Blood Pressure In Cats Research Articles

Effects of caffeine on carotid sinus nerve chemosensory discharge in kittens and cats.

Caffeine (C) decreases apneic episodes in premature infants and is thought to stimulate breathing mainly by a central mechanism. While the methylxanthines theophylline and aminophylline are known to alter the carotid chemoreceptor activity, there are little data on C. The aim of the study was to examine the effects of C on the carotid sinus nerve discharge (CSND) in developing animals. Nine kittens 17-21 days old and six adult cats that were anesthetized and artificially ventilated were studied. They received four consecutive doses of C, each of 10 mg/kg, administered at intervals of 20 min either as intravenous bolus injection (6 kittens, 3 cats) or continuous infusion (3 kittens, 3 cats). Bolus injections of C invariably induced a prompt but transient increase in the CSND from 4.1 +/- 0.6 to 8.1 +/- 1.0 (SE) impulses/s in kittens (P = 0.01) and form 3.9 +/- 0.1 to 7.9 to 1.0 impulses/s in cats (after the first injection). This response was associated with a significant decrease in arterial blood pressure. Continuous infusion of C did not induce any early change in either CSND or blood pressure in kittens or cats. Fifteen minutes after C injection or infusion was begun, CSND values in air, 8% O2-balance N2, or 100% O2 were not significantly different from control. Haloperidol administered at the end of the experiment in four cats and four kittens significantly increased CSND and did not suppress the early response to C injection. It is concluded that caffeine administered by bolus in the kitten induces a transient stimulation of the CSND that is associated with a decrease in the arterial blood pressure and is independent of the dopaminergic mechanisms in the carotid body. The lack of sustained effect implies the main mechanism to the ventilatory stimulation by C must be central.

The pharmacological basis for the use of dried sheep placenta in traditional obstetric practice in Nigeria

Dried sheep placenta is sometimes used in traditional medicine to facilitate labour. The effects of an extract of powdered dried sheep placenta with normal saline on guinea-pig uterus, ileum, spontaneously beating atrium and Langendorff heart, rat uterus and hindquarters, and cat blood pressure were therefore examined. It was found that 1 g of dried sheep placenta had, on the guinea-pig uterus, an oxytocic activity equipotent with 0.075-0.32 i.u. of oxytocin. The oxytocic activity was unaffected at pHs between 4 and 10 or by boiling for 30 min or autoclaving for 15 min. Neither atropine nor promethazine inhibited the oxytocic action, but promethazine inhibited, to the same degree, contractions induced in the ileum by equipotent doses of the infusion and histamine. Atropine, however, had no effect on infusion-induced contractions in the ileum. The vasoconstriction induced in the rat hindquarters was antagonized by promethazine and phentolamine. Cat blood pressure was reduced, but it had positive inotropic and chronotropic effects on the spontaneously beating guinea-pig atrium and on the guinea-pig Langendorff heart. It was concluded that the dried placenta contains a chorionic oxytocic substance the action of which is independent of stimulation of H 1 receptors or of muscarinic receptors.

Phenyl biguanide does not inhibit locomotion in conscious rabbits

Stimulation of cardiopulmonary vagal C fibers with phenyl biguanide (PBG) reflexly inhibits locomotion in addition to causing depression of blood pressure (BP), heart rate (HR), and respiration in cats and rats. We investigated whether PBG caused somatomotor inhibition during exercise in the rabbit, a species in which it is known that the hemodynamic and respiratory responses to PBG are mediated by cardiac rather than by pulmonary receptors. In eight New Zealand White rabbits, BP, HR, and hindlimb electromyographic (EMG) responses to 60 and 120 micrograms/kg PBG and saline vehicle were evaluated during two separate 3-min exercise bouts at 10 m/min at 0% grade. During exercise, 60 micrograms/kg PBG decreased BP (-27 +/- 4 mmHg) and HR (-95 +/- 16 beats/min) but did not inhibit locomotion as suggested by the EMG response (+112 +/- 8% of preinfusion EMG). Hemodynamic and EMG responses to 120 micrograms/kg PBG were similar to 60 micrograms/kg PBG. Saline infusion during exercise had no effect on HR, BP, or locomotion (+114 +/- 8% of preinfusion EMG). Locomotion is not inhibited by PBG in rabbits, which suggests that PBG-induced reflex somatomotor inhibition observed in other species is primarily mediated by pulmonary rather than by cardiac receptors.

