bluuebunny/crossref_metadata_2025_split huggingface dataset:
OLEIC ACID‐INDUCED INJURIES IN THE GUINEA‐PIG. EFFECTS OF ALLOPURINOL ON CELL DYNAMICS, ERYTHROCYTE‐CATALASE AND URIC ACID PLASMA LEVELS
Authors: Hultkvist‐Bengtsson U. , Mårtensson L. 
Published: June 2007

SUMMARY1. Oleic acid was used to produce adult respiratory distress syndrome‐like pulmonary micro‐vascular injuries. The resulting injuries have previously indicated involvement of accumulating neutrophils (Hultkvist et al. 1988). Activated neutrophils release oxygen free radicals that may be possible to detect in the plasma.2. The dynamics of neutrophils and platelets were studied in the guinea‐pig after oleic acid‐induced injury (0.03 ml/kg per 10 min).3. As an indication of oxygen free radical activity, plasma levels of uric acid and red blood cell (RBC)‐catalase, were analysed.4. Allopurinol (10 mg/kg, i.p.) was given prior to oleic acid infusion to block the production of uric acid.5. The neutropenia, in contrast to the thrombocytopenia seen at 15 min, was significantly inhibited in the allopurinol pretreated group compared with oleic acid and vehicle alone.6. The blood plasma concentration of uric acid was significantly elevated after 15 min from start of experiment. Allopurinol pretreatment significantly reduced the uric acid plasma level.7. The RBC catalase activity did not change with time within or between any groups.8. The results indicate that sequestration of activated neutrophils in the microvasculature are to some extent oxygen free radical dependent.
THE EFFECT OF VASOACTIVE INTESTINAL PEPTIDE (VIP) ON THE CONTRACTILE ACTIVITY OF HUMAN UTERINE SMOOTH MUSCLE
Authors: Leroy M. J. , Tanguy G. , Vial M. , Rostène W. , Malassiné A. , Ferré F. 
Published: June 2007

SUMMARY1. In the present study we examined the in vitro effect of vasoactive intestinal peptide (VIP) on spontaneous contractions in both inner and outer layers of non‐pregnant human myometrium. A dose‐dependent relaxation was observed, but with a marked difference in sensitivity to VIP between the two layers, with an IC50 value of 1 X 10−8 and 1 X 10−5 mol/L in the outer and inner layers, respectively.2. We also established that VIP did not directly stimulate the adenylate cyclase activity. The only slight stimulations were observed in non‐initial rate conditions. The maximal response of this indirect effect was obtained for VIP concentrations between 1 X 10−9 and 1 X 10−8 mol/L and this occurred to the same extent (an approximately 1.4‐fold increase) in both layers. However this response is specific, since structurally related peptides such as glucagon, gastric inhibitory polypeptide (GIP), secretin, or human growth hormone‐releasing factor (hGRF) had no effect in our preparations.3. Autoradiographic studies revealed that specific VIP binding sites were located on the vascularization of the intermediate vascular layer and on arterioles and venules distributed in the inner and outer myometrial layers. They were also present in the endometrium, but not on smooth muscle cells of either layer.4. Such observations could provide evidence for another signal transduction pathway to mediate the biological effect of VIP. An additional intermediate step on the vascularization distributed in all of the muscle cannot be excluded.
USE OF NICOTINE, BRADYKININ AND VERATRIDINE TO ELICIT CARDIOVASCULAR CHEMOREFLEXES IN UNANAESTHETIZED RABBITS
Authors: Evans Roger G. , Ludbrook John , Michalicek Jan 
Published: June 2007

