern in four of our subjects remained distinct from that in patients. Atropine could not prevent large BP swings in the hypoxic series. We conclude that SaO2 is a major determinant of periodic hypertension in recurrent apneas. Its effect probably results from chemoreflex modulation of peripheral resistance.
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PMID:Repetitive apneas induce periodic hypertension in normal subjects through hypoxia. 156 78

The purpose of this study was to investigate whether the muscarinic modulation of neostriatal acetylcholine release changes with senescence. Neostriatal slices from Fischer 344 rats aged 3, 10 and 28 months were prepared and incubated in Krebs-Ringer bicarbonate buffer oxygenated with 95% O2/5% CO2. Acetylcholine release from slices of each age group was monitored in the presence or absence of muscarinic agents, and the release in the presence of the drug was compared to the release from slices of age-matched controls in the absence of drug. The muscarinic agonist, oxotremorine, and two muscarinic antagonists, atropine and pirenzepine, were tested for their effects on acetylcholine release. Pirenzepine is selective in its interaction with the M1 muscarinic receptor subtype; atropine and oxotremorine are nonselective in their actions. Of the three drugs tested, pirenzepine displayed a significant age-related difference in its effects on acetylcholine release. Whereas the effects of pirenzepine (50 microM) on acetylcholine release modulation in slices from the 3-month rats were negligible, the M1-selective antagonist increased the release of acetylcholine from slices of 10- and 28-month rats by another 42 and 192% (P less than .05), respectively. Atropine (1 microM) was also tested, and an increase in acetylcholine release by another 64, 104 and 218% (all P less than .05) was observed in slices from the 3-, 10- and 28-month rats, respectively. In the presence of oxotremorine (50 microM), acetylcholine release decreased in slices from the 3-month rats by 35% (P less than .1), but changed by only 7 and 15% in the 10- and 28-month slices, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Age-related differences in the effects of some muscarinic agents on acetylcholine release from rat neostriatal slices. 186 53

The effect of cholinergic agents on proximal tubular absorption of bicarbonate and fluid were examined to investigate the possible role of the cholinergic receptor in the regulation of renal function. Proximal convoluted tubule (PCT) and peritubular capillaries were perfused with bicarbonate-Ringer's solution containing radioactive inulin. Bicarbonate (total CO2) was determined by microcalorimetry. The rates of bicarbonate absorption (JHCO3) and fluid absorption (Jv) were 143.3 +/- 7.2 pEq/min.mm and 2.52 +/- 0.23 nl/min.mm, respectively. Addition of carbachol (10(-8) M) to the capillary perfusate reduced JHCO3 by 17% and Jv by 32%. A higher dose of carbachol (10(-6) M) did not further inhibit JHCO3 or Jv. Simultaneous perfusion of atropine (10(-5) M) together with carbachol (10(-8) M) abolished the inhibitory effect of carbachol on PCT transport. Atropine itself, however, had no effect on PCT transport. The inhibitory effect of carbachol was also diminished by lanthanum chloride (10(-4) M). Carbachol (10(-6) M) had no effects from the luminal side. W-7, a calmodulin antagonist, inhibited carbachol-induced effects. Ionophore A-23187 also inhibited Jv and JHCO3. However, there was no additive effect when A-23187 and carbachol were combined in the capillary perfusate. These results suggest that there are functional cholinergic receptors on the basolateral side of the PCT that can regulate JHCO3 and Jv. Calcium influx may play a role in mediating the cholinergic effects on PCT transport.
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PMID:Cholinergic effect on rat proximal convoluted tubule. 210 2