Responses of neurons of the preoptic region to an increase in systemic blood pressure in cats

Responses of neurons of the lateral and medial parts of the preoptic regionRPO (LPO andMPO, respectively) and the supraoptic nucleus (SO) of the hypothalamus to an increase in systemic blood pressure were studied in acute experiments on ketamine-anesthetized cats. The blood pressure increase resulted from the injection of a 0.002% phenylephrine hydrochloride solution in the femoral vien. Responses of theRPO neurons to suprathreshold pressor stimulation were monophasic activation (48% of units), monophasic inhibition (10%), or two-phase activational-inhibitory complex (14%). The rest of the neurons did not respond to the systemic pressure increase. Pressor stimulations evoked the responses only of the first and third type inMPO neurons, and only of the first and second type inLPO neurons, whileSO neurons generated responses only of the first type. Hysteresis of a varying degree was manifested in the changes of neuronal spike activity accompanying shifts of the systemic pressure. In some neurons there was no strict correlation between the pressor effect and the onset of neuronal response. Osmosensitivity of a part of neurons was tested. The responses of most of theRPO andSO neurons to pressor influences and infusions of hypertonic saline were of similar direction, whereas responses to infusions of hypotonic saline were opposite.

Central muscarinic M-1 receptors in the regulation of the arterial blood pressure in cats

Central muscarinic M-1 receptors in the regulation of the arterial blood pressure in cats

Intravenous NBQX inhibits spontaneously occurring sympathetic nerve activity and reduced blood pressure in cats

2,3-Dihydroxy-6-nitro-7-sulfamoyl-benzo( F)quinoxaline (NBQX) has been demonstrated to be a specific and competitive non-N- methyl- D-aspartate (non-NMDA) glutamate receptor antagonist. Our previous data obtained with the NMDA receptor antagonist MK-801 indicate that blockade of the NMDA receptor affects blood pressure. The purpose of this study was to determine whether the same is true with blockade of the non-NMDA receptor. For this purpose we administered three doses of NBQX (1, 3 and 10 mg/kg i.v.) to anesthetized, artificially ventilated and paralyzed cats while monitoring spontaneously occurring cardiac sympathetic nerve activity, arterial blood pressure and heart rate. The 1 mg/kg dose of NBQX i.v. reduced both sympathetic nerve activity (−29 ± 7%, P < 0.05, n = 4) and blood pressure (−27 ± 5 mm Hg, P < 0.05). Injection of 3 mg/kg NBQX produced a greater decrease in sympathetic nerve activity (−78 ± 11%, P < 0.01, n = 8) and mean arterial pressure (−47 ± 5 mm Hg) and also reduced heart rate (−11 ± 2 beats/min, P < 0.01). The depressant effects of NBQX on sympathetic nerve activity, blood pressure and heart rate were similar regardless of whether activity was recorded from pre- or postganglionic cardiac nerves, or from animals subjected to baroreceptor denervation. Intravenous injection of a total dose of 10 mg/kg NBQX completely inhibited sympathetic nerve activity (−100 ± 0%, P < 0.05, n = 3) and this effect was associated with reductions in mean arterial pressure (−49 ± 10 mm Hg, P < 0.05) and heart rate (−30 ± 6 beats/min, P < 0.05). The data indicate that NBQX i.v. decreases sympathetic nerve activity, blood pressure and heart rate in a dose-dependent manner and that the primary site of these effects is likely in the central nervous system.

Effects of inhibition of nitric oxide synthase on systemic arterial pressure and renal vascular resistance in cats

