scholarly journals Spinal Sympathetic Reflexes in the Cat and the Pathogenesis of Arterial Hypertension

1974 ◽  
Vol 48 (s2) ◽  
pp. 259s-260s ◽  
Author(s):  
A. Malliani ◽  
F. Lombardi ◽  
M. Pagani ◽  
G. Recordati ◽  
P. J. Schwartz

1. In vagotomized anaesthetized cats with both common carotid arteries occluded, stretch of the thoracic aorta induced reflex increases in arterial blood pressure, heart rate and left ventricular dP/dtmax.. Similar responses were obtained in cats with spinal transection at the level of the first cervical nerve roots. 2. The hypothesis is advanced that sympathetic excitatory reflexes may contribute to the maintenance of hypertension through positive feedback.

1995 ◽  
Vol 78 (5) ◽  
pp. 1793-1799 ◽  
Author(s):  
M. Kamitomo ◽  
T. Ohtsuka ◽  
R. D. Gilbert

We exposed fetuses to high-altitude (3,820 m) hypoxemia from 30 to 130 days gestation, when we measured fetal heart rate, right and left ventricular outputs with electromagnetic flow probes, and arterial blood pressure during an isoproterenol dose-response infusion. We also measured the distribution of cardiac output with radiolabeled microspheres during the maximal isoproterenol dose. Baseline fetal arterial blood pressure was higher in long-term hypoxemic fetuses (50.1 +/- 1.3 vs. 43.4 +/- 1.0 mmHg) but fell during the isoproterenol infusion to 41.3 +/- 1.4 and 37.5 +/- 1.4 mmHg, respectively, at the highest dose. Heart rate was the same in both groups and did not differ during isoproterenol infusion. Baseline fetal cardiac output was lower in the hypoxemic group (339 +/- 18 vs. 436 +/- 19 ml.min-1.kg-1) due mainly to a reduction in right ventricular output. During the isoproterenol infusion, right ventricular output increased to the same extent in both hypoxemic and normoxic fetuses (approximately 35%); however, left ventricular output increased only approximately 15% in the hypoxemic group compared with approximately 40% in the normoxic group. The percent change in individual organ blood flows during isoproterenol infusion in the hypoxemic groups was not significantly different from the normoxic group. All of the mechanisms that might be responsible for the differential response of the fetal left and right ventricles to long-term hypoxia are not understood and need further exploration.


1981 ◽  
Author(s):  
G J Stewart ◽  
R G Schaub ◽  
R E Cartee

This study was done to correlate known cardiovascular responses to bradykinin (increased heart rate, lowered arterial blood pressure) with recently demonstrated endothelial damage and proposed venous dilation. Healthy dogs of mixed breed were used. Blood pressures and heart rate were monitored and recorded on a Narco physiograph. The diameter of a jugular vein was monitored with an ADR ultrasound machine using a 10 MHz probe with linear array of crystals and recorded on polaroid prints. Jugular veins and carotid arteries were removed and prepared for scanning electron microscopy after removal of blood and partial in situ fixation by whole body perfusion. The response of arterial pressure was dose dependent with no change at 6 ug/min, variable drop at 12 ug/min and 22-40% drop at 60 ug/min and above. Venous pressure increased in 1 dog but was unchanged in 4 others. The increase of heart rate paralled the drop in arterial blood pressure. The diameter of a jugular vein increased in 3 of 3 monitored dogs by 25, 33, 50% of baseline diameter (average increase 36%) with high (300 ug/min) bradykinin. Endothelial damage (microtears) occurred around 70-80% of branches, at some valves and on the main vessel occassionally. The tears were infiltrated with leukocytes and some red cells and platelets indicating that tearing occurred while blood was still circulating, i.e. before dissection for removal of vessels. Carotid arteries showed no tears. Dilation of arteries would be limited by their elastic layers (missing in veins). These observations show that venous dilation and endothelial tearing around side branches are part of the cardiovascular response to blood born bradykinin. They also show that venous dilation can be measured by ultrasound.


