Modulation of baroreflex by varying insulin and glucose in conscious dogs

1990 ◽  
Vol 258 (3) ◽  
pp. R624-R633 ◽  
Author(s):  
D. E. Fitzovich ◽  
D. C. Randall
Keyword(s):  
Plasma Insulin ◽  
Nervous Activity ◽  
Time Derivative ◽  
Cardiovascular Responses ◽  
Left Ventricular ◽  
Carotid Occlusion ◽  
Immunoreactive Insulin ◽  
State Reduction ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid

We developed a conscious, chronically instrumented canine preparation (n = 5 dogs) in which insulin concentration was precisely controlled to study the effects of controlled variations of plasma insulin and glucose concentrations on cardiac responses to bilateral carotid occlusion and dobutamine. Endogenous insulin secretion was reduced to negligible levels using alloxan and then replaced by continuous, constant intravenous insulin infusion at a rate (0.625 +/- 0.115 U/h) sufficient to maintain fasting normoglycemia (85 +/- 9 mg/100 ml); plasma immunoreactive insulin (IRI) in this basal "normal insulin, normal glucose" (NI,NG) condition was 0.362 +/- 0.45 ng/ml (NS vs. prealloxan fasting concentration). A fivefold increase of IRI from NI,NG levels with normoglycemia maintained (5 x NI,NG) reduced (P less than 0.05) the maximal first time derivative of left ventricular pressure (LV dP/dtmax) from 3,010 +/- 62 to 2,398 +/- 91 (SE) mmHg/s but had no effect on LV dP/dtmax when plasma glucose was elevated to 298 +/- 25 mg/100 ml (5 x NI,HG). The LV dP/dtmax increase during bilateral carotid occlusion (BCO) in the NI,NG state of 124 +/- 17 mmHg/s was significantly reduced (P less than 0.05) in the 5 x NI,HG state to 58 +/- 18 mmHg/s but was not altered in the 5 x NI,NG state. Reduction of plasma insulin to one-fifth of the normal fasting level had no effect on basal cardiac function or the responses to BCO. There were no other statistically significant effects of insulin or glucose concentration on cardiovascular responses to BCO or to infusion of dobutamine. Our data indicate that physiologically realistic variations in plasma IRI and glucose concentrations interact and may modulate cardiovascular responses to changes in autonomic nervous activity, even though previously reported effects of pharmacological doses of insulin were not observed.

Systemic responses to carotid occlusion in the anesthetized rat

1992 ◽  
Vol 72 (4) ◽  
pp. 1247-1254 ◽  
Author(s):  
J. M. Lash ◽  
E. Haase ◽  
A. A. Shoukas
Keyword(s):  
Pressor Response ◽  
Cardiovascular Responses ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Carotid Occlusion ◽  
Male Rats ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Common Carotid Artery ◽  
Bilateral Carotid ◽  
Common Carotid Artery Occlusion

We evaluated the effects of four standard anesthetization regimens on the systemic cardiovascular responses to bilateral common carotid artery occlusion in 28 adult male rats. Rats were randomly assigned to anesthesia groups: thiopental sodium (PT; 100 mg/kg ip), alpha-chloralose (CH; 100 mg/kg iv), ketamine hydrochloride plus acepromazine (KA; 135 mg/kg and 1.5 mg/kg sc), and pentobarbital sodium (PB; 50 mg/kg ip). PT and PB animals had similar baseline heart rates (HR; 333 and 345 beats/min, respectively) and arterial pressures (MAP; 126 and 118 mmHg, respectively), whereas both were lower in CH and KA (314 and 288 beats/min, 92 and 85 mmHg). During bilateral carotid occlusion, PT demonstrated the largest change in MAP (dMAP; +27 mmHg) but the smallest change in HR (dHR; +8 beats/min). CH and PB demonstrated similar dHR (+24 and +16 beats/min) and dMAP (+20 and +19 mmHg). KA demonstrated a significant dHR (+14 beats/min), but the average dMAP was not statistically significant (+3 mmHg). Therefore, carotid occlusion in rats anesthetized with PT, PB, or CH consistently elicits a systemic arterial pressor response comparable with that reported for conscious animals. When the magnitude and stability of baseline HR and MAP are also considered, PT and PB anesthetization seem to be the most reliable for evaluation of the carotid occlusion pressor response in rats.

