|
1. |
FURTHER EVIDENCE OF THE ROLE OF CYCLIC AMP AS A MEDIATOR OF THE DEPRESSANT EFFECTS OF β‐ADRENOCEPTOR AGONISTS AND PHOSPHODIESTERASE INHIBITORS ON SLOW‐CONTRACTING MAMMALIAN SKELETAL MUSCLES |
|
Clinical and Experimental Pharmacology and Physiology,
Volume 13,
Issue 6,
1986,
Page 441-445
Zainuddin Merican,
Paden Morat,
Rahim Dan,
B. A. K. Khalid,
Preview
|
PDF (326KB)
|
|
摘要:
SUMMARY1. The depressant effects of β‐adrenoceptor agonists and phosphodiesterase inhibitors on contractions of slow‐contracting mammalian skeletal muscles are associated with increased muscular cyclic AMP levels.2. A strong correlation was found to exist between the percentage depression of contraction and the percentage increase in cyclic AMP level, irrespective of the drug used and regardless of the mechanism of cyclic AMP production.3. The results strongly support the mediatory role of cyclic AMP in the depressant effects of β‐adrenoceptor agonists and phosphodiesterase inhibitors on slow‐contracting mammalian skeletal muscle con
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1986.tb00924.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
|
2. |
A COMPARISON OF THE EFFECTS OF END‐TO‐SIDE PORTACAVAL SHUNTING AND SIDE‐TO‐SIDE MESOCAVAL SHUNTING ON HEPATIC HAEMODYNAMICS IN THE DOG |
|
Clinical and Experimental Pharmacology and Physiology,
Volume 13,
Issue 6,
1986,
Page 447-452
S. A. Jenkins,
A. Taylor,
J. Johnson,
S. K. Shimlrty,
J. N. Baxter,
R. Shields,
Preview
|
PDF (332KB)
|
|
摘要:
SUMMARY1. Functional liver blood flow and hepatic artery flow were measured before and after either end‐to‐side portacaval or side‐to‐side mesocaval shunting in dogs.2. Functional liver blood fell by approximately 50% following both portacaval and mesocaval shunting.3. The hepatic artery response was variable after both portacaval and mesocaval shunts.4. It is concluded that side‐to‐side mesocaval shunts do not preserve hepatic blood flow or produce a greater compensatory increase in hepatic artery flow than conventional portac
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1986.tb00925.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
|
3. |
ACTION OF ALMITRINE BISMESYLATE ON VENTILATION‐PERFUSION MATCHING IN CATS AND DOGS WITH PART OF THE LUNG HYPOVENTILATED |
|
Clinical and Experimental Pharmacology and Physiology,
Volume 13,
Issue 6,
1986,
Page 453-467
R. A. Wach,
G. W. Gill,
A. J. Suggett,
D. Bee,
G. Barer,
Preview
|
PDF (854KB)
|
|
摘要:
SUMMARY1. Ventilation to one lobe of lung was reduced in anaesthetized open‐chest cats and dogs to simulate the ventilation/perfusion (V̇/Q̇) mismatching of chronic lung disease. Blood flow to this lobe fell less than ventilation; thus lobar V̇/Q̇ diminished.2. In seven cats almitrine (0.5 mg/kg + 10 μg/kg per min, i.v.) caused a rise in pulmonary artery pressure (PPA), increased flow through the hypoventilated lobe in six out of seven cats and both increased or decreased lobar vascular resistance (PVR); the lobar V̇/Q̇ ratio therefore fell. Arterial and lobar venous oxygen tension (Po2) fell.3. In five dogs almitrine caused a rise inPPAand PVR but lobar flow changes were variable. Arterial and lobar venousPo2fell.4. With fixed ventilation, almitrine failed to improve V̇/Q̇ matching; there was no improvement in gas exchange in the hypoventilated lobe.5. In eight dogs the hypoventilated lobe was perfused at constant flow with right atrial blood (i.e. while V̇/Q̇ was held constant). Almitrine caused a rise in perfusion pressure, vasoconstriction, followed, in five out of eight dogs, by vasodilatation.6. In six similar cat preparations, vasoconstriction but not vasodilatation was clearly shown. In two cats dilatation after almitrine was demonstrated during ventilation with Nitrogen.7. In all experiments there was no significant effect of the solvent.8. Thus the dual action of almitrine seen in other species was seen in a proportion of cats and dogs.9. Results do not support the view that improved arterial gas tensions in patients after almitrine are attributable to diversion of blood flow away from hypoxic lung. Alternative mechanisms a
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1986.tb00926.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
|
4. |