These studies were undertaken to examine the systemic and renal effects of the pharmacological inhibition of endothelium-derived nitric oxide ( EDNO) in cats. In six healthy cats, the intravenous infusion of nitro-L-arginine at a dose of 100 μg kg −1 bodyweight min −1 resulted in a marked increase (P<0·001) in mean arterial pressure from the control value of 116·7 ± 4·6 mmHg to 154·2 ± 6·8 mmHg and an increase (P<0·05) in renal vascular resistance from the control value of 3·69 ± 0·33 mmHg min ml −1 to 6·83 ± 1·15 mmHg min ml −1. The increase in renal vascular resistance was generalised, with comparable increments in preglomerular and postglomerular vascular resistance. Mean values for glomerular capillary pressure (61·1 ± 61·9 vs 1·9 ± 1·6 mmHg), calculated from the sum of arterial colloid osmotic pressure plus proximal tubule stop-flow pressure, did not change in response to the infusion of nitro-L-arginine. However, there was a marked reduction in renal blood flow (29·4 ± 3·1 to 16·9 ± 2·3 ml min −1, P<0·01) and glomerular filtration rate (5·22 ± 0·57 to 3·52 ± 0·45 ml min −1, P<0·01). These results provide evidence that EDNO plays an important role in the basal regulation of systemic arterial blood pressure and renal haemodynamics in cats.

Peptide leukotriene receptor antagonism in myocardial ischaemia and reperfusion.

The aim was to investigate the role of peptide leukotrienes in the pathophysiology of myocardial injury during reperfusion of previously ischaemic myocardium. Adult male cats (2.9-5.4 kg) were subjected to left anterior descending coronary artery occlusion for 3 h followed by 3 h of reperfusion. The peptide leukotriene receptor antagonist, LY-171883, was given intravenously only during the reperfusion period (3 mg.kg-1 bolus; 3 mg.kg-1 x h-1 infusion). Ischaemic injury was assessed by nitroblue tetrazolium staining and tissue creatine kinase activity; neutrophil infiltration was determined by myeloperoxidase activity of myocardial homogenates. There was no significant difference at any time point in the experimental protocol between mean arterial blood pressure or pressure-rate index in cats given LY-171883 (3 mg.kg-1) and cats given vehicle. The area at risk of infarction (AAR) was 24(SEM 2)% for vehicle treated cats and 22(2)% for the drug treated cats. The necrotic area was 48(5)% of the AAR for the vehicle group but only 29(5)% of the AAR for the group given LY-171883 (p < 0.02). Left ventricular maximum +dP/dt tended to be higher with drug treatment compared to vehicle at the end of the reperfusion period. Tissue from the area at risk was assayed for creatine kinase activity and neutrophil specific myeloperoxidase activity as an index of the accumulation of neutrophils in this region. Creatine kinase activity was significantly higher (p < 0.05) in the AAR for drug nu vehicle treated cats following reperfusion, confirming the histochemical analysis. Myeloperoxidase activity increased approximately 12-fold in the AAR of cats receiving vehicle. LY-171883 did not reduce the myeloperoxidase activity significantly in the area at risk. LY-171883 has a protective effect in ischaemia-reperfusion injury to the myocardium. These findings suggest a role for peptide leukotrienes both in the extension of ischaemic damage and in post-ischaemic ventricular dysfunction during reperfusion.

Evaluation of the Doppler ultrasonic method of measuring systolic arterial blood pressure in cats

Summary The accuracy of the Doppler technique for indirect systolic blood pressure measurement was assessed in 16 anesthetized cats. Eight cats were anesthetized with isoflurane and 8 were anesthetized with halothane. Anesthetic depth and mode of ventilation were varied to obtain a wide range of arterial blood pressure. A Doppler transducer was placed on the palmer surface of the left forelimb over the common digital branch of the radial artery to detect blood flow, and a blood pressure monitoring cuff with a width 37% the limb circumference was placed half way between the elbow and the carpus. To enable direct arterial pressure measurements, the left femoral artery was catheterized and the blood pressure waveforms recorded simultaneously. Systolic blood pressure measured by use of the Doppler ultrasonic technique was significantly lower than that obtained from the femoral artery catheter. Using linear regression, we determined a clinically useful calibration adjustment for Doppler indirect blood pressure measurement in cats: femoral systolic pressure = Doppler systolic pressure + 14 mm of Hg.

Pharmacological Effects of Gardenia erubescens in Mice, Rats and Cats

AbstractCrude extracts, mannitol and saponins obtained from Gardenia erubescens were tested for pharmacological effect in mice, rats and cats. When the saponins were injected intraperitoneally they did not produce anesthesia in mice but potentiated the duration of pentobarbital-induced sleep. They produced profound dose-dependent sedation but showed no anticonvulsant effects in mice. The saponins also produced a dose-dependent analgesia in adult rats and reduced the blood pressure of anesthetised cats. The water extract of the stem bark and mannitol isolated from the plant produced mild diuresis in rats when given orally. The LD50 of the methanolic extract and saponins were 550mg/kg and 119mg/ kg respectively.

