Pressure In Cats Research Articles

Positive end-expiratory pressure increases intraocular pressure in cats

The purpose of the present study was to examine the effect of various levels of positive end-expiratory pressure on intraocular pressure in cats. Fourteen healthy adult cats (2.6 to 3.7 kg) without evidence of ocular disease were anesthetized with pentobarbital, paralyzed, and placed on mechanical ventilation. Direct continuous measurements of heart rate (HR), mean arterial pressure (MAP), CVP, CSF pressure, and intraocular pressure were recorded at zero end-expiratory pressure, and at 5, 10, and 15 cm H2O positive end-expiratory pressure, applied in random order. There were no significant changes in pHa, Paco2, HR, MAP, hematocrit, and temperature. Intraocular pressure increased significantly from 17 (during zero end-expiratory pressure) to 20 mm Hg at 10 cm H2O positive end-expiratory pressure; at 15 cm H2O positive end-expiratory pressure, intraocular pressure increased significantly to 21 mm Hg. CVP and CSF pressure increased significantly in parallel with intraocular pressure at 5, 10, and 15 cm H2O positive end-expiratory pressure. We speculate that similar responses occur in man, and may be undesirable in patients with already increased intraocular pressure, when higher levels of positive end-expiratory pressure are used.

The Effect of Isoflurane for Intracranial Pressure in Cats

The Effect of Isoflurane for Intracranial Pressure in Cats

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)

Gradual reduction of coronary perfusion pressure in cats: Changes in transmural distribution of blood flow

We evaluated a model for regional myocardial hypoperfusion in cats with an extracorporeal shunt line to the left main coronary artery, and investigated the effects of reduced coronary perfusion pressure on the transmural distribution of left ventricular blood flow measured with radioactive microspheres. Shunt establishment did not alter cardiac function, myocardial tissue blood flow, or its transmural distribution. An artificial shunt stenosis, which clearly reduced coronary perfusion pressure without changing cardiac function, caused reduced endocardial blood flow, slight flow reduction in mid-myocardium, and no flow change in the epicardium. When a severe stenosis was applied, causing increased end-diastolic pressure and reduced shunt flow, endocardial and mid-myocardial flow further decreased whereas epicardial blood flow remained essentially unchanged. These results demonstrate a transmural profile of the coronary autoregulation capacity.

The Effect of Succinylcholine on the Intracranial Pressure in Cats

The Effect of Succinylcholine on the Intracranial Pressure in Cats

Effect of Portal Hypertension and Duct Ligature on Pancreatic Fluid Pressures in Cats

In two groups of cats recordings were performed, during laparotomy, of pancreatic tissue fluid pressure measured by a needle technique, interstitial fluid pressure measured by micropipette technique, pancreatic intraductal pressure, and portal vein pressure. In one group of cats the pressures were measured before and after acutely induced portal hypertension; in the other group of cats the pressures were measured after an overnight ligature of the pancreatic main duct. At rest the needle pressure was equal to duct pressure but significantly lower than interstitial fluid pressure and portal pressure. Acute portal hypertension caused no significant changes in micropipette, needle, or duct pressures. Pancreatic duct ligature increased duct pressure, interstitial fluid pressure, and needle pressure. We conclude that the fluid pressure in the pancreas is probably influenced by the production/drainage relation of the pancreatic juice rather than by haemodynamic conditions.

Intraretinal and preretinal PO2 response to acutely raised intraocular pressure in cats.

The effect of acutely raised intraocular pressure (IOP) on retinal oxygenation has been determined using oxygen-sensitive microelectrodes preretinally and intraretinally. Anesthetized cats were ventilated alternately with one of two oxygen concentrations, 21 or 100%, while the IOP was manipulated via a hydrostatic pressure head connected to the anterior chamber. Preretinal and inner retinal oxygen tension remained stable over a broad range of IOP for air breathing. In contrast, the outer retina was severely affected, with the PO2 reducing as IOP was raised, resulting in some areas becoming anoxic. Outer retinal oxygen consumption was reduced for perfusion pressures less than 50 mmHg. It is postulated that under air-breathing conditions the preretinal and inner retinal oxygen tension was stabilized by the autoregulatory capacity of the retinal circulation. The inability of the choroidal circulation to autoregulate was reflected in the reduction of outer retinal oxygen tension with increasing IOP. With 100% oxygen breathing, increases in IOP caused a significant reduction in PO2 throughout the entire retina and preretinal vitreous. It is proposed that the effect of the autoregulatory capacity of the retinal circulation on retinal oxygenation is reduced in hyperoxia.

