Age-related responses to stimulation of cardiopulmonary receptors in swine

1986 ◽  
Vol 251 (4) ◽  
pp. H748-H755 ◽  
Author(s):  
P. M. Gootman ◽  
B. J. Buckley ◽  
S. M. DiRusso ◽  
N. Gootman ◽  
A. C. Yao ◽  
...  
Keyword(s):  
Cardiovascular Responses ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Postnatal Maturation ◽  
Age Related ◽  
Bilateral Vagotomy ◽  
Cardiopulmonary Receptors ◽  
Mean Aortic Pressure ◽  
Stimulation Of

Cardiovascular responses to stimulation of cardiopulmonary receptors were evaluated in standard breed developing swine (1-2 days, 1-2 wk, and 2 mo of age) and sexually mature miniswine anesthetized with 0.25-0.50% halothane in O2. Cryptenamine, a mixture of veratrum viride alkaloids (VVA), was administered as right atrial or left ventricular bolus injections in doses of 5-20 micrograms/kg. In developing swine, mean aortic pressure (AoP) decreased after 10-20 micrograms/kg VVA in 1- to 2-wk olds and after 5-20 micrograms/kg VVA in 2-mo olds. Bradycardia was always elicited. Renal (Ren) and femoral (Fem) vasodilation occurred in the 1- to 2-wk-old and 2-mo-old groups after 5-20 micrograms/kg VVA. Mesenteric (Mes) vasodilation was elicited with 10-20 micrograms/kg VVA in the 1- to 2-wk-old group and with 5-20 micrograms/kg VVA in 2-mo olds. In the 1- to 2-day-old group, VVA did not significantly alter Ren, Fem, and Mes vascular resistance. In mature miniswine, 20 micrograms/kg VVA elicited decreases in AoP and heart rate that were similar in magnitude to responses obtained with only 5 micrograms/kg VVA in dogs. Cardiovascular responses to VVA were abolished after bilateral vagotomy but were not altered after denervation of the carotid sinuses. The results indicate postnatal maturation of the Bezold-Jarisch reflex in swine.

Stimulation of pancreatic afferents reflexly activates the cardiovascular system in cats

1983 ◽  
Vol 245 (6) ◽  
pp. R820-R826 ◽  
Author(s):  
G. A. Ordway ◽  
J. C. Longhurst ◽  
J. H. Mitchell
Keyword(s):  
Cardiovascular System ◽  
Cardiovascular Responses ◽  
Systemic Arterial Pressure ◽  
Left Ventricular ◽  
Chemical Stimulation ◽  
Potential Mechanism ◽  
Bilateral Vagotomy ◽  
Reflex Activation ◽  
Developed Pressure ◽  
Stimulation Of

Chemical stimulation of afferents from the stomach and gallbladder has been shown reflexly to activate the cardiovascular system. It is not known, however, whether stimulating afferents from the pancreas evoke similar reflex activity. Therefore we recorded the cardiovascular responses in cats anesthetized with methoxyflurane, while we applied capsaicin (200 micrograms/ml) and bradykinin (0.001-1,000 micrograms/ml) to the surface of the pancreas. Topically applying these algesic substances evoked cardiovascular responses that included increases in systemic arterial pressure, heart rate, left ventricular dP/dt at 40-mmHg developed pressure and systemic vascular resistance. Bilateral vagotomy at the level of the diaphragm did not diminish the cardiovascular responses evoked by capsaicin or bradykinin. In contrast, removal of the celiac and superior mesenteric ganglia abolished the cardiovascular responses demonstrated previously when capsaicin or bradykinin was applied to the pancreas. We conclude that afferent endings in the pancreas can be stimulated reflexly to increase cardiovascular function in cats. This reflex activation represents a potential mechanism for eliciting the cardiovascular changes observed during acute pancreatitis, particularly the marked vasoconstriction that may lead to renal failure.