Electrocardiographic evidence for cocaine cardiotoxicity in cat

Recent case studies suggest that cocaine overdose may produce life-threatening cardiac arrhythmias. We therefore investigated its effects on the electrocardiogram (leads II and V1) and arterial blood pressure in cats anesthetized with pentobarbital. Cocaine was administered by intravenous infusion over a 2-min interval at 1 mg/kg in 10 cats. In 5 out of 10 cats an additional infusion of 3 mg/kg cocaine was also administered after hemodynamic and electrocardiographic parameters had returned to control values (i.e., within 10 min). During and following infusion of 1 mg/kg cocaine, no significant change in heart rate or systolic or diastolic blood pressure were found, however the QRS duration increased by 38% (from 46 +/- 5 to 64 +/- 12 ms) (p less than 0.01). Evidence for bundle branch block and (or) premature ventricular beats was observed in 9 out of 10 cats after 1 mg/kg cocaine. Infusion of a further 3 mg/kg cocaine in five cats significantly lowered diastolic blood pressure (from 98 +/- 18 to 64 +/- 28 mmHg; 1 mmHg = 133.3 Pa) (p less than 0.01), and further prolonged QRS to 79 +/- 14 ms, a 75% increase from the mean control value (p less than 0.01). In addition, 1st and 2nd degree atrioventricular block, ventricular extrasystoles, and ectopic rhythms (AV junctional or idioventricular) were observed in four out of five cats given 3 mg/kg cocaine. Mean plasma concentrations of cocaine were 1.37 +/- 0.39 micrograms/mL (4.28 +/- 1.22 microM) (n = 5) at the end of a 1 mg/kg infusion and 2.93 +/- 0.43 micrograms/mL (9.16 +/- 1.34 microM) after a 3 mg/kg infusion (n = 3).(ABSTRACT TRUNCATED AT 250 WORDS)

Pharmacological activities of Grewia bicolor roots

Intraperitoneal administration of the ethanol extract of Grewia bicolor root (300 mg kg ) to rats in early pregnancy ( +1 – 4 days) did not affect the number of conception sites, but significantly increased resorption. In late pregnancy (+19–20 days), the extract (300 mg kg ) did not affect duration of the gestation period; however, 400 mg kg was lethal to all mother rats. The active compound, apparently a peptide, exerted a serotonin-like effect on rat uterus, rat fundus and rabbit jejunum. All these effects were abolished by methysergide. A transient serotonin-like rise in cat blood pressure was produced by the active fraction and this effect was also blocked by cyproheptadine.

Cardiovascular effects of 1-methyl-4-(1-naphthylvinyl) piperidine hydrochloride

1-Methyl-4-(1-naphthylvinyl)piperidine (B-120) produced a dose related decrease in blood pressure in cats. B-120 did not alter the cardiovascular response to acetylcholine or vagal stimulation. It did not affect the response of the nictitating membrane to both pre- and post-ganglionic stimulation. In isolated cortical synaptosomes, B-120 decreased calcium flux below basal levels. Thus, the blockade of calcium channels appeared to be related to the production of hypotension and may be the mechanism by which B-120 protected against organophosphate toxicity.

Effects of electrical stimulation on intracranial pressure and systemic arterial blood pressure in cats: Part II: Stimulation of cerebral cortex and hypothalamus

This experimental work was carried out to examine whether activation of autonomic cortical and hypothalamic areas by electrical stimulation is related to changes in the intracranial pressure (ICP) in cats anaesthetized lightly with sodium pentobarbital. Electrical stimulation was performed using a concentric electrode with a train of electrical pulses (pulse duration, 0.4 ms; frequency, 40 Hz; intensity, 50-400 microA). Stimulation of sites in the anterior cingulate gyrus produced a rise in ICP associated with a fall in systemic arterial blood pressure (BP) or with no change in BP. Stimulation of sites in the anterior hypothalamus produced a fall in BP with an increase in ICP. Stimulation of sites in the area extending from the anterior hypothalamus to the posterior hypothalamus produced rises in BP and ICP. These observations suggest that activation of autonomic cortical and hypothalamic areas is involved in changes in ICP.