SUMMARY1. We have characterized in unanaesthetized rabbits the reflex effects of injecting nicotine into the pericardial sac or left atrium on heart rate, arterial pressure, systemic vascular resistance and the amplitude and frequency of respiration. These effects were compared with those of atrial administration of nicotine and veratridine, and intrapericardial administration of veratridine and bradykinin.2. Injection of nicotine (6.25–400 μg) into the pericardial sac caused dose‐dependent falls of heart rate and arterial pressure, and a brief period of hypopnoea. The fall in arterial pressure was mainly due to a fall in systemic vascular resistance. The threshold dose was 25 μg. Near maximal falls in heart rate (108 beats/min) and arterial pressure (47 mmHg) occurred at a dose of 200–400 μg. The latency between injection and the onset of bradycardia was 3.0 s.3. The effects of intrapericardial nicotine on arterial pressure and respiration were antagonized in a dose‐dependent fashion by intrapericardial mecamylamine (1–100 μg/kg) but were unaffected by intrapericardial hyoscine methylbromide (10 μg/kg) or vecuronium (1–10 μg/kg). The haemodynamic and respiratory effects were abolished by intrapericardial procaine. The haemodynamic effects were increased, though not significantly, by sino‐aortic baroreceptor denervation. In decerebrate, artificially ventilated rabbits, bilateral cervical vagotomy converted the hypotensive and bradycardic response into a slowly developing tachycardia without change in arterial pressure.4. Left atrial injection of nicotine (6.25–100 μg) caused bradycardia, a rise in arterial pressure, and prolonged hyperpnoea preceded by transient hypopnoea. After sino‐aortic barodenervation it caused profound falls in heart rate and arterial pressure and transient hypopnoea, which were abolished by intrapericardial procaine.5. Intrapericardial injection of veratridine (50–100 μg) had no consistent effect under control conditions. After sino‐aortic barodenervation it caused falls in heart rate and arterial pressure which were abolished by intrapericardial procaine. Left atrial injection of veratridine caused highly variable haemodynamic effects.6. Intrapericardial bradykinin (2.5–25 μg) caused rises in both arterial pressure and heart rate. These were abolished by intrapericardial procaine.7. We conclude that when nicotine is injected into the pericardial sac of conscious rabbits the reflex haemodynamic and respiratory effects are due to the selective activation of neuronal‐type nicotinic cholinoceptors on vagal afferents that originate in the epicardium. The reflex effects of left atrial nicotine are probably due to the excitation of a combination of carotid chemoreceptors and cardiac receptors.SUMMARY8. The effects of nicotine, veratridine and bradykinin that we observed in conscious rabbits were profoundly different from those reported in anaesthetized rabbits.
THE INHIBITORY EFFECT OF BEVANTOLOL ON THE ACCUMULATION OF NON‐ESTERIFIED FATTY ACIDS DURING ISCHAEMIA IN THE DOG HEART IN SITU
Authors: Miura Itaru , Nasa Yoshihisa , Ichihara Kazuo , Abiko Yasushi 
Published: June 2007

SUMMARY1. The left anterior descending coronary artery (LAD) was completely ligated for 90 min (i.e. myocardial ischaemia was produced) in the dog anaesthetized with pentobarbital.2. Bevantolol, a β1‐adrenoceptor antagonist, was injected (1 mg/kg, intravenously) 5 min before LAD occlusion. The bevantolol injection decreased heart rate without affecting blood pressure.3. The myocardial samples were taken from the LAD area immediately after the end of LAD occlusion, and were subjected to analysis of the myocardial levels of non‐esterified fatty acids (NEFA).4. In dogs in which saline was injected, ischaemia produced accumulation of NEFA, especially arachidonic and palmitoleic acids, in the myocardium.5. In dogs in which bevantolol was injected, the accumulation of NEFA induced by ischaemia was almost completely inhibited.6. It is concluded that bevantolol inhibits ischaemia‐induced accumulation of NEFA in the myocardium, and that stimulation of the β1‐adrenoceptors is probably responsible for NEFA accumulation induced by ischaemia.
CLONIDINE SUPPRESSION TEST RELIABLY DIFFERENTIATES PHAEOCHROMOCYTOMA FROM ESSENTIAL HYPERTENSION
Authors: Bachmann Anthony W. , Gordon Richard D. 
Published: June 2007