Strips of trachealis muscle were dissected from the mid-cervical portion of the trachea from horses that were free of respiratory tract disease. The epithelium and mucosa were removed from one group of tissues and were left intact in a second group of tissues. Each tissue was suspended in a bath filled with Krebs-bicarbonate solution that was aerated with 5% CO2 in oxygen and maintained at 37 degrees C. Isometric tension was continuously recorded. The contractile response to square-wave electrical stimulations increased as frequency (3, 5, 10, 15, 20, 25, and 30 Hz), voltage (10, 15, 18, and 25 V), and pulse duration (0.2, 0.5, 1.0, 1.5, and 2.0 ms) increased in tissues with the epithelium and mucosa intact. A stimulus of 18 V, 20 Hz, and 0.5 ms induced maximal contraction. Atropine (10(-6) M) abolished the response to 18 V and 0.5 ms at all frequencies. The increase in active isometric tension was concentration dependent when acetylcholine (10(-9) to 10(-4) M) was added to the baths in 0.5-logarithmic increments. Tissues that were contracted in response to acetylcholine (10(-5) M) had a concentration-dependent decrease in active isometric tension when isoproterenol was added to the baths in 0.5-logarithmic increments (10(-9) to 10(-4) M). The contraction and relaxation curves were qualitatively similar, but quantitatively different in tissues with and without the epithelium and mucosa. Removing the epithelium and mucosa increased the contractile response to acetylcholine at bath concentrations of 3.1 x 10(-7) M and 10(-6) M. The presence of epithelium and mucosa enhanced the magnitude of isoproterenol-induced relaxations.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epithelium- and mucosa-dependent relaxation and contraction of normal equine trachealis muscle in vitro. 280 2

Respiratory and circulatory (measured and calculated) variables were obtained at the same time in resting eels, during normoxia and after 1 h exposure to environmental hypoxia (water PO2 of 40 torr). In normoxia, values of respiratory and circulatory variables appeared less than those reported for most other fish. These differences could be partly explained by a lower level of standard metabolism and a greater uptake of O2 through the skin. Hypoxia caused a marked decrease in heart rate (40%), cardiac output (37%), ventral and dorsal arterial blood pressures (22% and 32%), associated with a constriction of prebranchial veno-venous shunt, and an increase in branchial vascular resistance (30%). Atropine treatment during hypoxia reduced, but did not abolish, bradycardia, and branchial vascular resistance remained unchanged. The lack of increase in cardiac stroke volume as well as the slowing of the heart in atropine-treated eel, could be regarded as metabolic effects of sustained hypoxia. The increase in branchial resistance and constriction of prebranchial veno-venous shunt could be regarded as a direct myogenic effect of hypoxia. Hypoxic exposure resulted in an increase in ventilatory water flow Vg (more than twofold), a decrease in gill O2 uptake (50%) and oxygen partial pressure in arterial (PaO2 80%) and mixed venous blood (PvO2 78%), and in increase in the transfer factor for O2 of the gills, TO2, (+66%). The ventilatory convection requirement increased (fivefold) while extraction (EwO2%) and effectiveness (Eff%) of gill oxygen transfer were maintained in spite of hyperventilation. Hypoxic hyperventilation reduced partial pressure of CO2 (PaCO2 from 3.4 to 0.7 torr) and markedly raised pH (pHa from 7.98 to 8.33) in arterial blood, thus causing a typical respiratory alkalosis, which resulted in increased O2 affinity and capacity of eel haemoglobin.
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PMID:Ventilatory and circulatory adjustments in the European eel (Anguilla anguilla L.) exposed to short term hypoxia. 292 Aug 10

Strips of smooth muscle from the cervical tracheae of six adult male crab-eating monkeys (Macaca fascicularis) were studied in jacketed 25 ml organ baths filled with Krebs-bicarbonate solution maintained at 37 degrees C and gassed with 5% CO2 in oxygen. Isometric tissue tension increased in response to electrical field stimulation (18 V, 25 Hz, 0.5 msec), norepinephrine in the presence of propranolol, acetylcholine and histamine. Atropine abolished the contractile response to electrical stimulation. Tissues that were contracted with acetylcholine or pretreated with atropine then contracted with histamine relaxed when stimulated electrically. The relaxation was unaffected by propranolol but was abolished by tetrodotoxin. Isoproterenol relaxed tissues that were contracted with histamine, but failed to relax histamine-contracted tissues that had been pretreated with propranolol. Norepinephrine did not change isometric tension in untreated tissues or tissues pretreated with phentolamine. These results demonstrate the presence of excitatory and inhibitory nerves and noninnervated beta-adrenergic receptors in macaque trachealis. The excitatory nerves appear to be cholinergic. The inhibitory response to electrical stimulation is not mediated through muscarinic cholinergic or beta-adrenergic receptors. The inhibitory response to electrical field stimulation was likely mediated through nonadrenergic noncholinergic nerves.
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PMID:Innervation of crab-eating monkey trachealis muscle determined in vitro. 337 7