2008 ◽  
Vol 60 (2) ◽  
pp. 329-334 ◽  
Author(s):  
R.L. Linardi ◽  
J.C. Canola ◽  
C.A.A. Valadão

Cardiovascular effects due to intravenous (IV) xylazine (1.0mg/kg) or amitraz (0.1 or 0.4mg/kg) were evaluated in horses. Left ventricular function indexes, heart rate (HR), and cardiac output (CO) were measured by echocardiography. Second degree atrioventricular (AV) block was detected by electrocardiography. Invasive arterial blood pressure (AP) was also evaluated. All parameters were measured immediately before and during 60 minutes after drug injection. HR, CO, and second degree AV block were different between xylazine and amitraz-0.4mg/kg groups. Xylazine induced initial hypertension 10 minutes after injection, and hypotension was observed 30 minutes after amitraz-0.4mg/kg administration. Except for the second degree AV block which occurred only at five minutes, there was no change in the echocardiographic measurements after administration of amitraz-0.1mg/kg. Thus, amitraz-0.4mg/kg and xylazine (1.0mg/kg) induced similar cardiovascular side effects, but long-lasting action of amitraz-0.4mg/kg in the cardiovascular system was observed.


1971 ◽  
Vol 49 (5) ◽  
pp. 420-426 ◽  
Author(s):  
Paul F. Mercer

Renal function was studied in rats before and after section of the vagus nerves at the level of the common carotid arteries. In the control group of rats, sodium output and volume rate of urine flow increased following vagal section but glomerular filtration rate did not change. This response was not altered in other rats by desoxycorticosterone acetate, vasopressin, or renal nerve section. This response was similar to that seen in rats in which both common carotid arteries had been occluded. The natriuresis following bilateral vagotomy did not occur in rats in which the blood pressure was prevented from rising by means of aortic constriction. It is concluded that a natriuresis does occur following bilateral vagotomy. This natriuresis may be a result of the effect of arterial blood pressure following the vagotomy.


1996 ◽  
Vol 16 (3) ◽  
pp. 507-516 ◽  
Author(s):  
J. Michalicek ◽  
V. Gordon ◽  
G. Lambert

In cats anesthetized with α-chloralose, auto-regulation of blood flow (F) in the middle meningeal and common carotid arteries was assessed by bleeding and subsequently reinfusing the animals to achieve a 25% step reduction in mean arterial blood pressure (P), while maintaining the systolic blood pressure >80 mmHg. The integrity of autoregulation was assessed by calculating the gain factor Gf = 1 — [(ΔF/F)/(ΔP/P)]. Cats were examined intact, after hexamethonium (10 mg/kg), and after papaverine (6 mg/kg). Reduction of blood pressure of 25 to 60 mmHg produced equivalent drops in carotid blood flow ( Gf = 0.041 ± 0.34; mean ± standard deviation, n = 12). There were only small changes in flow in the middle meningeal artery during this procedure ( Gf = 0.91 ± 0.29). Hexamethonium did not block autoregulation in the middle meningeal artery ( Gf = 0.92 ± 0.13, n = 4). However, papaverine almost completely abolished the ability of the artery to autoregulate ( Gf = 0.10 ± 0.16, n = 7). The results suggest that the middle meningeal artery possesses an ability similar to that of the cortical circulation to autoregulate its blood flow through intrinsic, non-neuronal mechanisms. This will have important implications for the study of disturbances of dural arterial control in migraine and other headaches.


1979 ◽  
Vol 57 (s5) ◽  
pp. 209s-211s ◽  
Author(s):  
M. Pagani ◽  
M. Bergamaschi ◽  
A. Malliani

1. The effects of mechanical activation of aortic sympathetic sensory fibres have been studied in conscious dogs. 2. A cannula covered by an inflatable rubber balloon, previously implanted in the descending thoracic aorta, was used to stretch the aortic walls without obstructing blood flow. 3. Aortic stretch significantly increased mean arterial blood pressure and heart rate from control values in the absence of pseudo-affective reactions. 4. This response indicates that positive feedback sympathetic reflexes are operative in the conscious, fully innervated animal.