SUMMARY1. Clonidine resulted in significant suppression of both noradrenaline (NA) and adrenaline (ADR) in essential hypertensives (EHT) without any false positive findings. That is, every patient who failed to suppress had phaeochromocytoma (PH).2. The clonidine suppression test (CST) produced minimal suppression of NA in NA‐secreting PH (NA‐PH) and correctly identified two NA‐PH with normal basal plasma NA.3. In ADR‐secreting PH (ADR‐PH) the CST did not result in significant suppression of ADR levels, whether elevated or normal basally.4. The CST proved to be an accurate discriminator of PH from other forms of hypertension.noradrenaline
THE SYNDROME OF HYPERTENSION AND HYPERKALAEMIA WITH NORMAL GLOMERULAR FILTRATION RATE: IS THERE A DEFICIENCY IN VASODILATOR PROSTAGLANDINS?
Authors: Klemm Shelley A. , Hornych Antonin , Tunny Terry J. , Gordon Richard D. 
Published: June 2007

SUMMARY1. In Gordon's syndrome (GS; a syndrome of hypertension and hyperkalaemia with normal glomerular fitration rate), excessive proximal sodium reabsorption leads to suppression of renin and aldosterone, hyperkalaemia and hyperchloraemic acidosis.2. Low urinary levels of vasodilator prostaglandins (PG) have been reported in GS, suggesting renal hypoprostaglandinism as a pathophysiological mechanism.3. In four cases of GS, levels of vasodilator prostaglandins PGE2 and 6‐keto‐PGF1α were low.4. In one case of GS, low PGE2 levels were normalized by dietary salt restriction or diuretic therapy.
RELEVANCE OF THE WATERFALL PHENOMENON IN CONTINUOUS FINGER CUFF BLOOD PRESSURE MEASUREMENTS
Authors: Kobler H. , Cejnar M. , Hunyor S. N. 
Published: June 2007

SUMMARY1. Finger cuff blood pressure monitors that provide continuous presentation of arterial pressure at the finger are available.2. The operation of such instruments is based on ‘clamping’ arterial volume under a pressurized encircling cuff applied to a digit. Blood volume is detected by measuring infra‐red transmission across the finger.3. The compressed veins adopt cuff pressure and combine with the resistance of the peripheral vascular bed at the finger tip to control the blood flow. This results in waterfall behaviour in the veins under the cuff.4. With the cuff set just 5 mmHg below the undisturbed arterial pressure, adequate flow to the distal finger is maintained.5. Two potential sources of error affect the finger cuff blood pressure method. These are related to the increase in systolic pressure associated with moving peripherally and the variable value of occluding transmural pressure, both of which depend on muscular tone.
REDUCTION IN LEFT VENTRICULAR MASS IN NORMOTENSIVE AND SPONTANEOUSLY HYPERTENSIVE RATS GIVEN ENALAPRIL
Authors: Mooser Vincent , Casley David , Trinder Deborah , Paxton Donna L. , Johnston Colin I. 
Published: June 2007

SUMMARY1. To test the hypothesis that the reduction of left ventricular weight (LVW) observed during angiotensin‐converting enzyme (ACE) inhibition in rats is mainly a response to decreased cardiac load, the effect of enalapril on LVW and blood pressure (BP) in normotensive Sprague‐Dawley (SD) and in spontaneously hypertensive rats (SHR) was compared.2. Enalapril decreased BP by 10% in SD rats and 21% in SHR; and LVW by 6% in SD rats and 12% in SHR. A close linear correlation between BP and LVW was observed in SD (r= 0.65, n= 24, P<0.001) and SHR (r= 0.92, n= 15, P<0.001).3. The effect of enalapril on LVW, when related to BP, was almost identical in SD and SHR, as the average reduction of LVW (μg/g of bodyweight) per mmHg was 7.7 ± 1.9 versus 7.5 ± 0.9 in SD and SHR respectively.4. These data constitute additional evidence to support the view that, at least under ACE inhibition, reduction in LVW is mainly due to the fall in BP and the decreased cardiac load.
CHARACTERIZATION OF MONOCLONAL ANTIBODIES TO A RAT LIVER VASOPRESSIN RECEPTOR
Authors: Trinder Deborah , Mooser Vincent , Kelly Janice M. , Phillips Paddy A. , Casley David , Johnston Colin I. 
Published: June 2007

