Mechanisms of Respiratory Inhibition Produced by Sudden Aortic Obstruction

1958 ◽  
Vol 194 (1) ◽  
pp. 155-159 ◽  
Author(s):  
Thomas M. Gilfoil ◽  
Robert T. Schopp ◽  
Gail R. Norris ◽  
W. B. Youmans

External constriction of the descending aorta elicits immediate inhibition of breathing in dogs under Pentothal-chloralose anesthesia both before and after sino-aortic denervation. Impulses initiated by traction of a ligature on the aorta are conducted into the thoracic part of the cord. There is no indication that this mechanism is activated in experiments involving internal occlusion in the innervated animals. Internal occlusion of the descending aorta elicits inhibition of breathing in dogs under morphine sulfate-chloralose anesthesia having all neural pathways intact. The inhibition is related in large part to reflexes from the sino-aortic zones. In the majority of dogs studied the delayed inhibition of breathing following internal occlusion of the descending aorta was greatly reduced but usually not entirely eliminated by sino-aortic denervation. Therefore, some other respiration-inhibiting mechanism is involved. That the respiratory center may be relatively insensitive to changes in blood flow under the conditions of these experiments is indicated by the fact that in individual cases sudden severe changes in blood pressure in sino-aortic denervated animals were not accompanied by changes in respiration.

1961 ◽  
Vol 201 (1) ◽  
pp. 109-111 ◽  
Author(s):  
Noel M. Bass ◽  
Vincent V. Glaviano

Heart rate, mean blood pressure, adrenal blood flow, and adrenal plasma adrenaline and noradrenaline were compared before and after ligation of the anterior descending coronary artery in dogs anesthetized with chloralose. One group of 12 dogs responded to acute coronary occlusion with a sudden and marked decrease in mean blood pressure (mean, 31%) and heart rate (mean, 18%) followed by an early onset (mean, 227 sec) of ventricular fibrillation. Another group of nine dogs responded with slight decreases in mean blood pressure (mean, 13%) and heart rate (mean, 5%), during which time ventricular fibrillation occurred late (mean, 30 min) or not at all. While the two groups were statistically different in mean blood pressure and heart rate, the minute output of adrenal catecholamines in either group was not found to be related to the early or late occurrence of ventricular fibrillation.


Author(s):  
Juulia Lantto ◽  
Tiina Erkinaro ◽  
Mervi Haapsamo ◽  
Heikki Huhta ◽  
Leena Alanne ◽  
...  

A drop in arterial oxygen content activates fetal chemoreflex including an increase in sympathetic activity leading to peripheral vasoconstriction and redistribution of blood flow to protect the brain, myocardium, and adrenal glands. By using a chronically instrumented fetal sheep model with intact placental circulation at near-term gestation, we investigated the relationship between peripheral chemoreflex activation induced by hypoxemia and central hemodynamics. 17 Åland landrace sheep fetuses at 115-128/145 gestational days were instrumented. Carotid artery was catheterised in 10 fetuses and descending aorta in 7 fetuses. After a 4-day recovery, baseline measurements of fetal arterial blood pressures, blood gas values, and fetal cardiovascular hemodynamics by pulsed Doppler ultrasonography were obtained under isoflurane-anesthesia. Comparable data to baseline was collected 10 (acute hypoxemia) and 60 minutes (prolonged hypoxemia) after maternal hypo-oxygenation to saturation level of 70-80% was achieved. During prolonged hypoxemia, pH and base excess (BE) were lower, and lactate levels higher in the descending aorta than in the carotid artery. During hypoxemia mean arterial blood pressure (MAP) in the descending aorta increased, while in the carotid artery MAP decreased. In addition, right pulmonary artery pulsatility index values increased, and the diastolic component in the aortic isthmus blood flow velocity waveform became more retrograde. Both fetal ventricular cardiac outputs were maintained even during prolonged hypoxemia when significant fetal metabolic acidemia developed. Fetal chemoreflex activation induced by hypoxemia decreased the perfusion pressure in the cerebral circulation. Fetal weight-indexed LVCO or AoI Net Flow-ratio did not correlate with a drop in carotid artery blood pressure.