Outbred Mol:SPRD rats were maintained in surgical anaesthesia for two hours by using five different drug combinations: 1) pentobarbitone, 2) ketamine + diazepam, 3) ketamine + pentobarbitone, 4) atropine + diazepam + fentanyl + fluanisone, 5) atropine + etorphine + acepromazine. Respiratory rate, arterial O2 and CO2 tensions, arterial pH, base excess, mean arterial blood pressure and heart rate were recorded at set intervals from 30 to 120 min. from the initiation of anaesthesia. Atropine + diazepam + fentanyl + fluanisone caused no disturbance of acid-base balance, whereas the other drug combinations induced moderate to severe acidosis. Arterial blood pressure was reduced by all methods. Pentobarbitone and regimens including ketamine reduced heart rate, whereas combinations with etorphine and fentanyl caused a rise in heart rate.
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PMID:Influence of injectable anaesthetic combinations on blood gas tensions and acid-base status in laboratory rats. 393 15

Application of cholinergic agents on the ventrolateral surface of the medulla in areas in which the "central chemoreceptors" are believed to be located stimulates breathing. It is also known that cranial nerves, such as the hypoglossal, have respiratory modulated activity (greater in inspiration than expiration) that responds to many of the same stimuli which affect breathing. In the present study we compared effects of cholinergic agents (acetylcholine, carbachol, methacholine, eserine) directly applied to chemoreceptive areas on the ventral medullary surface on phrenic and hypoglossal nerve activity. Studies were performed in paralyzed, anesthetized, and artificially ventilated cats after vagotomy. All cholinergic agents increased hypoglossal activity significantly more than phrenic activity in animals ventilated with O2 or 7% CO2 in O2 whether or not the carotid sinus nerves were intact. Atropine applied topically to the same medullary area blocked the respiratory effects of locally administered acetylcholine. The results suggest that cholinergic agents applied centrally can increase both phrenic and hypoglossal activity. Moreover the effects of the drugs are relatively greater on XII nerve activity than on phrenic discharge, suggesting that the drive from medullary cholinergic structures is distributed with unequal weight to different respiratory motoneurons.
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PMID:Hypoglossal and phrenic responses to cholinergic agents applied to ventral medullary surface. 639 Dec 8

In the conscious, undisturbed toad, Bufo marinus, pulmonary arterial blood flow increased during periods of lung ventilation and decreased in intervening periods of pulmonary apnea. In unidirectionally ventilated, anesthetized toads, lung inflation produced by increasing the outflow resistance to pulmonary gas flow to 3 cmH2O caused a significant increase in pulmonary arterial blood flow and a significant decrease in cutaneous arterial blood flow. Changes in flow were associated with reciprocal changes in calculated vascular resistance. Mean pulmocutaneous pressure and cardiac frequency did not change significantly. Thus lung inflation (in the absence of changes in the composition of intrapulmonary gases) increased the proportion of total pulmocutaneous flow routed to the lungs and decreased the proportion directed to the skin. Unidirectional ventilation with air + 5% CO2 at constant lung volume produced a significant decrease in pulmonary arterial blood flow, an increase in calculated pulmonary arterial flow resistance, and a small increase in the flow to the cutaneous artery. Concomitant mild hypoxia potentiated the effects of pulmonary hypercapnia, although hypoxia alone was less effective than hypercapnia alone in decreasing pulmonary flow. Pulmonary arterial blood flow was decreased by infusion of acetylcholine into the pulmocutaneous artery, but epinephrine had no effect on either the pulmonary or cutaneous artery at doses below those that produced systemic effects. Atropine blocked all changes in pulmonary arterial blood flow. This and other evidence suggest that calculated arterial resistance changes are due to reflex changes in the tone of vascular smooth muscle. Intrapulmonary CO2-sensitive mechanoreceptors possess appropriate response characteristics to mediate the afferent limb of the reflex.
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PMID:Factors influencing pulmonary and cutaneous arterial blood flow in the toad, Bufo marinus. 643 53


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