SUMMARY1. Balb/c mice were immunized against a vasopressin binding protein purified from rat liver. The hybrids produced from two cell fusions were screened against this receptor. Three hybrids were selected, cloned and expanded in serum‐free media. The monoclonal antibodies (MoAb) secreted by these three hybrids were of the subclass IgM and were able to immunoprecipitate [125I]‐labelled purified receptor.2. All three MoAb bound to the purified solubilized receptor, crude liver and kidney membranes in a concentration‐dependent manner. However, the binding of MoAb to the membranes did not inhibit the binding of [125I]‐[d(CH2)5, Sar7]AVP, a selective V1 receptor radioligand, to the liver membrane‐bound receptor.3. These results suggest that the three MoAb recognize epitopes on the V1 receptor which are not denatured by solubilization, but are common to both rat liver and kidney membranes.
ANGIOTENSIN‐CONVERTING ENZYME IN MACRO‐AND MICROVESSELS OF THE RAT
Authors: Jandeleit Karin , Jackson Bruce , Perich Rose , Paxton Donna , Johnston Colin 
Published: June 2007

SUMMARY1. Angiotensin‐converting enzyme (ACE) was measured in the aorta, cerebral and mesenteric microvessels of Wistar‐Kyoto rats using a specific radioligand assay.2. Ligand binding studies revealed a four‐fold increase in concentration of ACE in mesenteric microvessels, compared with aorta or brain microvessels. The dissociation constant (Kd) was similar in all tissues.3. The effects of oral administration of the ACE inhibitor S9650 on vascular ACE in vivo were measured.4. S9650 produced a dose‐dependent inhibition of vascular ACE from brain and mesenteric microvessels.
RENIN GENE EXPRESSION IN VARIOUS TISSUES DETERMINED BY SINGLE‐STEP POLYMERASE CHAIN REACTION
Authors: Lou Yi‐kun , Smith D. Lynne , Robinson Bruce G. , Morris Brian J. 
Published: June 2007

SUMMARY1. Renin mRNA is present in the kidney and, in lower concentrations, in many extrarenal tissues and serves as an index of renin gene activity, as well as potential renin or prorenin synthesis in cell populations within those tissues. Unfortunately the quantity can be very low.2. A new, highly sensitive technique is described for detection of renin mRNA that involves the enzyme Taq polymerase for both reverse transcription of renin mRNA into renin cDNA and for amplification of the 769–1099 nucleotide segment by the polymerase chain reaction (PCR), all of which involves a single reaction mixture.3. In this way renin mRNA was detected in kidney and several extrarenal tissues as a PCR product of ∼330 base pairs on agarose gels by ethidium‐bromide staining or hybridization probing. The region of renin mRNA chosen for amplification spanned several intron sites in the coding sequence so that the presence of amplicants derived from genomic DNA could be readily discriminated, as a band of ∼1.5 kilobases.4. Thus single‐step PCR offers a powerful new approach to detection of renin mRNA.
HAEMODYNAMIC RESPONSES TO N‐NITRO‐l‐ARGININE IN CONSCIOUS RABBITS
Authors: Du Z. Y. , Dusting G. J. , Woodman O. L. 
Published: June 2007

SUMMARY1. The effect of N‐nitro‐l‐arginine (NOLA) on mean arterial pressure (AP), hindlimb vascular resistance (HVR) and heart rate (HR) was examined in conscious rabbits.2. NOLA (15 mg/kg, i.v.) increased AP (ΔAP = 14 ± 3 mmHg) and HVR (ΔHVR = 0.8 ± 0.3 U) and decreased HR (ΔHR = ‐ 66 ± 8 beats/min). AP remained elevated for at least 2 h following NOLA infusion but had returned to control levels after 24 h. In contrast, the hindlimb vasoconstriction and bradycardia were sustained for at least 48 h but had returned to control levels after 72 h.3. In the presence of total autonomic blockade (hexamethonium 30 mg/kg; propranolol 1 mg/kg and atropine 0.1 mg/kg) NOLA continued to have a pressor (ΔAP = 33 ± 9 mmHg) and hindlimb vasoconstrictor action (ΔHVR = 0.4 ± 0.1 U) but did not affect HR (ΔHR = ‐ 1 ± 3 beats/min).4. NOLA has a prolonged pressor and vasoconstrictor action which is independent of any action in the central nervous system and which results in a marked reflex bradycardia. These results suggest that the peripheral biosynthesis of nitric oxide is important in regulation vascular tone and arterial pressure.
ON MAKING MULTIPLE COMPARISONS IN CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY
Authors: Ludbrook John 
Published: June 2007