Effects of electrical stimulation on intracranial pressure and systemic arterial blood pressure in cats. Part I: Stimulation of brain stem.

It has been suggested that brain stem activity is involved in the occurrence of pressure waves. Different sites in the brain stem were activated by electrical stimulation in cats anaesthetized with sodium pentobarbital, to produce an increase in intracranial pressure (ICP) similar to the pressure waves. Then the effect of artificial ventilation on the occurrence of the pressure wave-like response produced under spontaneous respiration was examined since Lundberg's A-waves appear even in artificial ventilation, and B-waves are effaced during artificial ventilation. This results in a brain stem map of ICP and systemic arterial blood pressure (BP) produced by electrical stimulation during spontaneous respiration. Stimulation of the rostral medullary reticular formation produced a rise in ICP and BP in association with a change in the rhythm of the spontaneous respiration; with artificial ventilation, stimulation produced a rise in BP but ICP kept almost at the same level. However, the rise in ICP that was produced by stimulation of the caudal medullary reticular formation during spontaneous respiration also occurred with a depressor response of BP during controlled ventilation. The pressure wave-like responses could be classified, therefore, into two types. One was the response seen during both spontaneous and controlled ventilation, which we designated the 'alpha' wave. The other was the response seen only during spontaneous ventilation, the 'beta' wave. These observations suggest that the origins of A- and B-waves may be related to those of 'alpha' and 'beta' waves, respectively.

Attenuation of postischemic cerebral hypoperfusion by the 21-aminosteroid U74006F.

The ability of the nonglucocorticoid 21-aminosteroid U74006F, a potent inhibitor of iron-dependent lipid peroxidation, to antagonize progressive brain hypoperfusion after a 5-minute episode of global brain ischemia was examined in alpha-chloralose-anesthetized cats. Immediately after a 5-minute episode of near-total tourniquet-induced brain ischemia, cortical blood flow returned to normal or above normal. Thereafter, cortical blood flow fell progressively to a level 71.7% below normal by 3 hours after ischemia. In contrast, in cats that received 1 mg/kg i.v. U74006F 15 minutes after the ischemic episode, cortical blood flow remained significantly greater than that seen in vehicle-treated cats. At 3 hours, cortical blood flow had declined by only 45.7% (p less than 0.04 compared with vehicle). In addition, U74006F treatment significantly improved postischemic maintenance of blood pressure and recovery of somatosensory evoked potentials and reduced postischemic arterial blood acidosis. U74006F had no effect on cortical blood flow, somatosensory evoked potentials, or blood pressure in nonischemic cats. Our results suggest that U74006F may be useful in the early treatment of global cerebral ischemia.

Central and baroreflex control of sympathetic nerve activity to the heart and kidney in a daily life of the cat.

We measured simultaneously and continuously the sympathetic nerve activity to the heart (CSNA) and kidney (RNA) together with heart rate (HR) and arterial blood pressure (AP) in conscious cats. The time course and magnitude of their responses to behavioral stimuli and norepinephrine iv administration were analyzed quantitatively. The increases in CSNA and RNA occurred almost simultaneously with the onset of standing, walking or eating behavior. The abrupt increases in CSNA and RNA were not preceded by a decrease in AP so it was unlikely to have been a reflex initiated by baroceptors. Rather, the increases in CSNA and RNA were followed by increases in HR and AP. The lag time ranged from 2 to 10 sec. Relative response magnitude of CSNA differed significantly from that of RNA. Thus, when AP increased spontaneously by behavioral stimuli, there was always preceding nonuniform increases in CSNA and RNA. On the other hand, when AP was elevated by norepinephrine iv administration, CSNA and RNA were inhibited proportionally to a rise in AP due to baroreflexes. At rest, the baroreflex effect on CSNA was greater than that on RNA. Cardiac-related discharges of CSNA and RNA, which were induced reflexly by baroceptor input, occurred dominantly at rest. However, with excitement or at the onset of body movements, they were diminished significantly. Our results suggested that AP adjustment associated with various behavior was made directly by a nonuniform central activation of the sympathetic nerve activity to the heart and blood vessels and partly by a central modulation of the baroceptor input.

Responses of intracranial pressure (ICP) produced by stimulating the pressor area in the brainstem at various levels of blood pressure and ICP in cats.

