Cardiovascular Responses to Pressure Alterations Within the Urinary Tract of the Dog

1958 ◽  
Vol 193 (2) ◽  
pp. 260-262 ◽  
Author(s):  
Leonard B. Berman ◽  
John C. Rose

Acute changes in pressure within the bladders and renal pelves of intact, anesthetized dogs were produced by the infusion of normal saline. Direct and continuous observations were made of aortic, right ventricular and intravesical or intrapelvic pressures, as well as the electrocardiogram. No significant cardiovascular alterations were observed during acute and extreme increments and decrements of intraluminal urinary tract pressures. These results are in marked contrast with those seen in reptilia and amphibia.

1962 ◽  
Vol 202 (2) ◽  
pp. 249-252 ◽  
Author(s):  
Santiago A. Pereda ◽  
John W. Eckstein ◽  
François M. Abboud

Cardiovascular responses to intravenous administration of insulin were studied in lightly anesthetized dogs treated with a neuromuscular blocking agent. An early transient pressor response was observed. This abrupt increase in arterial pressure appeared 2–9 min after insulin was given. It was accompanied by increases in cardiac output and right atrial pressure. It occurred in the presence of hyperglycemia and in the absence of hypoglycemia. It was not altered by glucagon but it could be antagonized by ganglionic and adrenergic blocking drugs and by pentobarbital. The response could be produced when insulin was given in the carotid artery in doses that caused no effect when injected in a systemic vein. The experiments suggest that insulin may have a direct action on the brain.


1991 ◽  
Vol 261 (3) ◽  
pp. H720-H727 ◽  
Author(s):  
F. L. Belloni ◽  
T. H. Hintze

The effects of the ATP-sensitive K(+)-channel blocker glibenclamide on the cardiovascular responses to adenosine in dogs were determined. Adenosine (0.01-20 mumol/kg iv) caused coronary vasodilatation, arterial hypotension, and bradycardia in dogs with either combined beta-adrenergic and muscarinic receptor blockade or with bilateral cervical vagotomy plus beta-adrenergic receptor blockade. The 50% effective dose for adenosine-induced coronary dilatation was increased from 0.13 +/- 0.04 mumol/kg in the control state to 1.1 +/- 0.5 mumol/kg after 2 mg/kg of glibenclamide (P less than 0.001). Adenosine at 5 mumol/kg reduced heart rate by 19 +/- 5% from a baseline of 158 +/- 6 beats/min in five anesthetized dogs. After glibenclamide (10 mg/kg), this dose of adenosine failed to cause a significant change in heart rate. The arterial hypotensive effects of adenosine were also attenuated by glibenclamide. Thus glibenclamide inhibited adenosine-induced bradycardia, hypotension, and coronary dilatation. On the other hand, glibenclamide did not affect the reductions in heart rate caused by vagus nerve stimulation. The mechanism of this adenosine antagonism is not known but, in the case of bradycardia, it does not appear to involve any of the steps shared in common by both adenosine-induced and vagal responses of the sinoatrial node.


2019 ◽  
Vol 6 (2) ◽  
pp. 45-50
Author(s):  
Sujita Manandhar ◽  
Kishor Manandhar

Introductions: Catheter-related bladder discomfort (CRBD) is common in patients with urinary catheterization. Centrally acting intravenous opioid like Tramadol inhibits detrusor activity and incidence of CRBD. Present study aims to analyze efficacy of intravenous (IV) Tramadol in prevention of CRBD in patients undergoing upper urinary tract surgery. Methods: Adult patients undergoing elective open upper urinary tract surgeries at Bir Hospital, National Academy of Medical Sciences (NAMS), Nepal, over a period of six months, requiring urinary catheterization were randomly divided into Control (C) and Tramadol (T) groups. After general anesthesia, patients in T-group received IV Tramadol 1.0 mg/kg and C-group received normal saline 30 minutes before extubation. In post-operative ward, CRBD was graded as mild, moderate or severe at 0, 1, 2 and 6 hours. Post-operative Ramsay sedation score and nausea vomiting were compared in two groups. Results: There were total 70 patients, 35 in each of groups-T and C. Incidence of CRBD in T-group was significantly low compared to the C-group at all points of evaluation (p<0.05). Postoperative sedation score, analgesic requirement and nausea vomiting were not significantly different in two groups. Conclusions: Intravenous Tramadol administered before extubation in upper urinary tract surgery reduces the incidence of CRBD.