Cardiac responses to stimulation of thoracic afferents in the primate and canine

1976 ◽  
Vol 231 (4) ◽  
pp. 1279-1284 ◽  
Author(s):  
DR Kostreva ◽  
GL Hess ◽  
EJ Zuperku ◽  
J Neumark ◽  
RL Coon ◽  
...  
Keyword(s):  
Carotid Sinus ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Cardiac Responses ◽  
Afferent Nerves ◽  
Before And After ◽  
Blood Pressures ◽  
Bilateral Vagotomy ◽  
Upper Thoracic ◽  
Stimulation Of

Excitatory cardiovascular responses to electrically stimulated upper thoracic sympathetic afferent nerves were observed in halothane-anesthetized mongrel dogs and monkeys. The central end of the transected ventral limb of the left ansa subclavia was stimulated before and after several types of denervation. Significant increases in right and left ventricular maximum systolic pressures, systolic and diastolic systemic blood pressures, and aortic flow were observed. The carotid sinuses were denervated bilaterally and stimulation of the ansa was repeated. The cardiovascular responses to stimulation of the ventral ansa after carotid sinus denervation were greater in magnitude than those observed prior to denervation. This carotid sinus modulation of cardiovascular responses was observed in dogs and monkeys. Cardiovascular responses to stimulation of the ventral ansa after bilateral vagotomy were significantly less than the responses observed after carotid sinus denervation prior to vagotomy. However, the responses after vagotomy were statistically identical to responses obtained while stimulating the ventral ansa when the carotid sinuses and vagi remained intact.

scholarly journals Acute stimulation of the soluble guanylate cyclase does not impact on left ventricular capacitance in normal and hypertrophied porcine hearts in vivo

2018 ◽  
Vol 315 (3) ◽  
pp. H669-H680 ◽  
Author(s):  
Alessio Alogna ◽  
Michael Schwarzl ◽  
Martin Manninger ◽  
Nazha Hamdani ◽  
Birgit Zirngast ◽  
...  
Keyword(s):  
Guanylate Cyclase ◽  
Soluble Guanylate Cyclase ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Concentric Hypertrophy ◽  
Ventricular Compliance ◽  
Left Ventricular Compliance ◽  
Stimulation Of

Experimental data indicate that stimulation of the nitric oxide-soluble guanylate cyclase(sGC)-cGMP-PKG pathway can increase left ventricular (LV) capacitance via phosphorylation of the myofilamental protein titin. We aimed to test whether acute pharmacological sGC stimulation with BAY 41-8543 would increase LV capacitance via titin phosphorylation in healthy and deoxycorticosteroneacetate (DOCA)-induced hypertensive pigs. Nine healthy Landrace pigs and 7 pigs with DOCA-induced hypertension and LV concentric hypertrophy were acutely instrumented to measure LV end-diastolic pressure-volume relationships (EDPVRs) at baseline and during intravenous infusion of BAY 41-8543 (1 and 3 μg·kg−1·min−1 for 30 min, respectively). Separately, in seven healthy and six DOCA pigs, transmural LV biopsies were harvested from the beating heart to measure titin phosphorylation during BAY 41-8543 infusion. LV EDPVRs before and during BAY 41-8543 infusion were superimposable in both healthy and DOCA-treated pigs, whereas mean aortic pressure decreased by 20–30 mmHg in both groups. Myocardial titin phosphorylation was unchanged in healthy pigs, but total and site-specific (Pro-Glu-Val-Lys and N2-Bus domains) titin phosphorylation was increased in DOCA-treated pigs. Bicoronary nitroglycerin infusion in healthy pigs ( n = 5) induced a rightward shift of the LV EDPVR, demonstrating the responsiveness of the pathway in this model. Acute systemic sGC stimulation with the sGC stimulator BAY 41-8543 did not recruit an LV preload reserve in both healthy and hypertrophied LV porcine myocardium, although it increased titin phosphorylation in the latter group. Thus, increased titin phosphorylation is not indicative of increased in vivo LV capacitance. NEW & NOTEWORTHY We demonstrate that acute pharmacological stimulation of soluble guanylate cyclase does not increase left ventricular compliance in normal and hypertrophied porcine hearts. Effects of long-term soluble guanylate cyclase stimulation with oral compounds in disease conditions associated with lowered myocardial cGMP levels, i.e., heart failure with preserved ejection fraction, remain to be investigated.

