Changes In Systemic Arterial Pressure Research Articles

Hypotension following cimetidine administration during cardiopulmonary bypass.

Intravenous administration of cimetidine may occasionally cause profound hypotension. Cimetidine 200 mg was administered as a bolus injection to patients whilst on cardiopulmonary bypass and subsequent changes in systemic arterial pressure were recorded. A statistically significant fall in arterial pressure was observed (p less than 0.001), which was attributable to a fall in systemic vascular resistance.

Pulmonary petechiae: ventilatory-circulatory interactions.

Summary: Pulmonary petechial hemorrhages are typically observed in sudden infant death syndrome (SIDS), but their cause has not been determined. Some data suggest that SIDS infants die with an obstructed airway. Inspiratory efforts against the closed airway can decrease the efficiency of the cardiac pump by increasing the afterload on the left ventricle and/or by decreasing left ventricular compliance. If these effects are augmented by hypoxia-induced decreases in cardiac contractility as occlusion is maintained, the resultant failure of the left ventricle could produce a large increase in end-diastolic pressure. Increases in left ventricular end-diastolic pressure will then increase pressures in the pulmonary circuit, where rupture of small blood vessels gives rise to petechial hemorrhages. To evaluate this postulated mechanism of petechiae formation, lightly anesthetized adult rabbits were sacrificed using three 1-min end-expiratory airway occlusions plus a fourth occlusion maintained until death; systemic arterial, intratracheal, and pulmonary wedge pressures (the latter approximating left atrial pressure) were measured during inspiratory efforts and expiratory intervals. Those animals showing minimal evidence of left heart failure, as evidenced by a relatively small difference between wedge and intratracheal pressures during obstructed breathing, showed few pulmonary petechiae. When the above pressure difference was large (greater than 25 mmHg during inspiratory efforts and greater than 10 mmHg during expiratory intervals) numerous pulmonary petechiae (usually n > 40) could be observed. Progressive increases in pulmonary wedge pressure and bradycardia during occlusion suggested that direct and/or reflex hypoxic depression of the myocardium contributed to the observed effects. The occlusions produced little change in systemic arterial pressure. These results are consistent with the possibility that mechanical interactions between the heart and lung pumps, along with hypoxia-induced decreases in cardiac contractility accompanying airway obstruction, account for intrathoracic petechiae in SIDS.

EFFECTS OF EDTA AND VERAPAMIL ON RENIN RELEASE IN DOGS

EDTA or verapamil was infused into the renal artery of the anesthetized dog, and the effects on renin release and renal function were examined in an attempt to elucidate the role and action site of calcium ion in the renin secretory system. Both EOT/(25 mg/min) and verapamil (50 μ/mm) increased RSR and RBF with a concomitan increase of urine flow, although there was no change in systemic arterial pressure. An infusion of verapamil in combination with ouabain produced a significant increase in RBF which was similar to that seen with verapamil alone. Urine flow and urinary excretin of electrolytes were also increased, but these changes did not differ from those seen with ouabain infusion alone. Ouabain alone did not affect RSR, but its infusion combined with verapamil resulted in a significant increase in RSR. Therefore, the effects of EDTA and verapamil on renin release may reflect the action of both drugs on the vascular component of the juxtaglomerular apparatus. If a change in calcium movement similar to the one in vascular smooth muscle occurs in the juxtaglomerular cells, the altered concentration of calcium may be considered to induce, in part, the stimulation of renin release by EDTA or verapamil.

Effects of EDTA and verapamil on renin release in dogs.