1973 ◽  
Vol 86 (6) ◽  
pp. 788-797 ◽  
Author(s):  
David E Fixler ◽  
Joseph P Archie ◽  
Daniel J Ullyot ◽  
Julien I.E Hoffman

1984 ◽  
Vol 62 (7) ◽  
pp. 769-774 ◽  
Author(s):  
C. E. King ◽  
S. M. Cain ◽  
C. K. Chapler

To compare with earlier studies of anemic hypoxia obtained by hemodilution, O2 carring capacity was decreased by carbon monoxide (CO) hypoxia. Arterial O2 content was reduced either 50% (moderate CO) or 65% (severe CO). In two groups of anesthetized dogs (moderate and severe CO) hindlimb innervation remained intact while in a third group (moderate CO) the hindlimb was denervated. Measurements were obtained prior to and at 30 and 60 min of CO hypoxia. Cardiac output was elevated at 30 min of CO hypoxia in all groups (p < 0.01) and in the severe CO group at 60 min (p < 0.01). Hindlimb blood flow remained unchanged during CO hypoxia in the intact groups. In the denervated group, hindlimb blood flow was greater (p < 0.05) than that in the intact groups throughout the experiment. A decrease in mean arterial pressure (p < 0.01) in all groups was associated with a fall in total resistance (p < 0.01). Hindlimb resistance remained unchanged during moderate CO hypoxia in the intact group but increased (p < 0.05) in the denervated group. In the severe CO group hindlimb resistance was decreased (p < 0.05) at 60 min. The results indicate that the increase in cardiac output during CO hypoxia was directed to nonmuscle areas of the body and that intact sympathetic innervation was required to achieve this redistribution.


1964 ◽  
Vol 206 (6) ◽  
pp. 1279-1280 ◽  
Author(s):  
Skoda Afonso ◽  
George G. Rowe ◽  
Cesar A. Castillo ◽  
Charles W. Crumpton

The present study relates to metabolic, and systemic and coronary hemodynamic effects of methylene blue in five anesthetized dogs (group I) and of electrically induced tachycardia in ten dogs pretreated with methylene blue (group II). In group I body oxygen consumption increased slightly. In group II coronary blood flow, cardiac metabolic rate for oxygen, and right ventricular work increased significantly while coronary vascular resistance decreased significantly. The observed pattern of changes is not different from that produced by induced tachycardia in untreated dogs. Methylene blue does not alter the usual response of coronary circulation to cardiac acceleration.


1956 ◽  
Vol 186 (1) ◽  
pp. 85-88
Author(s):  
Paul K. Mooring ◽  
John Rathe ◽  
Walter S. Root

Intravenous injection of Adrenalin (1 ml of 1:300,000–1:25,000) into 10 normal, anesthetized (Nembutal) dogs produced an average increase in mean arterial pressure which amounted to about 25 at the lower and 100 mm Hg at the higher doses. Essentially the same responses were shown by seven anesthetized, vagotomized dogs and five anesthetized, vagotomized animals in which the carotid regions were denervated. Eight anesthetized dogs with spinal cords cut between C8 and T1 showed after Adrenalin injection an average percentage increase in mean arterial pressure which was some threefold greater than that found in normal, anesthetized animals. This difference was increased still further by bilateral section of the vagi in eight spinal dogs. Section of the spinal cord one or two segments below C8 to T1 (4 dogs) decreased the response to Adrenalin. The increase in mean arterial pressure induced by the intravenous injection of Adrenalin was greater in six spinal dogs (C8 to T1) anesthetized with Nembutal than in two similar unanesthetized animals. Acute changes in plasma volume did not influence the magnitude of the blood pressure response to Adrenalin shown by four high spinal animals.


2011 ◽  
Vol 300 (6) ◽  
pp. H1983-H1989 ◽  
Author(s):  
Cinzia Perrino ◽  
Giuseppe Gargiulo ◽  
Gianluigi Pironti ◽  
Anna Franzone ◽  
Laura Scudiero ◽  
...  

Exercise adaptations result from a coordinated response of multiple organ systems, including cardiovascular, pulmonary, endocrine-metabolic, immunologic, and skeletal muscle. Among these, the cardiovascular system is the most directly affected by exercise, and it is responsible for many of the important acute changes occurring during physical training. In recent years, the development of animal models of pathological or physiological cardiac overload has allowed researchers to precisely analyze the complex cardiovascular responses to stress in genetically altered murine models of human cardiovascular disease. The intensity-controlled treadmill exercise represents a well-characterized model of physiological cardiac hypertrophy because of its ability to mimic the typical responses to exercise in humans. In this review, we describe cardiovascular adaptations to treadmill exercise in mice and the most important parameters that can be used to quantify such modifications. Moreover, we discuss how treadmill exercise can be used to perform physiological testing in mouse models of disease and to enlighten the role of specific signaling pathways on cardiac function.


Sign in / Sign up

Export Citation Format

Share Document