1975 ◽  
Vol 79 (2) ◽  
pp. 337-350 ◽  
Author(s):  
Per Olof Janson ◽  
Ivan Albrecht ◽  
Kurt Ahrén

ABSTRACT In the search for data supporting the hypothesis that the luteolytic effect of prostaglandins (PG) is initiated by a vascular mechanism, some haemodynamic parameters including ovarian blood flow and vascular resistance were measured in pseudopregnant anaesthetized rabbits before and after exogenous administration of PGF2α. The measurements were performed on days 5–10 of pseudopregnancy induced by 500 IU HCG iv. Infusion of 50 μg/kg PGF2α iv over a one-minute period caused significant falls in cardiac output, heart rate and blood pressure after 1–3 min. Blood pressure and cardiac output were normalized after 16–49 min. Blood flow in the ovarian vein (direct measurements) decreased and returned to initial values parallel to the blood pressure and no change in resistance in the vascular bed drained by the vein was noted. Total ovarian blood flow and resistance, as measured in surgically intact ovaries before and after PG infusion, using 35 or 15 μm 169Yb and 46Sc-labelled microspheres, changed and remained constant respectively, according to the same pattern as in the direct measurements. The distribution of blood flow between the corpora lutea and the interstitial tissue of the ovary measured by 15 μm radioactive microspheres. PGF2α caused an interstitial vasodilation whereas no significant change in luteal vascular resistance was noted. Since luteal blood flow represented a predominant part of total ovarian flow in the type of ovary studied, the interstitial vasodilatation caused only negligible changes in blood flow to the whole ovary. The present study does not support the hypothesis of a PG-induced luteal blood flow reduction preceding luteolysis. The possible significance of the interstitial vasodilatation for luteal function remains to be elucidated.


2020 ◽  
Vol 15 (2) ◽  
pp. 81-89
Author(s):  
Nadia Aryani ◽  
Nofri Zayani

Hydrotherapy non-pharmacological treatment for hypertension during pregnancy needs to be developed because it is safe for mother and fetus. Hydrotherapy soaking feet using warm water can increase vasodilation and increase blood flow, thereby lowering blood pressure. The purpose of this study was to determine the effectiveness of foot soaking with warm water to reduce hypertension in pregnant women. The pre-experimental research design was one group pretest posttest, which measured blood pressure before and after warm water therapy was given to pregnant women with hypertension for three days. The research sample was selected using purposive sampling method and the number was 15 people. Data analysis was performed by using paired sample T-Test. Results: Giving hydrotherapy soaking feet using warm water reduced systolic and diastolic blood pressure in pregnant women (p = 0.000 <0.05). Hydrotherapy is effective in reducing systolic blood pressure by 13-16 mmHg and diastolic by 8-9 mmHg. Conclusion: Hydrotherapy soaking feet using warm water is effective in reducing hypertension of pregnant women who go to dr. Jerry Kp. Kulon waterfall. Suggestion: Apply the foot soaking method with warm water as a non-pharmacological method of hypertension in pregnant women.


2002 ◽  
Vol 92 (6) ◽  
pp. 2554-2564 ◽  
Author(s):  
Aidan K. Curran ◽  
Daniel Peraza ◽  
Cheryl A. Elinsky ◽  
J. C. Leiter

The rostral ventral medulla (RVM) may be important in the control of cardiorespiratory interactions. We hypothesized that inhibition of the RVM would enhance inhibition of breathing associated with transient blood pressure elevations. In 25 piglets 3–16 days of age, we studied the effect of acutely increasing blood pressure, by systemic infusion of phenylephrine, on respiratory activity before and after inhibition of neural activity in the RVM by dialysis of 10 mM muscimol, a GABAA-receptor agonist. Muscimol dialysis through probes that were placed along the ventral medullary surface from ∼1 mm rostral to the facial nucleus to ∼0.5 mm caudal to the facial nucleus augmented the respiratory inhibition associated with acute increases in blood pressure. No similar enhancement of respiratory inhibition after phenylephrine treatment was seen in six control animals that did not receive muscimol dialysis. We conclude that the piglet RVM participates in cardiorespiratory interactions and that dysfunction of homologous regions in the human infant could lead to cardiorespiratory instability and may be involved in the pathogenesis of sudden infant death syndrome.


1987 ◽  
Vol 252 (6) ◽  
pp. H1243-H1248
Author(s):  
D. J. DiPette ◽  
J. F. Burris ◽  
A. Rogers ◽  
B. Waeber ◽  
H. R. Brunner

Acute beta-adrenoreceptor blockade results in an enhanced blood pressure-lowering effect in glucocorticoid hypertensive rats in the absence of the adrenals. To evaluate the possible mechanism of this enhanced blood pressure-lowering effect, systemic and regional hemodynamics were determined by the radioactive microsphere technique before and after propranolol administration in bilaterally adrenalectomized (AX) and sham-operated (SH) glucocorticoid hypertensive rats. Propranolol decreased mean blood pressure (BP) and heart rate (HR) to a greater extent in the AX animals. In response to propranolol, cardiac output (CO) decreased equally in both the AX and SH animals. Regional vascular responses to propranolol were similar between the AX and SH animals, except in muscle. In muscle propranolol significantly decreased blood flow and increased resistance in the SH animals. In marked contrast, in the AX animals propranolol significantly increased blood flow and decreased vascular resistance. The results of this study show that in adrenalectomized glucocorticoid hypertensive rats, the enhanced BP lowering effect of acute beta-adrenoreceptor blockade is not mediated by changes in CO. Additionally, in glucocorticoid hypertensive rats acute beta-adrenoreceptor blockade causes selective vasodilation in skeletal muscle.


Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 711-711
Author(s):  
Cecilia M Sayago ◽  
William H Beierwaltes

P100 The stimulatory second messenger for renin is cAMP, which is degraded by phosphodiesterase (PDE)-3. PDE-3 is inhibited by cGMP, while PDE-5 degrades cGMP. We hypothesized that if endogenous cGMP was increased, it could inhibit PDE-3, increasing cAMP, and stimulating renin. We used the selective PDE-5 inhibitor Zaprinast at a dose we determined would not change either blood pressure or renal blood flow (RBF). In inactin-anesthetized rats, renin secretion rate (RSR) was determined by collecting arterial and renal venous blood while measuring RBF before and 75 min after administering 20 mg/kg bw Zaprinast (n=9) ip, or vehicle (n=7). Blood pressure before and after Zaprinast was unchanged at 102 ±2 and 98 ±2 mmHg, respectively, similar to vehicle controls (107 ±3 to 105 ±4 mmHg). RBF was unchanged by either Zaprinast (5.57 ±0.38 to 5.77 ±0.41 ml/min/gkw) or vehicle (6.21 ±0.47 to 6.25 ±0.42 ml/min/gkw). Zaprinast increased RSR 6-fold (from 2.95 ±1.74 to 17.62 ±5.46 ng Ang1/hr/min, p <0.024), while vehicle had no effect (4.08 ±2.02 to 3.87 ±1.53 ng Ang1/hr/min). Zaprinast also increased renal cGMP excretion from 12.75 ±1.57 to 18.67 ±1.87 p mol/min (p<0.003), while cGMP excretion was unchanged by vehicle (13.07 ±1.76 to 12.42 ±2.16 p mol/min). Thus, inhibition of cGMP degradation by the PDE-5 inhibitor Zaprinast increased endogenous cGMP (as reflected in excretion) and also stimulated renin secretion, despite not significantly changing renal hemodynamics. These data suggest that endogenous cGMP may indirectly regulate renin through its direct effect on cAMP degradation.


1958 ◽  
Vol 193 (2) ◽  
pp. 360-364 ◽  
Author(s):  
Allan V. N. Goodyer ◽  
Louis R. Mattie ◽  
Allen Chetrick

In anesthetized dogs, bleeding (1.5–3% of the body weight) was allowed while renal arterial pressure was maintained at constant levels by graded changes of mechanical aortic obstruction. The renal hematocrit decreased, (as measured with I131 albumin and acid hematin, and as compared to the blood hematocrit), primarily as a result of an increased renal plasma volume. These changes are correlated with previously identified alterations of sodium excretion, all independent of renal innervation or arterial blood pressure. It is proposed that hemorrhage may involve an intrarenal redistribution of blood flow favoring diversion of plasma to cell-poor capillaries or to lymphatic spaces.


2015 ◽  
Vol 114 (9) ◽  
pp. 1427-1437 ◽  
Author(s):  
Emma L. Wightman ◽  
Crystal F. Haskell-Ramsay ◽  
Jonathon L. Reay ◽  
Gary Williamson ◽  
Tristan Dew ◽  
...  

AbstractSingle doses of resveratrol have previously been shown to increase cerebral blood flow (CBF) with no clear effect on cognitive function or mood in healthy adults. Chronic resveratrol consumption may increase the poor bioavailability of resveratrol or otherwise potentiate its psychological effects. In this randomised, double-blind, placebo-controlled, parallel-groups study, a total of sixty adults aged between 18 and 30 years received either placebo or resveratrol for 28 d. On the 1st and 28th day of treatment, the performance of cognitively demanding tasks (serial subtractions, rapid visual information processing and 3-Back) (n 41 complete data sets) was assessed, alongside blood pressure (n 26) and acute (near-IR spectroscopy (NIRS)) and chronic (transcranial Doppler) measures of CBF (n 46). Subjective mood, sleep quality and health questionnaires were completed at weekly intervals (n 53/54). The results showed that the cognitive effects of resveratrol on day 1 were restricted to more accurate but slower serial subtraction task performance. The only cognitive finding on day 28 was a beneficial effect of resveratrol on the accuracy of the 3-Back task before treatment consumption. Subjective ratings of ‘fatigue’ were significantly lower across the entire 28 d in the resveratrol condition. Resveratrol also resulted in modulation of CBF parameters on day 1, as assessed by NIRS, and significantly increased diastolic blood pressure on day 28. Levels of resveratrol metabolites were significantly higher both before and after the day’s treatment on day 28, in comparison with day 1. These results confirm the acute CBF effects of resveratrol and the lack of interpretable cognitive effects.


Sign in / Sign up

Export Citation Format

Share Document