EDTA or verapamil was infused into the renal artery of the anesthetized dog, and the effects on renin release and renal function were examined in an attempt to elucidate the role and action site of calcium ion in the renin secretory system. Both EDTA (25 mg/min) and verapamil (50 micrograms/min) increased RSR and RBF with a concomitant increase of urine flow, although there was no change in systemic arterial pressure. An infusion of verapamil in combination with ouabain produced a significant increase in RBF which was similar to that seen with verapamil alone. Urine flow and urinary excretion of electrolytes were also increased, but these changes did not differ from those seen with ouabain infusion alone. Ouabain alone did not affect RSR, but its infusion combined with verapamil resulted in a significant increase in RSR. Therefore, the effects of EDTA and verapamil on renin release may reflect the action of both drugs on the vascular component of the juxtaglomerular apparatus. If a change in calcium movement similar to the one in vascular smooth muscle occurs in the juxtaglomerular cells, the altered concentration of calcium may be considered to induce, in part, the stimulation of renin release by EDTA or verapamil.

Baroreceptor control of systemic haemodynamic at incremental halothane levels in the dog.

The open-loop carotid sinus reflex control of systemic haemodynamics was studied in an acute dog preparation with isolated perfused carotid sinuses at three end-tidal halothane levels of 0.66 +/- 0.02% (HI); 0.88 +/- 0.02% (H2); and 1.17 +/- 0.02% (H3), in order to investigate the dose dependency of the carotid sinus reflex operating characteristics for halothane. Corresponding to the above halothane levels were reflex operating point pressures (set point pressures) of 104.9 +/- 2.9, 103.3 +/- 4.1 and 76.0 +/- 3.8 mmHg, respectively. Carotid sinus reflex gain decreased significantly with progressively increasing halothane levels (1.4. +/- 0.18; 0.84 +/- 0.12; 0.48 +/- 0.09), as did the range of reflex changes in systemic arterial pressure for equal overall changes in carotid sinus pressure (87.1 +/- 7.9; 64.1 +/- 7.4; 33.6 +/- 5.1 mmHg; P less than 0.01). For halothane levels below approximately 0.9%, this depression was not dependent upon changes in mean systemic arterial pressure. The relationship between reflex gain and halothane concentration could be described by a first-order exponential which suggested virtual ablation of the carotid sinus reflex control of mean arterial pressure at an end-tidal halothane concentration exceeding about 1.6%.

Dopamine-induced ventilatory depression in the rat, mediated by carotid nerve afferents

In pentobarbitone-anesthetized rats, i.v. injections of dopamine (DA) at 10 −8–10 −5 g/kg led to transient ventilatory depression, usually not associated with changes in systemic arterial pressure. DA-induced ventilatory depression consisted of decreases in tidal volume and respiratory frequency in 12 rats, and in bradypnea without changes in tidal volume in 5 rats. After bilateral section of the carotid nerves, ventilatory responses to DA were abolished or greatly diminished. It is concluded that DA inhibits carotid body chemosensory discharges in the rat. The possibility that chemosensory activity directly affects respiratory frequency is discussed.

Effects of vasoactive polypeptides on the uterine vasculature

Estrogen-induced increases in uterine blood flow appear to require de novo protein or polypeptide synthesis. In the present experiments a chronically catheterized nonpregnant sheep preparation was used to determine the uterine vascular effects of vasoactive intestinal polypeptide (VIP), neurotensin, and substance P. These effects were compared to those of bradykinin and the most potent vasodilator prostaglandin, prostacyclin. An intra-arterial catheter was placed in a branch of the main uterine artery to allow administration of the compounds directly into the uterine vasculature. Uterine blood flow was continuously monitored via an electromagnetic flow transducer on the main uterine arteries. VIP, bradykinin, and prostacyclin were equally potent as vasodilators of the uterine vasculature, while neurotensin and substance P were totally devoid of vasoactivity. Unlike estradiol, bradykinin and VIP produced significant changes in systemic arterial pressure and heart rate, suggesting that these compounds may not be responsible for mediating the uterine vascular response observed after estrogen. However, VIP was a potent uterine vasodilator and was able to totally ablate uterine contractile activity, suggesting that this endogenously occurring polypeptide may be important in regulating uterine hemodynamics and contractile activity.

Effect of carotid sinus baroreceptor reflex on responses to phenylephrine and nitroprusside in anesthetized cats.