Pulmonary and systemic vasodilator effects of the newly discovered prostaglandin, PGI2

1978 ◽  
Vol 45 (3) ◽  
pp. 408-413 ◽  
Author(s):  
P. J. Kadowitz ◽  
B. M. Chapnick ◽  
L. P. Feigen ◽  
A. L. Hyman ◽  
P. K. Nelson ◽  
...  
Keyword(s):  
Vena Cava ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Vascular Bed ◽  
Vasodilator Activity ◽  
Pulmonary Arterial ◽  
Vascular Beds ◽  
Renal Vascular ◽  
Dose Dependent

The effects of the newly discovered bicyclic prostaglandin, prostacyclin (PGI2), on the pulmonary and systemic vascular beds were investigated in the anesthetized dog. PGI2 decreased systemic and pulmonary arterial pressures in a dose-related manner when injected into the vena cava in doses of 1--30 microgram. Since left ventricular end-diastolic, left atrial, and right atrial pressures were unchanged, and since cardiac output was increased or unchanged, pulmonary and systemic vascular resistances were decreased. PGI2 was 10 times more potent than prostaglandins E1 or E2 in decreasing aortic pressure when injected intravenously, and the effects of PGI2 on the systemic vascular bed were similar when injected into the vena cava or the left atrium. These data indicate that inactivation of PGI2 is minimal in the lung. The stable prostacyclin metabolite, 6-keto-PGF1alpha, had little hemodynamic effects, suggesting that responses to PGI2 were not due to formation of this metabolite. PGI2 produced dose-dependent increases in blood flow in the mesenteric and renal vascular beds. These data demonstrate that PGI2 has marked vasodilator activity in the pulmonary and systemic vascular beds and suggest that prostacyclin is the only known metabolite of arachidonic acid that dilates the pulmonary and systemic circulations.

Arterial pressure-flow relations in the awake standing dog

1975 ◽  
Vol 229 (5) ◽  
pp. 1261-1270 ◽  
Author(s):  
W Enrlich ◽  
FV Schrijen ◽  
TA Solomon ◽  
E Rodriguez-Lopez ◽  
RL Riley
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Rate Increase ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Right Atrial ◽  
Heart Rate Increase ◽  
Underlying Mechanisms ◽  
The Right

The transient circulatory changes following paced heart rate increase are reported from 133 trials with 6 unanesthetized dogs with chronically implanted monitoring devices for heart rate, cardiac output, aortic blood pressure, and mean right atrial pressure. In 62 trials with 2 of the dogs, pulmonary artery, and left ventricular end-diastolic pressure, as well as left ventricular dP/dt were also studied. The sequence of changes in pressures and flows is analyzed in terms of probable underlying mechanisms, particularly with respect to the nature of vascular resistances. The rise in aortic pressure and flow during the first 3 s of paced heart rate increase, before arterial stretch receptor reflexes become active, is more consistent with an effective downstream pressure of about 49 mmHg, presumably at the arteriolar level, than with an effective downstream pressure close to 0 mmHg at the right atrial level. In the pulmonary circulation where vascular reflex effects are less prominent, the pattern of pulmonary arterial pressure and flow for the entire 30 s of observation is consistent with an effective downstream pressure of 9 mmHg, presumably at the alveolar or pulmonary arteriolar level, rather than at the level of the left ventricular end-diastolic pressure.

Role of spinal NK1 receptors in cardiovascular responses to chemical stimulation of the gallbladder

1995 ◽  
Vol 268 (2) ◽  
pp. H526-H534 ◽  
Author(s):  
H. L. Pan ◽  
A. C. Bonham ◽  
J. C. Longhurst
Keyword(s):  
Intrathecal Injection ◽  
Left Ventricular Pressure ◽  
Cardiovascular Responses ◽  
Pressure Change ◽  
Left Ventricular ◽  
Chemical Stimulation ◽  
Intrathecal Catheter ◽  
Nk1 Receptors ◽  
Stimulation Of

