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Biomedical subjects

K G Cornish

Publications and source records attributed to K G Cornish.

At least 37 records · Page 2Linked to original sources
PubMed1988

Pentobarbital potentiates natriuretic response to acute volume expansion in monkeys.

We determined the influence of pentobarbital sodium on the renal responses of the monkey to acute intravascular volume expansion. Before volume expansion, the anesthetized animals had a significantly lower blood pressure and creatinine clearance and a significantly higher urine flow and sodium excretion than the conscious animals. After volume expansion with an isotonic, isoncotic, dextran solution, sodium excretion and urine flow increased significantly in both groups of animals. However, both responses were significantly greater in the anesthetized animals. The greater natriuresis in the anesthetized animals was associated with a greater fractional sodium excretion than in the conscious animals. The potentiated response of the anesthetized animal may be the result of a direct renal tubular effect of pentobarbital and/or the result of the anesthetic removing an inhibitory influence on sodium excretion.

Animals↗
PubMed1988

Hypotension produced by vagal block in primates.

In many species, the vagus has been reported to contain afferents that inhibit sympathetic tone. Vagal block (VB) increases blood pressure in both the intact and sinoaortic-denervated (SAD) dog. In the present study, VB was produced in intact and SAD monkeys by infiltrating the vagi with a local anesthetic. This was done in conjunction with blood volume expansion or head-out water immersion. The cardiovascular parameters monitored were heart rate (HR), blood pressure (BP), and left atrial pressure (LAP). VB decreased BP (-13 +/- 2.8 mmHg) in the control group and the SAD animals (-47 +/- 6.7 mmHg) without changing HR. Volume expansion decreased BP in the SAD animals (-6 +/- 3.4) but not in the intact monkeys (1.8 +/- 2.27), whereas HR did not change. Volume expansion after VB increased BP in both the SAD and the intact animals while producing a decrease in HR. Volume expansion caused LAP to increase in all groups (SAD 13.9 +/- 6.3; control VB 11.6 +/- 1.8, control 9.3 +/- 0.89, SAD VB 7.66 +/- 3.46). Immersion in the VB SAD animals increased BP to a greater extent than volume expansion. VB in the monkey must be removing input from peripheral receptors, which maintain sympathetic tone. Because immersion with VB increases BP more than volume expansion with VB, it is concluded that VB causes predominantly venous pooling. Because cardiopulmonary receptors generally inhibit sympathetic tone, it is concluded that those receptors responsible for the observed hypotension are located in the venous system, probably in the chest or the abdominal cavity.

Animals↗
PubMed1987

Carotid and aortic baroreceptor control of heart rate in conscious monkey.

This study looks at the difference between the aortic and the carotid baroreceptors in controlling the heart rate of conscious monkeys in the cage vs. the laboratory. Macaca mulatta and M. radiata underwent sequential baroreceptor denervation by first stripping the aortic arch, then one carotid sinus, and finally the second carotid sinus [sinoaortic denervation (SAD)]. Four monkeys had the carotid sinuses denervated before denervation of the aortic arch. Mean arterial blood pressure (MABP)-heart rate (HR) curves were determined by infusing nitroprusside and phenylephrine hydrochloride. The peak sensitivity (PS) was significantly less for all animals (control and denervated) in the laboratory than in the cage (P less than 0.05) with the exception of the SAD animals, which showed no difference. There was no significant difference in sensitivity between control and aortic-denervated animals in the cage. The PS decreased significantly after denervation of aortic arch and one carotid sinus. Monkeys with only the aortic baroreceptors intact had gains for the baroreflex curves that were similar to that of the SAD animals. After complete SAD the PS were essentially zero. We concluded that 1) the maximum slope of the MABP-HR reflex is greater when the monkey is in the cage than it is in the laboratory, probably resulting from an increase in the sympathetic tone; and 2) the carotid baroreceptors exert a greater influence on the HR component of the baroreflex in the conscious monkey than do the aortic baroreceptors.

Animals↗
PubMed1987

Effects of left ventricular receptor stimulation on coronary blood flow in conscious dogs.