This study attempted to measure the extent to which the carotid sinus baroreceptor reflex attenuates the acute changes in arterial pressure during infusions of phenylephrine and nitroprusside, and to express these effects as equations which could be used in a simple computer model of the circulation. Arterial pressure and cardiac output were measured in vagotomized cats anesthetized with chloralose or pentobarbital. The carotid arteries were perfused to allow sinus pressure either to follow changes in systemic arterial pressure or to be held at the preinfusion control level, thereby eliminating the effects of the reflex. There was a linear relationship between arterial pressure in the presence and absence of the reflex, and the changes in arterial pressure were attenuated to one-third by the reflex while cardiac output was not significantly changed. These effects are described by simple equations involving peripheral resistance, heart rate, and venous compliance. The activity of the reflex was not significantly different in cats anesthetized with pentobarbital or chloralose, and our data do not support the view that these anesthetic agents depress the vasomotor component of the carotid sinus reflex.

Adaptive function of the sympathetic innervation of the cerebral vessels during rapid changes in systemic arterial pressure

Acute hemorrhagic hypotension followed by hypertension induced by rapid blood reinfusion was simulated in acute experiments on anesthesized rats with unilateral denervation of cerebral vessels (cervical sympathectomy). The quantity of hypertension-induced small hemorrhages in the denervated hemisphere was twice as large as in the intact one. No hemorrhages were obtained in both hemispheres in experiments without preliminary hypotension. Thus the reflector activation of the sympathetic neuronal system increases during hypotension the resistance of the brain vascular bed to the following hypertension.

Localization of Baroreceptors and Gain of the Baroreceptor-Heart Rate Reflex in the Lizard Trachydosaurus Rugosus

ABSTRACT The location of arterial baroreceptors was studied in unanaesthetized Trachydosaurus rugosus by inflation of strategically placed perivascular cuffs. There was no evidence for baroreceptors at the site homologous with the carotid sinus of mammals or at the site homologous with the aortic arch baroreceptors of mammals and birds. The baroreceptors of T. rugosus probably lie in the truncus arteriosus. When the sensitivity or gain of the cardiac response to changes in systemic arterial pressure was expressed as change in heart period per unit change in mean aortic blood pressure, the value for 6 animals was 1370 ms/ kPa (100 ms/mmHg). This is very much greater than reported values for rabbits. If, instead, gain was calculated as the percentage increase in heart rate per unit fall in mean aortic pressure, a mean gain of 98%/kPa (7·2%/ mmHg) was obtained. It is suggested that the latter method provides the better comparative value. Adrenergic neurone blockade with bretylium and muscarinic blockade with atropine or hyoscine indicated that sympathetic fibres probably play the dominant role in generating the gain of the cardiac baroreflex.

Ontogeny of single nephron filtration distribution in canine puppies.

The ontogeny of single nephron filtration distribution was studied in 29 canine puppies two hr to 42 days old using the [14C] ferrocyanide method as modified by Coehlo (9). The ratio of 14C counts in outer cortical nephrons (OC) to counts in juxtamedullary nephrons (JM) were plotted against age for each puppy. This ratio (OC:JM) provided an index for comparing the single nephron glomerular filtration between regions. A four-fold increase in OC:JM occurred from two days to four wk. The youngest puppy, two hr old, showed a ratio of zero because no counts were detected in OC at that age. The most rapid increase occurred in the first 8 days of life. By the fourth wk, the mean OC:JM ratio was 0.72 +/- 0.06, approaching values reported by other laboratories for adult dogs. In contrast to age-related changes in OC:JM ratio, the ratio of middle cortical to JM counts showed no age-related increase. Cortical blood flow distribution was determined by the microsphere method. The ratio of blood flow to outer and inner cortex increased from 0.43 at one-half a day to a mean of 2.93 after one wk. The ratio of OC:JM single nephron filtration of OC/inner cortical nephron renal blood flow was 0.36 from 3 days to 26 days (n = 12) and did not change significantly with age, indicating that changes in zonal filtraion matched the alterations in cortical blood flow distribution.

Effect of carotid pressoreceptor stimulation on integrated systemic venous bed.