The present study examined the role of substance P (SP) as a sensory neurotransmitter in cardiovascular responses to bradykinin applied on the gallbladder. Experiments were performed in anesthetized cats in which sympathetic chains were transected at the T5-T6 level, and the tip of the intrathecal catheter was positioned at T6-T7 to limit the injectate between T6 and L2. Bradykinin (10 micrograms/ml) was applied onto the gallbladder before and after intrathecal injection of [D-Pro2,D-Phe7,D-Trp9]SP (100–200 micrograms, NK1/NK2-receptor antagonist), CP-99,994 (50–100 micrograms, selective NK1 antagonist), MEN-10,376 (100–500 micrograms, selective NK2 antagonist), or vehicle. Intrathecal injection of NK1 but not NK2 antagonist significantly reduced increases in mean arterial pressure, heart rate, and maximal rate of left ventricular pressure change by 28 +/- 2 mmHg (33 +/- 4%), 4 +/- 1 beats/min (42 +/- 5%), and 497 +/- 46 mmHg/s (36 +/- 4%), respectively. Intrathecal injection of NK1 or NK1/NK2 antagonist had no effect on cardiovascular responses evoked by electrical stimulation in the rostral ventral lateral medulla. These data suggest that endogenous SP, acting as a sensory neurotransmitter, is involved in the excitatory cardiovascular reflex caused by chemical stimulation of the gallbladder through its action on NK1 receptors in the spinal cord.

Chemically induced cardiovascular reflexes arising from the stomach of the cat

1984 ◽  
Vol 247 (3) ◽  
pp. H459-H466 ◽  
Author(s):  
J. C. Longhurst ◽  
C. L. Stebbins ◽  
G. A. Ordway
Keyword(s):  
Blood Pressure ◽  
Smooth Muscle ◽  
Muscle Tension ◽  
Cardiovascular Responses ◽  
Smooth Muscle Contraction ◽  
Left Ventricular ◽  
Cardiovascular Reflexes ◽  
Bilateral Vagotomy ◽  
Celiac Ganglionectomy ◽  
Developed Pressure

We examined the potential for cardiovascular reflexes caused by the application of either bradykinin or capsaicin to the serosal or mucosal surface of the stomach. After application to the serosa, bradykinin (10 micrograms/ml) evoked increases in mean arterial pressure of 12 +/- 2 mmHg, heart rate of 5 +/- 1 beats/min, left ventricular dP/dt (at 40 mmHg developed pressure) of 305 +/- 54 mmHg/s and systemic vascular resistance of 0.04 +/- 0.01 PRU. Capsaicin (200 microgram/ml) caused similar cardiovascular responses. There were no cardiovascular responses when either substance was applied to the gastric mucosa. The responses to both chemicals were abolished by celiac ganglionectomy but not by bilateral vagotomy. To determine whether the cardiovascular responses evoked by bradykinin were caused by smooth muscle contraction, we compared the increases in gastric smooth muscle tension and blood pressure elicited by bradykinin, bethanechol, or acetylcholine. Bethanechol and acetylcholine caused greater increases in tension than bradykinin, whereas bradykinin evoked greater increases in blood pressure than either bethanechol or acetylcholine. We conclude that stimulation of gastric afferents by capsaicin or bradykinin causes cardiovascular reflexes, primarily through activation of chemosensitive receptors.

β2-Adrenergic receptor agonists stimulate L-type calcium current independent of PKA in newborn rabbit ventricular myocytes

2007 ◽  
Vol 293 (5) ◽  
pp. H2826-H2835 ◽  
Author(s):  
Leon P. Collis ◽  
Shekhar Srivastava ◽  
William A. Coetzee ◽  
Michael Artman
Keyword(s):  
Ventricular Myocytes ◽  
Ventricular Myocardium ◽  
Adult Rabbit ◽  
Patch Clamp Technique ◽  
Postnatal Maturation ◽  
Newborn Rabbit ◽  
Age Related ◽  
Rabbit Ventricular Myocardium ◽  
Rabbit Ventricular Myocytes ◽  
Stimulation Of