Intraocular pressure in cats is lowered by drops of hornet venom

1. Nine cats were given an intravenous injection of the Oriental hornet ( Vespa orientalis, Vespinae; Hymenoptera) venom sac extract (VSE) and seven cats had the same VSE administered as eye drops. 2. When injected intravenously, the hornet VSE decreased the intraocular pressure in both eyes sharply during the first 20 min and with a slower rate later on until the end of the 3 hr experiment. The intraocular pressure dropped to zero in some cases. 3. VSE eye drops decreased the intraocular pressure only in the treated eye, while in the second eye (left as a control) the intraocular pressure remained the same throughout the experiment. 4. The decrease in the intraocular pressure was sharp during the first 20 min and slowed down afterwards until the end of the experiment. 5. The intraocular pressure did not reduce to zero. 6. This study shows that the active components of the hornet venom which caused a decrease in the intraocular pressure can cross the cornea and exert a hypotensive effect in the eye.

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.

The Effects of Vecuronium on Hemodynamics and Intracranial Pressure in Cats

The Effects of Vecuronium on Hemodynamics and Intracranial Pressure in Cats

Effect of hepatic nerves, norepinephrine, angiotensin, and elevated central venous pressure on postsinusoidal resistance sites and intrahepatic pressures in cats

Portal venous pressure was controlled by resistance localized to specific sites in hepatic lobar veins in cats. All of the pressure drop from the portal vein to the vena cava occurred across postsinusoidal vessels; portal pressure, lobar venous pressure, and, therefore, sinusoidal pressure were not significantly different. Norepinephrine and angiotensin infusions (intraportal) caused elevation in portal pressure due to constriction of hepatic venous resistance sites as well as some constriction of presinusoidal (portal or sinusoidal) resistance sites. At low doses of norepinephrine presinusoidal constriction dominated whereas at higher doses the postsinusoidal constriction increased proportionately more. Hepatic nerve stimulation produced a similar response measured at an early time (1 min), but by 3 min the presinusoidal constriction showed complete escape so that elevated portal pressure was entirely due to hepatic venous constriction. The same site that provided basal vascular resistance also provided the increased hepatic venous resistance with nerve stimulation and infusion of angiotensin and norepinephrine. Rapid elevation of central venous pressure (CVP) caused elevated sinusoidal pressure. At high CVP (16 mm Hg), 75% of a rise in CVP was transmitted whereas at normal CVP (<4.5 mm Hg) less than 20% transmission occurred. The presence of a high resistance in the hepatic veins protected intrahepatic pressure from the effects of normal fluctuation of CVP.

The effect of intraocular silicone oil on anterior chamber oxygen pressure in cats.

Intraocular silicone oil has been observed to lessen the incidence of neovascular glaucoma in patients with a high risk of anterior segment neovascularization. In order to test the hypothesis that the presence of silicone oil in the vitreous cavity acts as a diffusion/convection barrier to oxygen and prevents the decrease in anterior chamber oxygen tension that occurs after lensectomy and vitrectomy, we measured anterior chamber oxygen pressure in six cats that had undergone lensectomy-vitrectomy in one eye and lensectomy-vitrectomy with silicone oil placement in the other eye ten to 21 days previously. The anterior chamber oxygen tension was 17.8 +/- 6.9 mm Hg (mean +/- SD) in the eyes that had undergone lensectomy-vitrectomy and 34.8 +/- 3.5 mm Hg in the silicone oil-treated eyes (P less than .001). Silicone oil does appear to act as a diffusion/convection barrier to oxygen and may alter the stimulus for anterior segment neovascularization.

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.

ネコ外リンパ圧の実験的研究

The aims of this study are to demonstrate the presence of a pressure equalizing system between the inner ear fluids (perilymph and endolymph) and the cerebrospinal fluid (CSF) and the roles of the cochlear aqueduct (CA) and endolymphatic duct (ED) in that system.The following conclusions are drawn from the measurement of perilymphatic and CSF pressures in cats.1. After obstruction of the CA, perilymphatic and CSF pressures are identical and interdependent, indicating that they are transmitted by a route other than the CA.2. After obstruction of both the CA and ED, the perilymphatic pressure becomes independent of the CSF pressure.3. The respiratory variations in the CSF pressure are partially transmitted to the perilymph after obstruction of the CA and are further reduced when the ED is also occluded.4. Artificially increased CSF pressure is transmitted to the perilymph without attenuation in normal cats. However, this transmission is markedly reduced when the CA is obstructed. This indicates that there is a limit to the transmission of variations of CSF pressure through the ED. This conclusion raises the question whether equalization of the pressures of the perilymph and endolymph in the presence of abnormal variations in the CSF pressure is possible.5. After the administration of 30% urea (1g/kg) to cats with patent CAs, the perilymphatic and CSF pressures behaved identically. This suggests that a direct osmotic effect of urea on the perilymphatic pressure cannot be determined if the CA is patent.6. After the administration of urea to cats with obstructed CAs, the perilymphatic and CSF pressures behaved differently. The fact that the perilymphatic perssure is lower than the CSF pressure, particularly during the first 45 minutes, shows the direct osmotic effect of urea on the perilymphatic pressure.