In 9 mongrel dogs, venous return was completely drained from the caval veins to an oxygenator and returned to the femoral arteries with a roller pump. Perfusion rate of systemic circulation and blood pressures in both caval veins were kept constant. Changes in the oxygenator weight were recorded and reflected reciprocal changes in integrated systemic venous blood volume. The vagal nerves were dissected. The carotid sinuses were separately perfused with blood by means of a pump. In 25 experiments, increases in carotid sinus pressure of 15 to 74 mm Hg resulted in decreases in systemic arterial pressure of 10 to 57 mm Hg and increases in systemic venous blood volume of 1.1 to 4.7 ml/kg. On an average, systemic venous blood volume was changed by 1.25 +/- 0.08 ml/kg when the change in systemic arterial pressure was 10 mm Hg. It is concluded that the carotid sinus pressoreceptor reflex considerably alters the systemic venous capacity which in tern alters venous return and cardiac output. These changes in cardiac output are expected to be small, but sufficient to alter the arterial pressure considerably. Thus, they might contribute nearly as much as the reflex effect on total peripheral resistance to the reflex control of arterial pressure.

Effects of acute changes in systemic arterial pressure on left ventricular diastolic stiffness and mass.

Effects of acute changes in systemic arterial pressure on left ventricular diastolic stiffness and mass.

Haemodynamic variables during repeated exercise in chronic lung disease.

1. Pulmonary and systemic haemodynamics during repeated exercise were studied in 28 patients with chronic lung disease of various etiology, 16 of whom suffered from chronic bronchitis. They performed a moderate exercise repeated after a 20 min rest period. Ventilatory variables, blood gas tensions, cardiac output and vascular pressures (right ventricular end-diastolic, pulmonary arterial, wedge and systemic arterial) were measured at rest, during exercise and again at rest and during the same exercise. 2. Ventilation and blood gas tensions were similar during the two rest and exercise periods; there was, however, a slightly significant difference in oxygen consumption and hydrogen ion concentration between the first and the second exercise period. Pulmonary arterial and wedge pressures were lower during the second rest and exercise, right ventricular filling pressure was lower at rest, and systemic arterial pressure during the second exercise. Cardiac output and pulmonary vascular resistance were unchanged. 3. Changes in systemic arterial pressure were significantly different in a group of patients with arterial oxygen desaturation or perfusion defects, compared with those patients without such impairment.

Mechanism underlying systemic arterial pressure changes in cats in response to alteration in sodium ion concentration of cerebrospinal fluid: S.R. Maitra. Department of Physiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India

Mechanism underlying systemic arterial pressure changes in cats in response to alteration in sodium ion concentration of cerebrospinal fluid: S.R. Maitra. Department of Physiology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India

Gastric inhibitory polypeptide increases mesenteric blood flow.

SummaryGastric inhibitory polypeptide (GIP) induces dose-dependent increases in superior mesenteric blood flow in the anesthetized cat. There was no concommitant change in systemic arterial pressure or in femoral blood flow indicating a specific decrease in mesenteric vascular resistance.

The effects of changes in arterial pressure on sinus nerve efferent activity.

The carotid body is a peripheral arterial chemoreceptor which senses arterial blood pH, PC0 2 and P0 2. Neuronal activity from the carotid body is conveyed to the central nervous system by the carotid sinus nerve, a branch of the ninth cranial nerve. In 1968 Biscoe and Sampson1 recorded neuronal activity from the central end of the sinus nerve. This activity was of two types. The first type displayed a respiratory rhythm in firing rate and was shown to arise from the sympathetic nervous system via the superior cervical ganglion. The second type appeared to originate directly from the central nervous system and displayed a random firing pattern. This second type of activity is termed sinus nerve efferent activity, and has been shown by Sampson and Biscoe2 and by Neil and O’Regan3, 4 to be capable of inhibiting carotid chemoreceptor afferent activity. We have investigated the response of sinus nerve efferent activity to changes in systemic arterial pressure induced passively by bleeding and by reinfusion of the animal’s own blood. Some of these results have been presented to the Physiological Society5.