The present study was undertaken to determine the effects of intracoronary administration of the veratrum alkaloid veratridine on coronary blood flow and resistance in conscious, chronically instrumented intact and sinoaortic denervated dogs. Ten dogs were instrumented with a Doppler flow probe on the left anterior descending coronary artery. A chronic catheter was placed in the left circumflex coronary artery and in the aorta and left atrium. A Konigsberg pressure cell was placed in the left ventricle, and pacing leads were attached to the left atrium and ventricle. While heart rate was kept constant, bolus intracoronary injections of veratridine (0.1-0.4 microgram/kg) were administered in the unblocked state after beta 1-receptor blockade, after alpha-receptor blockade, and after cholinergic blockade. In the unblocked state, late diastolic coronary resistance fell by 34.7 +/- 5.0%. The maximum response was achieved at a time when arterial pressure was not significantly different from control. After beta 1-blockade, coronary resistance fell by 29.1 +/- 7.9%. After combined alpha- and beta-blockade, coronary resistance fell by 25.4 +/- 6.5% in response to veratridine. The addition of atropine completely blocked the decrease in coronary resistance, changing it by an average of -0.10 +/- 2.5%. The responses in sinoaortic denervated dogs were similar to those in intact animals. The response was abolished by vagotomy. We conclude that cardiac receptor stimulation causes a reflex decrease in coronary resistance in the awake dog that is completely accountable by a cholinergic mechanism.

Animals↗
PubMed1986

Acute aortic stenosis in the conscious dog: effects of inotropic state on heart rate.

Effects of acute distension of the left ventricle on heart rate were studied in conscious, instrumented dogs. In intact dogs, increasing left ventricular (LV) systolic pressure by a maximum of 77.6 +/- 3.6 mmHg from a control of 123.1 +/- 3.6 and LV end-diastolic pressure by a maximum of 24.1 +/- 2.0 mmHg from a control of 8.5 +/- 1.3 did not result in any consistent change in heart rate. Reduction of arterial pressure with sodium nitroprusside caused an increase in heart rate to 143.9 +/- 13.8 beats/min. With baroreceptors unloaded, increasing LV pressure by a similar degree as in the control group now resulted in consistent and significant bradycardia. Removal of arterial baroreceptors in a final group of dogs abolished the baroreflex. Increasing LV pressure by aortic stenosis now resulted in a stimulus-dependent decrease in heart rate that was significantly greater than that in the nitroprusside group. Both administration of atropine and bilateral cervical vagotomy abolished bradycardia. The second part of this study was concerned with effects of increases in LV inotropic state on heart rate change evoked by aortic stenosis. Each group was infused with intracoronary epinephrine. Infusion of epinephrine (12.5-50.0 ng . kg-1 . min-1) significantly increased LV dP/dt without any significant change in heart rate or mean arterial blood pressure. Aortic stenosis during epinephrine infusion did not result in any significant difference in heart rate responses in any group studied. It is concluded that LV distension can cause a reduction in heart rate that is opposed by the presence of arterial baroreceptors and that increases in LV myocardial contractility do not have any effect on the magnitude of this response.

Animals↗
PubMed1985

Imparied atrial receptor modulation or renal nerve activity in dogs with chronic volume overload.

Left atrial receptors with vagal afferents are reset and become less sensitive in dogs with chronic high output congestive heart failure (Zucker et al J Clin Invst 1977;60:323). We determined if the normal reflex inhibition of renal sympathetic nerve activity (RNA) which occurs in response to left atrial distension is altered in dogs with chronic volume overload produced by an aorto-vena caval fistula (AVF). In addition, we examined the ability of the arterial baroreflex to alter RNA. In normal dogs, left atrial distension decreased RNA by 6.8 +/- 1.8% per mmHg change in left atrial pressure (LAP). After carotid sinus denervation (CSD), this inhibition was increased to 10.9 +/- 1.4% per mmHg change in RNA in response to left atrial distension. Vagotomy completely abolished any change in RNA in response to left atrial distension. In contrast, dogs with chronic AVF's demonstrated an increase in RNA in response to left atrial distension by 4.5 +/- 3.9% per mmHg change in LAP. The response of the AVF dogs was significantly different from the normal dogs (P less than 0.005). This was also the case after CSD. Loading and unloading of the arterial baroreceptors with norepinephrine and nitroprusside demonstrated that the modulation of RNA by arterial baroreceptors was similar in AVF dogs compared with normal dogs. The present study demonstrates that chronic volume overload results in a decrease in the peripheral sympathetic inhibitory effects of left atrial receptor stimulation at a time when arterial baroreceptor function is preserved.

Animals↗
PubMed1985

Sino-aortic denervation in the monkey.