An increase in intracranial pressure (ICP) was produced by stimulating brainstem pressor sites in cats anesthetized with alpha-chloralose. The ICP responses were augmented by lowering prestimulus BP and reduced by elevating prestimulus BP. In contrast, stimulus-induced pressor response of BP showed no consistent correlation to prestimulus BP. When the mean amplitude of stimulus-induced ICP responses at the control prestimulus ICP (within 18 mmHg) was plotted against the mean of the prestimulus BP levels for each site examined, the sites were classified into 2 groups by the regression line; sites generating a marked ICP response above the line and those generating a small ICP response on and under the line. The former sites were located in the paramedian region of the reticular formation including nuclei parvocellularis and gigantocellularis. The latter sites scattered throughout the brainstem pressor area. The ICP response at the former sites was markedly increased at an elevated prestimulus ICP. The peak ICP response at 30-50 mmHg of prestimulus ICP was 70-100 mmHg, similar to plateau waves. The ratio of ICP response size to BP response size was negatively correlated to prestimulus BP and the regression line was 2-5 times steeper at an elevated prestimulus ICP (18-60 mmHg) than at the control ICP. On the other hand, the negative relation between the response ratio and the BP for the latter sites produced no such change at the increased prestimulus ICP. These findings suggest that the ICP response is produced primarily by neurogenic intracranial vasodilation, which works most effectively at moderately decreased cerebral perfusion pressure. This mechanism may be involved in a series of events that results in plateau waves.

Animal pharmacology of guanfacine

The pharmacologic data obtained from animal experiments with guanfacine, a novel, centrally acting antihypertensive agent, are reviewed. When given orally, guanfacine lowers systemic blood pressure in conscious DOCA-NaCl-hypertensive rats, Grollman rats and spontaneously hypertensive rats in a dose-dependent manner. It is also effective in renal hypertensive cats. Guanfacine reduces blood pressure in cats, rabbits and rats after injection into the lateral cerebral ventricle and in dogs after infusion into the vertebral artery at intravenously ineffective doses. Vagally mediated reflex bradycardia in dogs is enhanced. The preganglionic splanchnic (sympathetic) nerve activity is reduced in cats. In rats, guanfacine reduces the noradrenaline turnover in the brain stem. All these findings indicate a central site of action. Peripheral α-adrenoceptor stimulant properties of guanfacine have been demonstrated in various studies. In addition to postsynaptic stimulant effects, presynaptic guanfacine-induced inhibition of sympathetic heart nerve stimulation is antagonized by rauwolscine but not by prazosin, indicating a highly preferential α 2-agonistic presynpatic action of the drug. In receptor binding studies using rat cortex membranes and human platelets, guanfacine exhibited a high selectivity for α 2 adrenoceptors. Guanfacine has the advantage over other centrally acting antihypertensives of being less sedative and causing no rebound hypertension after discontinuation of treatment. The latter is mainly due to its pharmacokinetic properties.

Effects of 4-aminopyridine on cat blood pressure in relation to the sympathetic nervous system

The pressor effect of 4-aminopyridine (4-AP) was studied in anesthetized cats and in isolated cat aortic ring preparations. A significant increase in blood pressure (38.9 ± 11.4 mHg) was observed following intravenous administration of 4-AP (0.3 mg/kg). The elevated blood pressure lasted for 1.3 h and returned to the control level after 1.5 h. The pressor effect of 4-AP was not blocked by prior administration of phentolamine (2 mg/kg i.v.) or by pretreatment with reserpine (2 mg/kg i.m., once a day for two consecutive days). In vitro, a dose-dependent tonic contraction of aortic ring was noted after addition of 4-AP into the bathing fluid. The ED 50 of 4-AP was significantly greater than that of norepinephrine (NE) (8×10 −4 M vs. 10 −7 M). Phentolamine (10 −6 M) antagonized the contractile response to NE but not that to 4-AP, whereas verapamil (10 −5 M) attenuated the 4-AP induced contractile response. A diminished contractile effect was also obtained when aortic ring preparations were bathed in calcium-free solution. These data suggest that the sympathetic nervous system plays a minor role in the pressor offect of 4-AP and that the increased calcium influx may account, at least partially, for the vasoconstricting effect of 4-AP.