SUMMARY1. It is a central thesis of this review that in clinical and experimental pharmacology and physiology the goal of statistical analysis should be to minimize the risk of making any false–positive inferences from the results of an experiment (experimentwise Type I error).2. It is common in clinical and experimental pharmacology and physiology for the effects of several treatments to be tested within a single experiment. Specific intercomparisons of these several effects, made in a pairwise or more complex fashion, inflates the risk of making false–positive inferences unless special statistical procedures are used.3. A number of multiple comparison procedures is described and their ability to control experimentwise Type I error is evaluated critically.4. When only a few (< 5) of all possible pairwise or more complex comparisons are made between treatment groups, the Dunn‐Šdák procedure provides maximum protection against excessive experimentwise Type I error and is very convenient to use.5. When a control group is compared with all other treatment groups in a pairwise fashion, especially when the number of groups is large, the Dunnett procedure is more powerful than the Dunn‐Šidák.6. If investigators insist on making all possible pairwise comparisons among treatment groups, the Tukey‐Kramer procedure provides maximum protection against false‐positive inferences but inflates the Type II error rate. If it is especially important to avoid Type II error then the more complicated, stepwise procedures of the Ryan‐Peritz‐Welsch variety should be considered.
CONTRIBUTION OF α2‐ADRENOCEPTORS TO THE CENTRAL CARDIOVASCULAR EFFECTS OF CLONIDINE AND S 8350 IN ANAESTHETIZED RATS
Authors: Deckert Valérie , Lachaud Valérie , Parini Angelo , Elghozi Jean‐Luc 
Published: June 2007

SUMMARY1. The α2‐adrenoceptor agonist clonidine elicits centrally mediated effects through an interaction with both α2‐adrenoceptors and imidazoline binding sites.2. We selected a new oxazoline derivative, S 8350, which competes with [3H]‐yohimbine for binding to cerebral α2‐adrenoceptors (IC50, 67 ± 17 nmol/L) and displays a higher affinity (35‐fold) for α2‐ than for α1‐adrenoceptors.3. As observed for clonidine, intravenous (i.v.) administration of S 8350 resulted in a brief pressor effect followed by a prolonged hypotension. When S 8350 was administered i.v. to spinally pithed rats, only a rise in blood pressure was observed.4. In order to discriminate the cardiovascular effects related to the central imidazoline receptor or α2‐adrenoceptor activation, the effects of intracisternal (i.c.) administration of clonidine and S 8350 were investigated in the rat.5. In the anaesthetized rat, both clonidine and S 8350 displayed a profound central (i.c. route) hypotensive effect associated with a bradycardia.6. The cardiovascular effects of S 8350 were abolished by the central administration of the selective α2‐adrenoceptor antagonist rauwolscine. Conversely, rauwolscine completely prevented bradycardia but it induced only a partial reversion of the hypotension elicited by clonidine.7. These results suggest that central α2‐adrenoceptors are responsible for hypotension and bradycardia while imidazoline binding sites do not apparently contribute to heart rate control.
EFFECT OF TOLERANCE TO GLYCERYL TRINITRATE ON VASCULAR RESPONSES IN CONSCIOUS RABBITS
Authors: Du Z. Y. , Dusting G. J. , Woodman O. L. 
Published: June 2007