The aortic arch and carotid sinuses were denervated in eleven monkeys. The monkeys were subjected to four sequential surgeries which involved: (1) implantation of an aortic and left atrial catheter; (2) stripping of the adventitia from the aortic arch; (3) stripping the left carotid sinus and associated vessels; and (4) stripping the right carotid sinus and associated vessels. Blood pressure and pulse rate were recorded 6 days after each surgical procedure. Records were taken over a 6 h period while the monkeys were in their home cages. Baroreceptor denervation was confirmed by: (1) absence of heart rate response to blood pressure changes and (2) an increase in the variability of blood pressure. Veratridine given into the left atrium caused a Bezold-Jarisch reflex both before and after denervation verifying the integrity of the afferent and efferent vagus. Denervation of the baroreceptors resulted in a significant increase in blood pressure when measured from monkeys who were restrained in chairs in the laboratory; however, blood pressure was not significantly elevated in the baroreceptor denervated monkeys while they were tethered in their home cages. It is concluded that denervation of the sino-aortic baroreceptor does not result in a significant increase in systemic blood pressure.

Animals↗
PubMed1984

Renal and iliac vascular responses to left ventricular receptor stimulation in conscious dogs.

The purpose of the present study was to investigate the relative responses of the renal and iliac vascular beds to the selective chemical stimulation of left ventricular receptors in the conscious dog. Twenty dogs were chronically instrumented to obtain measurements of arterial blood pressure, renal blood flow, and iliac blood flow before and after a bolus intracoronary injection of veratridine (0.4-1.0 micrograms/kg in 0.5-ml vol) with the heart paced. The responses to intracoronary veratridine were a significant reduction in arterial blood pressure averaging 25 mmHg accompanied by a simultaneous reduction in renal blood flow of 25%. Renal resistance did not change throughout the course of the response analyzed (50 s). Iliac blood flow, however, increased, reaching a peak of 35% above control due to a 51% decrease in iliac resistance. After sinoaortic denervation, renal resistance still failed to show a decrease, although the recovery of arterial blood pressure and iliac resistance was prolonged. After a mild hypotensive hemorrhage (20 ml/kg), a greater decrease in iliac resistance occurred with intracoronary veratridine injections, but renal resistance still did not change. The reduction in iliac resistance with intracoronary veratridine was significantly attenuated after phentolamine administration (2 mg/kg iv) but not after atropine alone (0.2 mg/kg iv). A significant cholinergic receptor component of iliac vasodilation was observed only after prior alpha-adrenergic-receptor blockade. The results of this study are consistent with the conclusion that in the conscious dog, left ventricular receptors exert a preferential neural control over skeletal muscle vascular resistance and do not influence renal vascular resistance.

Animals↗
PubMed1984

Intracoronary epinephrine attenuates baroreflex control of heart rate in the conscious dog.

In the present study, the reflex effects of low-dose (12.5-50 ng X kg-1 X min-1) intracoronary epinephrine infusion on the arterial baroreflex control of heart rate were studied. Mean arterial blood pressure-heart rate curves were constructed by changing mean arterial blood pressure with graded occlusions of the descending aorta and inferior vena cava. Intracoronary epinephrine increased left ventricular dP/dtmax by an average of 309 +/- 67.0 mmHg/s but did not alter resting mean arterial blood pressure or heart rate. Peak sensitivity, the maximum absolute slope along the mean arterial blood pressure-heart rate curve, and heart rate range were 32.7 +/- 3.2 and 26.7 +/- 2.5% less during intracoronary epinephrine compared with control, respectively. Intracoronary epinephrine did not alter the median, threshold, or saturation pressure of the mean arterial blood pressure-heart rate curve. Lidocaine block of the pericoronary nerves, which blocked the ventricular afferent pathway, eliminated the effects of intracoronary epinephrine on the arterial baroreflex. Atropine abolished the effects of intracoronary epinephrine on arterial baroreflex control of heart rate. We conclude that intracoronary epinephrine reflexly attenuates the arterial baroreflex control of heart rate in the conscious dog through activation of ventricular receptors. This response is mediated by cardiac parasympathetic efferents common to both reflex arcs.

Animals↗
PubMed1984

Sinoaortic baroreceptors and the control of blood volume in the nonhuman primate.