2017 ◽  
Vol 20 (6) ◽  
pp. 554-562 ◽  
Author(s):  
Einar Johard ◽  
Anna Tidholm ◽  
Ingrid Ljungvall ◽  
Jens Häggström ◽  
Katja Höglund

Objectives Sedative agents are occasionally used to enable echocardiographic examination when screening cats for heart disease, such as hypertrophic cardiomyopathy (HCM). Owing to their haemodynamic effects, sedative agents may alter echocardiographic measurements. The aim of the study was to evaluate the effects of the sedative combination dexmedetomidine and buprenorphine on echocardiographic variables, blood pressure (BP) and heart rate (HR) in healthy cats. Methods Fifty healthy, client-owned cats were prospectively recruited and included after physical examination. Cats were sedated intramuscularly with dexmedetomidine and buprenorphine, according to body weight. Blood pressure and HR measurements, echocardiographic and Doppler examinations were performed prior to sedation and repeated once cats had achieved acceptable sedation. Results Left ventricular internal diameter at end-diastole and systole, right ventricular internal diameter at end-diastole, left atrium (LA), pulmonary artery (PA) deceleration time, and systolic, diastolic and mean arterial blood pressure increased after sedation ( P ⩽0.022). Aortic and PA maximum velocity, fractional shortening, PA acceleration/deceleration time and HR decreased after sedation ( P <0.0001). Interventricular septum at end-diastole and systole, left ventricular posterior wall at end-diastole and systole, aortic diameter (Ao), left atrial/aortic diameter (LA/Ao) and pulmonic acceleration time did not change. Conclusions and relevance Blood pressure increased and HR decreased post-sedation. While wall thickness and LA/Ao were not affected by sedation, indices of LA and left ventricular size increased. Further studies are needed using cats with HCM to assess the effect of this sedative combination on HCM screening results.


1989 ◽  
Vol 256 (6) ◽  
pp. R1299-R1307
Author(s):  
A. J. Gorman ◽  
J. S. Chen

The purpose of the present study was to determine the effects of left ventricular (LV) outflow obstruction on plasma renin activity (PRA) and the contribution from afferent receptors located in the LV myocardium. In chronically instrumented, conscious dogs (n = 12), changes in PRA during a 15- to 20-mmHg decrease in arterial blood pressure were assessed during 1) intravenous infusions of nitroprusside (NP) alone and 2) infusions of NP while peak systolic LV pressure was elevated by acute ascending aortic occlusion (AAO + NP). Infusions of NP alone elicited significant increases in heart rate (24.9 +/- 5.1 beats/min; P less than 0.01) and in PRA [3.31 +/- 0.53 ng angiotensin I (ANG I).ml-1.h-1; P less than 0.01]. These were accompanied by decreases in both LV pressure (-13.8 +/- 3.6 mmHg; P less than 0.05) and left atrial pressure (-3.0 +/- 0.7 mmHg; P less than 0.05). During AAO + NP, LV pressure was elevated to an absolute level of 169.2 +/- 4.6 mmHg (+53.3 +/- 4.2 mmHg; P less than 0.001), whereas left atrial pressure was not changed. Both the hypotension-induced rise in PRA and tachycardia were significantly inhibited during AAO + NP (+0.59 +/- 0.29 ng ANG I.ml-1.h-1 and +6.3 +/- 4.6 beats/min, respectively; NS). The topical application of a local anesthetic in the region of the main coronary artery, sufficient to block the heart rate and arterial blood pressure responses to selective LV receptor stimulation by intracoronary veratridine (0.1-0.4 microgram/kg), resulted in significant increases in PRA and heart rate during AAO + NP.(ABSTRACT TRUNCATED AT 250 WORDS)


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