SUMMARY1. The effect of tolerance to glyceryl trinitrate (GTN) on vasodilator and vasoconstrictor responses was examined in conscious rabbits and isolated rabbit aortic rings.2. In conscious rabbits, depressor responses to 5 min infusions of GTN (10–40 μg/kg per min intravenously (i.v.)), sodium nitroprusside (SNP, 5–20 μg/kg per min i.v.) and acetylcholine (ACh, 3–12 μg/kg per min i.v.) were examined before and after transdermal treatment with GTN (20 mg/48 h). GTN pretreatment significantly attenuated GTN‐induced depressor responses, indicating the development of tolerance, but did not affect the reductions in arterial pressure induced by SNP or ACh.3. Similarly, aortic rings taken from GTN pretreated rabbits exhibited tolerance to GTN but the relaxant responses to SNP or the calcium ionophore A23187 were not affected. In the aortic rings from GTN‐tolerant rabbits contractile responses to serotonin or the thromboxane‐mimetic U46619 were significantly attenuated, in contrast to the responses to the α1‐adrenoceptor agonist phenylephrine (PE) which were significantly enhanced.4. Similarly, in conscious rabbits, PE‐induced increases in arterial pressure and hindlimb vascular resistance were significantly enhanced by GTN pretreatment but the responses to the α2‐adrenoceptor agonist BHT 920 were unaffected.5. In conclusion, tolerance to GTN does not affect endothelium‐dependent vasodilatation but does cause a selective enhancement of α1‐ but not α2‐adrenoceptor‐mediated vasoconstriction.
DISTRIBUTION AND INHIBITION OF NEUTRAL METALLOENDOPEPTIDASE (NEP) (EC 3.4.24.11), THE MAJOR DEGRADATIVE ENZYME FOR ATRIAL NATRIURETIC PEPTIDE, IN THE RAT KIDNEY
Authors: Kanazawa Masayuki , Johnston Colin I. 
Published: June 2007

SUMMARY1. Atrial natriuretic peptide (ANP) is degraded by neutral metalloendopeptidase (NEP) (EC 3.4.24.11) and the kidney is a major site of ANP clearance.2. The regional distribution of NEP in the rat kidney was investigated.3. The activity of NEP, measured with an enzymatic fluorimetric method employing N‐dansyl‐D‐alanyl‐glycyl‐L‐4‐nitrophenylalanyl‐glycine as a synthetic substrate, was 18 times and eight times higher in the outer stripe of the medulla and inner cortex than in the outer cortex (OC).4. Low concentrations of NEP were found in the OC, inner stripe and inner medulla.5. NEP activity in the rat kidney was inhibited by the specific NEP inhibitors (SCH39370, phosphoramidon and thiorphan) at micromolar concentrations.6. The present result suggests that degradation of ANP by NEP occurs mainly in the proximal tubules of the juxtamedullary nephrons, rather than cortical nephrons, and that the convoluted tubule in the OC is not a major site of location of NEP.7. The relationship between NEP activities in the kidney in vitro and plasma clearance of ANP in vivo remains to be clarified.
DIGOXIN‐LIKE IMMUNOREACTIVITY INCREASES WITH INTRAVENOUS INFUSION OF SALINE IN RATS
Authors: Takahashi Hakuo , Matsusawa Makoto , Nishimura Masato , Ikegaki Iwao , Nakanishi Tadashi , Yoshimura Manabu 
Published: June 2007

SUMMARY1. The effects of sodium‐loading on releases of endogenous digitalis‐like substance were investigated by measuring digoxin‐like immunoreactivity (DLI) during intravenous infusions of isotonic (0.15 mol/L) and hypertonic (1 mol/L) saline in anaesthetized rats. Plasma DLI was measured after death by a digoxin‐radioimmunoassay.2. The infusion of isotonic saline and hypertonic saline elevated the central venous pressure to similar levels. The plasma DLI concentration in both the infused groups rose significantly compared with that in the control rat not receiving the intravenous infusion.3. The difference in the hypothalamic concentrations of DLI was not significant among the three groups, however, there was a significant inverse relationship between the plasma and hypothalamic concentrations of DLI.4. Results indicate that the central venous pressure, but not sodium concentration, is essentially involved in the release of DLI, possibly from the hypothalamus.