The purpose of this study was to determine the role of the aortic and carotid baroreceptors in regulating blood volume in the conscious non-human primate. Eighteen control animals were surgically instrumented to permit the recording of blood pressure, pulse rate, and left atrial pressure. After a urethral catheter was inserted into the bladder, the animals were given an intravenous infusion equal to 20% of the estimated blood volume. Renal function was determined before and after the volume expansion. Nine monkeys received the same infusion after undergoing chronic sinoaortic denervation. The denervated animals responded with a potentiated diuresis and natriuresis. The control animals excreted 24% of the infused volume and 4% of the infused salt while the sinoaortic-denervated animals excreted a volume equal to 113% of that infused and an amount of sodium equal to 46% of that infused. We conclude that high-pressure receptors exert an inhibitory influence on whatever mechanisms are involved in the renal response to acute volume expansion.

Animals↗
PubMed1983

The role of cardiopulmonary sympathetic afferents in blood volume homoeostasis in the non-human primate.

1. Four Macaca fascicularis monkeys were bilaterally sympathectomized by removing the thoracic sympathetic chain from the middle cervical ganglion to the T-6 sympathetic ganglion. This was done chronically, allowing adequate recovery time. While under light pentobarbital anaesthesia, the animals were then subjected to blood volume expansions with isotonic, isooncotic dextran or to head-out immersions. Seven immersions and seven volume expansions were carried out. 2. With immersion, there were significant increases in blood pressure, central venous pressure, urine flow, sodium excretion, potassium excretion, glomerular filtration rate, percentage of filtered sodium excreted and free water clearance. Although blood pressure and central venous pressure initially increased during the first immersion period, heart rate continued to increase with the immersion, while blood pressure and central venous pressure remained constant. Volume expansion caused an increase in central venous pressure, urine flow, sodium and potassium excretion, osmolar clearance, free water clearance, percentage of filtered sodium excreted and glomerular filtration rate. 3. Since these results with both the immersions and volume expansions were not qualitatively different from those observed in control animals, it is concluded that cardiopulmonary sympathetic afferents are not necessary for the renal response to head-out immersion or blood volume expansion in the non-human primate.

Afferent Pathways↗
PubMed1983

Influence of left ventricular receptor stimulation on plasma vasopressin in conscious dogs.

The current study was undertaken to determine whether receptors in the left ventricle are capable, when stimulated, of inhibiting plasma arginine vasopressin (AVP) in the conscious dog. Dogs were instrumented to measure aortic pressure and heart rate. In addition, a catheter was implanted in the left circumflex coronary artery. Left ventricular receptors were stimulated by the intracoronary infusion of veratrine, which evoked a hypotension and bradycardia. Control experiments consisted of intravenous infusion of veratrine. Plasma AVP, osmolality, and sodium and potassium concentrations were measured at intervals following the infusion. Similar experiments were done during the intravenous infusion of sodium nitroprusside (NP) to lower aortic pressure to the same extent as that seen with intracoronary infusion of veratrine. Experiments were also performed in chronic sinoaortic-denervated dogs. Intracoronary infusion of veratrine resulted in a significant decrease in aortic pressure from 93.9 +/- 2.8 to 70.5 +/- 4.5 mmHg. Control plasma AVP averaged 2.13 +/- 0.25 pg/ml and did not change significantly during this time. NP infusion lowered aortic pressure to a similar degree, and plasma AVP rose to 21.17 +/- 3.79 pg/ml after 5 min. There were no significant changes in any other plasma constituents. The results were similar in sinoaortic-denervated dogs. We conclude from the results of this study that receptors in the left ventricle are not capable of decreasing plasma AVP from low basal levels or from augmented levels.

Animals↗
PubMed1983

Is there a serotonin-induced hypertensive coronary chemoreflex in the nonhuman primate?

The purpose of this study was to investigate the nature of the serotonin-induced coronary chemoreflex in the conscious monkey. Ten chronically prepared and four acute monkeys were used in this study. Five chronically prepared animals had catheters in the left atrium, ascending aorta, descending aorta, and, bilaterally, in the common carotid arteries. In addition, Silastic catheters were placed next to both vagi to permit vagal block with 2% lidocaine. Serotonin was injected (12-200 micrograms/kg) into the left atrium, ascending aorta, descending aorta, or, bilaterally, into the carotid arteries while blood pressure, heart rate, and respiratory movements were recorded. Injections of serotonin were associated with hypertension and bradycardia followed by tachycardia, all of which were preceded by a cough response. Atropine blocked the bradycardia, whereas atropine and phentolamine eliminated the cardiovascular components of the reflex. Vagal blockade eliminated the bradycardia but otherwise did not alter the response to left atrial serotonin. Three monkeys were prepared with aortic and left atrial catheters. Subsequently, they were subjected to sinoaortic deafferentation. Serotonin injected into these animals did not alter blood pressure or respiration. The results of this study show that serotonin injected into the left atrium of the conscious monkey produces respiratory and cardiovascular alterations by its effect on aortic and carotid chemoreceptors, and that there is no coronary chemoreflex in the conscious monkey.