Effects of dopamine analogues and antagonists on carotid body chemosensors in situ.

1. The effects of dopamine, its analogues and antagonists on the chemosensory discharges originating from carotid bodies in situ were studied in anaesthetized cats. 2. Intracarotid (I.C.) injections of 100 ng or more of dopamine produced transient depression of the frequency of carotid nerve chemosensory discharges. Short term (1-5 sec) complete inhibition was usually elicited by 2 microgram dopamine. 3. I.V. injections of dopamine also produced inhibition of chemosensory discharges, an effect observed with doses which were still too low to produce changes in systemic arterial pressure. Half-maximal inhibition (ID50) of chemoreceptors was elicited with a mean dose of 84 ng.kg-1. 4. I.C. and I.V. injections of apomorphine and amantadine also produced transient inhibition of chemosensory activity. Higher doses of these analogues of dopamine were needed to produce this effect, and the resulting inhibition usually did not silence the nerve discharges. Apomorphine inhibition was slightly more prolonged than that with dopamine. 5. Large doses of amphetamine and tyramine, inducers of dopamine release, did not produce inhibition of chemosensory discharges. 6. The effects of two classes of dopamine antagonists were tested. Dose-response curves for dopamine and apomorphine inhibition were displaced to the right by administration of phenothiazines (chlorpromazine and perphenazine) and butyrophenones (haloperidol and spiroperidol). In animals treated with perphenazine or spiroperidol, dopamine became a stimulator of chemoreceptor activity. 7. It is suggested that dopamine present in carotid body may operate as a modulator of chemosensory activity.

Comparison of microvascular pressures and diameters in the innervated and denervated rat intestine

Direct pressure and diameter measurements were recorded in the innervated and denervated microcirculation of rat intestinal muscle at control (100–110 mm Hg) and reduced systemic arterial pressures. The measurements were made with a servo-null pressure transducer and video micrometer system. The goals of the study were (1) to determine if significant differences exist between the pressure distributions in innervated and denervated intestinal muscle microvessels at normal and reduced systemic pressures; (2) to see if neural and local vascular mechanisms influence capillary pressures and microvascular pressure distributions in intestinal muscle; and (3) to ascertain the relative contribution of individual microvascular segments to the pressure distribution within the intestinal microcirculation. The results indicate that there is a simple, linear relationship between microvascular pressures and systemic pressure, with no significant difference ( P > 0.05) between the results from innervated and denervated tissues, except for second-order venules. Denervation did not alter the pressure distribution within the microcirculation. However, denervation did cause a significant dilation ( P < 0.05) of the small arterioles and a very large increase in the diameter of venous microvessels. Thus, the major effect of denervation was to cause a decrease in the postcapillary to precapillary resistance ratio and an increase in flow through the intestinal muscle without any significant or measurable change in the microvascular pressure distribution. Furthermore, capillary pressures in both innervated and denervated tissues were not significantly different ( P > 0.05) at normal or reduced systemic pressures, but changed in direct linear proportion to changes in systemic arterial pressure. This result is in direct opposition to the idea of an “autoregulatory” mechanism for local control of capillary hydrostatic pressure, but is consistent with the concepts of local blood flow regulation.

Isoproterenol in offsetting adverse effects of vasopressin in cirrhotic patients

Vasopressin administered as a peripheral infusion (40 U/hr) significantly reduced portal vein pressure in ten awake patients with cirrhosis and portal hypertension. A vasopressin-induced reduction in cardiac output occurred in five of the ten patients (50 per cent). Vasopressin-induced changes in systemic arterial pressure, heart rate, and portal venous pressure were independent of alterations in cardiac output. When the five patients with vasopressin-induced reductions in cardiac output were given a combination of vasopressin and isoproterenol, cardiac output was maintained and the reduction in portal vein pressure was equal to that observed with unopposed vasopressin therapy. Thus, the addition of isoproterenol prevented a vasopressin-induced reduction in cardiac output while permitting vasopressin to reduce portal vein pressure.