BRAIN NORADRENALINE AND THE DEVELOPMENT OF HYPERTENSION: THE EFFECT OF TREATMENT WITH CENTRAL 6‐HYDROXYDOPAMINE OR DSP‐4 |
|
Clinical and Experimental Pharmacology and Physiology,
Volume 13,
Issue 6,
1986,
Page 469-476
Maarten Buuse,
Dirk H. G. Versteeq,
Wybren Jong,
Preview
|
PDF (508KB)
|
|
摘要:
SUMMARY1. The relative role of brain catecholamines in the development of hypertension in the spontaneously hypertensive rat (SHR) was studied.2. Treatments consisted in five weeks old SHR of central injections of 6‐hydroxydopamine (6‐OHDA), 3 × 200 μg either intracerebroventricularly (i.c.v.) or intracisternally (i.c.), or of intraperitoneal (i.p.) injections of DSP‐4, either once or three times 50 mg/kg.3. Compared to the pronounced attenuation of the development of hypertension following i.c.v. 6‐OHDA treatment, the i.c. 6‐OHDA treatment and the multiple DSP‐4 treatment were less effective. A single injection of DSP‐4 had only minor effects on blood pressure. Heart rate was markedly lower in i.c.v. 6‐OHDA treated SHR, but the other treatments induced no effects on this parameter.4. Noradrenaline depletion was found in various parts of the brain particularly after i.c.v. 6‐OHDA or either DSP‐4 treatment. Brain dopamine and adrenaline were depleted to a lesser extent. However, the best correlation between blood pressure and brain catecholamine concentration was found for dopamine in the hippocampus and hypothalamus and for adrenaline in the hypothalamus. Noradrenaline levels were also correlated with blood pressure, but to a lesser extent.5. These results suggest that the depletion of dopamine or adrenaline in the brain may be of more importance in the effects of neurotoxic treatments on the development of hypertension than the effects on brain noradrenaline. Thus, these experiments lend support to the hypothesis that brain noradrenaline systems may not play an important role in the development of hy
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1986.tb00927.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
|
5. |
RELATION OF INTRAMYOCARDIAL PRESSURE TO CORONARY PRESSURE AT ZERO FLOW |
|
Clinical and Experimental Pharmacology and Physiology,
Volume 13,
Issue 6,
1986,
Page 477-486
Hani N. Sabbah,
Mario Marzilli,
Zhi‐quan Liu,
Paul D. Stein,
Preview
|
PDF (523KB)
|
|
摘要:
SUMMARY1. The purpose of this study was to determine the extent to which coronary pressure at zero coronary flow (Pf=0) may relate to extravascular compressive forces determined by direct measurements of left ventricular intramyocardial pressure.2. Studies were performed in nine open‐chest anaesthetized dogs in which the anterior descending coronary artery was cannulated and perfused from the carotid artery. Coronary pressure was measured at the tip of the cannula.3. Intramyocardial pressure was measured with a 1 mm diameter micromanometer inserted directly into the subepicardium. The atrioventricular node was obliterated by cautery and the heart was electrically paced. Long diastolic pauses, sufficient to allow coronary flow to reach zero, were produced by the cessation of electrical pacing.4. In the autoregulated coronary bed,Pf=0, 47 mmHg (s.e.m. = 9), exceeded subepicardial pressure at zero flow, 23 mmHg (s.e.m. =2;P<0.001). During maximal vasodilatation with adenosine,Pf=0, 16 mmHg (s.e.m. = 11), was not significantly different from subepicardial pressure at zero flow, 21 mmHg (s.e.m. =4). These observations indicate that, in addition to coronary vasomotor tone, diastolic myocardial tissue pressure is important in the genesis ofPf=
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1986.tb00928.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
|
6. |
EFFECTS OF A SYNTHESIZED PHOSPHODIESTERASE INHIBITOR, ZSY‐27, ON PANCREATIC EXOCRINE SECRETION OF THE DOG |
|
Clinical and Experimental Pharmacology and Physiology,
Volume 13,
Issue 6,
1986,
Page 487-494
K. Iwatsuki,
F. Yamagishi,
S. Chiba,
Preview
|
PDF (430KB)
|
|
摘要:
SUMMARY1. The effects of a synthesized phosphodiesterase inhibitor, ZSY‐27, on the secretion of pancreatic juice were investigated in dog isolated and blood‐perfused pancreas, and compared with those of secretin and dopamine.2. Intravenous administration of ZSY‐27 (0.3‐1 mg/kg) elicited increases in pancreatic secretion. Intra‐arterial (i.a.) administration of ZSY‐27 (0.1‐1 mg) also elicited increased secretion. The secretory activity of ZSY‐27 (1 mg) was approximately equal to that of 0.1 units of secretin and 2.5 μg of dopamine.3. The concentration of bicarbonate in the pancreatic juice induced by ZSY‐27 i.a. was increased, but the protein concentration was not increased significantly. These effects are analogous to those of secretin and dopamine.4. ZSY‐27‐induced pancreatic secretion was not modified by pretreatment with phentolamine, propranolol, atropine, sulpiride and cimetidine.5. Secretin‐induced secretion was significantly potentiated by infusion of ZSY‐27 (25 μg/min) but dopamine‐induced one was not.6. These results suggest that ZSY‐27 increases pancreatic secretion acting directly on the ductular cells of the dog pancreas, at least in part, through the increase of intra‐cellular cyclic AMP concentration by inhi
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1986.tb00929.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
|
7. |
FRUSEMIDE INHIBITION OF SYMPATHETIC VASOCONSTRICTION IN THE RATIN SITUBLOOD PERFUSED MESENTERY |
|
Clinical and Experimental Pharmacology and Physiology,
Volume 13,
Issue 6,
1986,
Page 495-503
Stuart J. Armsworth,
John F. Gerkens,
Anthony J. Smith,
Preview
|
PDF (513KB)
|
|
摘要:
SUMMARY1. Mesenteric perfusion pressure was measured in thein situblood‐perfused mesentery of anaesthetized rats. Increases in perfusion pressure were produced by mesenteric periarterial electrical stimulation at 3, 6 and 10 Hz before and after the administration of frusemide 5 mg/kg intravenously (i.v.) or vehicle. Loss of volume due to diuresis was prevented by replacement with intravenous saline.2. Frusemide did not cause any changes in blood pressure or baseline perfusion pressure. Responses to electrical stimulation were inhibited by frusemide (P<0.05) but unchanged by vehicle administration.3. Acute bilateral nephrectomy or treatment with indomethacin (2 mg/kg i.v.) prevented the inhibitory effect of frusemide on responses to sympathetic nerve stimulation.4. Responses to sympathetic nerve stimulation were potentiated by an infusion of angiotensin II (12 ng/min) into the mesenteric artery. This infusion did not alter either blood pressure or baseline perfusion pressure. Administration of frusemide 5 mg/kg i.v. attenuated the potentiating effect of angiotensin II on vasoconstrictor responses to electrical nerve stimulation.5. Frusemide may lead to the release of a prostanoid or prostanoid precursor which inhibits vascular constrictor response
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1986.tb00930.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
|
8. |
EFFECTS OF AROTINOLOL, AN α‐ AND β‐ADRENOCEPTOR ANTAGONIST, ON RENIN RELEASE FROM RAT KIDNEY CORTICAL SLICES |
|
Clinical and Experimental Pharmacology and Physiology,
Volume 13,
Issue 6,
1986,
Page 505-510
S. Morimoto,
N. Miyawaki,
Y. Sasaki,
Y. Matsumura,
Preview
|
PDF (342KB)
|
|
摘要:
SUMMARY1. The effects of arotinolol on changes in renin release in rat kidney cortical slices in response to isoproterenol (IP) or norepinephrine (NE), were studied in comparison with those of AC‐623, a main metabolite of arotinolol, and other typical adrenoceptor antagonists.2. Arotinolol, at concentrations of 10−8to 10−4mol/l, inhibited the increasing effect of 10−6mol/l IP on renin release, in a concentration‐dependent manner. Similar results were observed with AC‐623, propranolol or labetalol, although the inhibitory potencies of these agents were considerably lower than that of arotinolol.3. The blocking effect of arotinolol on the 10−5mol/l NE‐induced decrease in renin release was much less potent than seen with other α‐adrenoceptor blocking agents such as prazosin, phenoxybenzamine and labetalol.4. These data suggest that the potent blocking effects of arotinolol and its metabolite on the increased renin release in response to β‐adrenoceptor stimulation may contribute to the antihypertensive
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1986.tb00931.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
|
9. |
ERRATUM |
|
Clinical and Experimental Pharmacology and Physiology,
Volume 13,
Issue 6,
1986,
Page 511-511
Preview
|
PDF (30KB)
|
|
ISSN:0305-1870
DOI:10.1111/j.1440-1681.1986.tb00932.x
出版商:Blackwell Publishing Ltd
年代:1986
数据来源: WILEY
|
|