Does B-HT 920 lower intraocular pressure in cats by interacting with alpha 2- and/or DA2 adrenoceptors?

Topical administration of B-HT 920 (50 micrograms) to the eyes of normal unanesthetized cats produced decreases in intraocular pressure and pupil diameter. The ocular hypotensive effect of B-HT 920 was eliminated by sympathectomy and pretreatment with sulpiride (2 mg/kg, s.c.). B-HT 920 also produced dose-related inhibition of contractions of the cat nictitans elicited by stimulating the pre- and postganglionic sympathetic trunks. B-HT 920-induced suppression of the contracting nictitans was antagonized more effectively by relatively selective DA2 antagonists, sulpiride and domperidone, than by rauwolscine, a relatively selective alpha 2-adrenoceptor antagonist. These data suggest that B-HT 920 produces ocular hypotension in the cat by interacting predominantly with DA2 receptor on peripheral sympathetic nerves.

Pial arterial pressure in cats following middle cerebral artery occlusion. II. Relationship to regional disturbance of energy metabolism.

Focal cerebral ischemia was produced in 16 cats by occluding the left middle cerebral artery (MCA) for 120 min. Cortical blood flow and pial artery pressure were determined prior to vascular occlusion and after 15, 60 and 120 min. At the end of the experiments (after 120 min MCA occlusion) heads were frozen in situ with liquid nitrogen. Cooled brains were cut into 0.5 cm thick slices. From these slices twenty-micron sections passing through the territory of the MCA were prepared in a cryostat and used in the pictorial presentation of glucose and ATP. NADH-fluorescence was recorded from the tissue slice, immersed in liquid nitrogen. In addition, tissue samples were taken from regions of interest and used for quantitative determination of biochemical substrates. In all but two animals permanent MCA occlusion led to disturbances in the energy-producing metabolism, as indicated by reduction in glucose and ATP, and increase in lactate. The regions exhibiting bright NADH-fluorescence were much smaller than those in which ATP was absent. In 6 animals NADH-fluorescence was not increased but even decreased in areas with disturbed energy-producing metabolism. A close correlation was obtained after comparing cortical blood flow measured 15 min after MCA occlusion with the area of ATP-depletion at the end of the experiments. However, the size of ATP-depletion did not correlate with flow measured 60 or 120 min after MCA occlusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Pathophysiology of periventricular tissue changes with raised CSF pressure in cats.

Intraventricular pressure (IVP) is increased in the early stages of acute hydrocephalus. Pressure falls, however, when compensatory routes for cerebrospinal fluid (CSF) absorption develop. In order to better understand the pathophysiology of acute hydrocephalus, the authors performed ventriculocisternal perfusions on adult cats with outflow pressures maintained at either -5, 20, or 40 cm H2O. Cerebral blood flow (CBF) was determined by the iodoantipyrine method. Penetration of an extracellular marker, horseradish peroxidase (HRP), was visualized histologically. Capillary transfer of radiolabeled molecules from CSF to blood was measured by steady-state tissue clearance. Increased IVP had several effects: 1) significant reduction in mean CBF in the periventricular white matter; 2) penetration of the HRP into deep white matter; and 3) prolongation of steady-state tissue clearance half-time for (14C)-ethylene glycol in the caudate nucleus. Reduced blood flow to periventricular white matter and impaired molecular clearance in the caudate nucleus may contribute to the clinical symptoms in acute hydrocephalus.

Pial arterial pressure in cats following middle cerebral artery occlusion. 1. Relationship to blood flow, regulation of blood flow and electrophysiological function.

In lightly anesthetized cats, the left middle cerebral artery was occluded using a transorbital approach. Pial arterial pressure was measured with a feedback-controlled micropressure recording system in the territory of the occluded artery, and compared with changes of cortical blood flow, cortical steady potential and cortical EEG activity. After middle cerebral artery occlusion pial artery pressure fell from 56.2 +/- 1.6 to 7.8 +/- 0.4 mm Hg; during the following two hours it again slowly rose to about 15 mm Hg. Cortical heat conductance, as a measure of blood flow, decreased from 15.1 +/- 0.2 to 11.9 +/- 0.2 X 10(-4) cal X cm-1 X sec-1 X degrees C-1, and remained at this level throughout the observation period. Cortical steady potential shifted by 9.1 +/- 0.7 mV towards negativity, and EEG amplitude was reduced by about 50%. Pial arterial pressure correlated with blood flow, cortical steady potential and EEG amplitude, but not with EEG frequency. Autoregulation and CO2 reactivity of blood flow were disturbed after middle cerebral artery occlusion. Calculation of extra- and intracortical vascular resistances revealed that this disturbance was entirely due to intracortical vasoparalysis whereas the collateral vessels supplying the ischemic territory continued to react to both pressure and CO2 changes. Maintained vascular reactivity of collateral vessels, therefore, is a decisive factor for the efficiency of therapeutic blood flow improvement after acute middle cerebral artery occlusion.