Animals↗
PubMed1983

Attenuation of arterial baroreflex control of heart rate by left ventricular receptor stimulation in the conscious dog.

The purpose of this investigation was to determine whether left ventricular receptor stimulation attenuates the arterial baroreflex control of heart rate in the conscious dog and to determine the role of cardiac efferent sympathetic and parasympathetic pathways in any interaction observed. Mean arterial blood pressure-heart rate function curves, which characterized arterial baroreflex control of heart rate, were constructed before (control) and during an infusion of veratrine into the left circumflex coronary artery. Peak sensitivity, the maximum absolute slope along the mean arterial blood pressure-heart rate curve, and heart rate range (maximum minus minimum heart rate) were reduced during intracoronary infusion of veratrine. The mean arterial blood pressure-heart rate relationship also was shifted to a lower pressure during intracoronary infusion of veratrine. In order to study the role of cardiac efferents in this interaction, we constructed mean arterial blood-pressure-heart rate curves during cholinergic blockade, cholinergic blockade plus intracoronary infusion of veratrine, beta 1-adrenergic blockade, and beta 1-adrenergic blockade plus intracoronary infusion of veratrine. The addition of intracoronary infusion of veratrine during cholinergic blockade produced a shift of the mean arterial blood pressure-heart rate curve down the ordinate axis (heart rate) and to a lower pressure; however, peak sensitivity and heart rate range remained unchanged. The addition of intracoronary infusion of veratrine during beta 1-adrenergic blockade resulted in reductions in peak sensitivity and heart rate range. These data indicate that left ventricular receptor stimulation attenuates arterial baroreflex control of heart rate and that the reduction of sensitivity and heart rate range is mediated by parasympathetic motoneurons common to both reflex arcs. On the other hand, resetting to a lower operational set point may be mediated by cardiac sympathetic motoneurons common to both reflex arcs.

Acetylcholine↗
PubMed1982

Increased left atrial pressure does not alter renal function in the conscious primate.

To study the functional role of the atriorenal reflex in the nonhuman primate, we chronically instrumented six Macaca fascicularis with left atrial snares and left atrial and aortic catheters. After inserting a bladder catheter, we determined hemodynamic and renal responses of the conscious chair-restrained monkey to increased left atrial pressure. In 23 snare experiments, no significant changes in renal or cardiovascular function were observed even though left atrial pressure increased from 6.5 +/- 3.3 to 16.2 +/- 3.4 mmHg. The animals were subjected also to blood volume expansion with isoncotic isotonic dextran solutions (+15% of calculated blood volume). They responded normally to this volume stimulus. Conscious dogs prepared in the same manner as the nonhuman primate exhibited diuresis in response to elevations of atrial pressure. We conclude that left atrial stretch receptors are not importantly involved in volume homeostasis in the nonhuman primate.

Animals↗
PubMed1981

Angiotensin I conversion by the microcirculation of the nonhuman primate.

Previous studies have shown that angiotensin I (AI) is converted to angiotensin II (AII) by converting enzyme (CE) or by tonin. Since all work on tonin has been done in the rodent, its relevance to the primate is yet to be shown. This study examines the conversion of AI to AII by the cheek pouch microcirculation of the monkey (macaca fascicularis). In 9 of the 11 monkeys studied, the conversion of AI to AII was blocked by converting enzyme inhibitor (CEI). However, in 2 older monkeys, AI conversion was not altered by CEI although the vascular response to AI was attenuated by both the AII antagonist (saralasin) and the antibody to AII (Ab-AII). In these 2 older animals, renin substrate caused vasoconstriction that was not altered by CEI, but was reduced by saralasin and Ab-AII. It is concluded that the tonin-angiotensin system is not active in the young macaque, but may be present in the older animals.

Aging↗