Selective stimulation of β2-adrenergic receptors (ARs) in newborn rabbit ventricular myocardium invokes a positive inotropic effect that is lost during postnatal maturation. The underlying mechanisms for this age-related stimulatory response remain unresolved. We examined the effects of β2-AR stimulation on L-type Ca2+ current ( ICa,L) during postnatal development. ICa,L was measured (37°C; either Ca2+ or Ba2+ as the charge carrier) using the whole-cell patch-clamp technique in newborn (1 to 5 days old) and adult rabbit ventricular myocytes. Ca2+ transients were measured concomitantly by dialyzing the cell with indo-1. Activation of β2-ARs (with either 100 nM zinterol or 1 μM isoproterenol in the presence of the β1-AR antagonist, CGP20712A) stimulated ICa,L twofold in newborns but not in adults. The β2-AR-mediated increase in Ca2+ transient amplitude in newborns was due exclusively to the augmentation of ICa,L. Zinterol increased the rate of inactivation of ICa,L and increased the Ca2+ flux integral. The β2-AR inverse agonist, ICI-118551 (500 nM), but not the β1-AR antagonist, CGP20712A (500 nM), blocked the response to zinterol. Unexpectedly, the PKA blockers, H-89 (10 μM), PKI 6-22 amide (10 μM), and Rp-cAMP (100 μM), all failed to prevent the response to zinterol but completely blocked responses to selective β1-AR stimulation of ICa,L in newborns. Our results demonstrate that in addition to the conventional β1-AR/cAMP/PKA pathway, newborn rabbit myocardium exhibits a novel β2-AR-mediated, PKA-insensitive pathway that stimulates ICa,L. This striking developmental difference plays a major role in the age-related differences in inotropic responses to β2-AR agonists.

Reversal of myocardial dysfunction in endotoxin shock with insulin

1978 ◽  
Vol 56 (1) ◽  
pp. 132-138 ◽  
Author(s):  
L. T. Archer ◽  
B. K. Beller ◽  
J. K. Drake ◽  
T. L. Whitsett ◽  
L. B. Hinshaw
Keyword(s):  
Insulin Infusion ◽  
Diastolic Pressure ◽  
Myocardial Dysfunction ◽  
Aortic Pressure ◽  
Endotoxin Shock ◽  
Left Ventricular ◽  
Lactate Uptake ◽  
Blood Glucose Concentrations ◽  
Mean Aortic Pressure ◽  
Canine Myocardium

Recent data reported from this laboratory have documented myocardial functional depression in endotoxin shock. The purpose of the present study was to determine the effects of insulin on the dysfunctioning canine myocardium subjected to lethal endotoxin shock. Experiments were conducted on isolated working left ventricular preparations in which LD90–100 endotoxin was administered prior to, or following, isolation of the heart. Determinations of myocardial performance were conducted under the conditions of controlled mean aortic pressure and cardiac output. Myocardial dysfunction occurred between 2 and 6 h postendotoxin, as evidenced by significantly increased left ventricular end-diastolic pressure, decreased power, and depressed negative dP/dt, although blood glucose concentrations were maintained at control values. Intraatrial infusions of insulin at rates of 6 U/min reversed all signs of myocardial dysfunction. During insulin infusion, heart rates decreased (p < 0.02) and myocardial lactate uptake increased (p < 0.02), while oxygen uptake and coronary blood flow were insignificantly altered.

Interaction of aortic pressure and left ventricular end-diastolic pressure in the dog

1977 ◽  
Vol 232 (6) ◽  
pp. H697-H704
Author(s):  
J. R. Foster ◽  
E. R. Powers ◽  
W. J. Powell
Keyword(s):  
Performance Improvement ◽  
Fiber Length ◽  
Diastolic Pressure ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Stroke Work ◽  
Ventricular Performance ◽  
Aortic Blood Pressure ◽  
Mean Aortic Pressure ◽  
Right Heart Bypass

Fiber length (preload) is an important determinant of left ventricular performance. Mean aortic blood pressure also influences ventricular performance. The present study was undertaken to examine the influence of mean aortic pressure on the fiber length-ventricular performance relationship. Fifteen anesthetized, adrenergically blocked dogs were studied on right-heart bypass at constant heart rate and coronary blood flow. An increase in mean aortic pressure permitted a greater improvement in performance as evaluated by stroke work for a given increase in left ventricular end-diastolic pressure. A given increase in mean aortic pressure at a constant stroke volume produced a greater rise in stroke work over intermediate ranges of left ventricular end-diastolic pressure than occurred with higher or lower left ventricular end-diastolic pressure. Thus, the degree of afterload-induced performance improvement depended on the magnitude of the preload. External circumference-left ventricular end-diastolic pressure data suggested a possible relationship between isovolumic systolic circumferential expansion and the improvement of ventricular performance at higher mean aortic pressures.

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