Effect of myocardial ischemia on hemodynamic response to carotid occlusion

1989 ◽  
Vol 256 (3) ◽  
pp. H672-H680
Author(s):  
G. E. Billman ◽  
D. H. Marsh
Keyword(s):  
Contractile Function ◽  
Left Ventricular Pressure ◽  
Hemodynamic Response ◽  
Left Ventricular ◽  
Vagal Afferents ◽  
Carotid Occlusion ◽  
Aortic Blood Flow ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Bilateral Vagotomy

Fourteen mongrel dogs were anesthetized and instrumented to measure arterial pressure (AP), left ventricular pressure (LVP), aortic blood flow, and heart rate (HR). Hydraulic occluders were placed around the left anterior descending (LAD, n = 9) and left circumflex (LCC, n = 14) coronary arteries. A bilateral carotid occlusion (BCO) was made before and during either anterior (LAD occlusion) or posterior (LCC occlusion) ischemia. Posterior ischemia significantly (P less than 0.01) reduced the BCO-induced increases in mean AP (by 44.3 +/- 7.3%), systolic LVP (by 65.5 +/- 6.9%), first derivative of LVP (dLVP/dt, by 95.7 +/- 44.3%), and aortic resistance (by 117.7 +/- 26.9%). In contrast, anterior ischemia failed to alter significantly the hemodynamic response to BCO. Bilateral vagotomy attenuated or eliminated many of the effects of posterior ischemia on the BCO response. In fact, the change in aortic resistance was no longer affected by the ischemia and increased to the same extent, as noted during the control BCO. However, mean AP (38.7 +/- 6.8%), systolic LVP (40.3 +/- 8.7%), and dLVP/dt (62.4 +/- 11.0%) remained significantly reduced when compared with the control (no coronary occlusion) response. These data suggest that 1) posterior ischemia elicits a greater reduction in the BCO response than anterior ischemia, and 2) vagal afferents as well as depression of contractile function may both contribute to the BCO response inhibition noted during posterior ischemia.

scholarly journals Severe autogenously fecal peritonitis in Wistar rats with permanent bilateral carotid occlusion. Response to intra peritoneal moxifloxacin combined with dexamethasone

2014 ◽  
Vol 29 (2) ◽  
pp. 76-81 ◽  
Author(s):  
Maria Cecília Santos Cavalcanti Melo ◽  
Diego Nery Benevides Gadelha ◽  
Thárcia Kiara Beserra Oliveira ◽  
Carlos Teixeira Brandt
Keyword(s):  
Wistar Rats ◽  
Carotid Occlusion ◽  
Fecal Peritonitis ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid

Constriction of lymphatics by catecholamines, carotid occlusion, or hemorrhage

1988 ◽  
Vol 255 (3) ◽  
pp. H514-H524
Author(s):  
J. M. Dabney ◽  
M. J. Buehn ◽  
D. E. Dobbins
Keyword(s):  
Lymphatic Vessel ◽  
Perfusion Pressure ◽  
Sympathetic Nerves ◽  
Carotid Occlusion ◽  
Central Venous ◽  
Lymphatic Function ◽  
Hemorrhagic Hypotension ◽  
Arterial Blood ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid

Regulation of lymphatics by sympathetic nerves or hormones seems probable. To elucidate this, we perfused a lymphatic vessel in the paw of the anesthetized dog while measuring lymphatic perfusion pressure. We studied the effects of norepinephrine, epinephrine, hemorrhage, and carotid occlusion on lymphatic pressure. Blood was pumped to the forelimb via the brachial artery. Cannulas were placed to measure systemic, central venous, and forelimb vascular pressures. Catecholamines, whether added to the lymphatic perfusate or infused into the forelimb arterial blood, and bilateral carotid occlusion significantly increased lymphatic perfusion pressure. Perfusion of prenodal lymphatics disconnected from downstream vessels and nodes indicated that this increase occurred primarily in prenodal lymph vessels. Hemorrhagic hypotension to 55 mmHg did not affect lymphatic pressure but reduction to 35 mmHg did. The increase in lymphatic pressure produced by epinephrine and norepinephrine was blocked by phentolamine. Increased lymphatic perfusion pressure subsequent to exogenous catecholamines, severe hemorrhagic hypotension, or bilateral carotid occlusion supports the possibility that lymphatic function is modulated by adrenergic mechanisms in physiological and/or pathophysiological states.

Effect of Bilateral Occlusion of Common Carotid Arteries on Cardiac Output and Oxygen Content of Arterial and Venous Blood in the Anesthetized Dog

1956 ◽  
Vol 185 (3) ◽  
pp. 483-486 ◽  
Author(s):  
Shirley H. Brind ◽  
Joseph R. Bianchine ◽  
Matthew N. Levy
Keyword(s):  
Cardiac Output ◽  
Oxygen Content ◽  
Venous Blood ◽  
Carotid Occlusion ◽  
Systemic Hypertension ◽  
Arterial Blood ◽  
Venous Oxygen Content ◽  
Bilateral Carotid Occlusion ◽  
Bilateral Carotid ◽  
Common Carotid Arteries

Changes in cardiac output, mean arterial blood pressure, hematocrit ratio, and arterial and venous oxygen content resulting from bilateral carotid occlusion were investigated. Cardiac output exhibited no significant alteration during endosinusal hypotension, and the systemic hypertension engendered was attributed to an increase in vasomotor tone. Arterial and venous oxygen content, as well as hematocrit ratio, increased significantly during the period of carotid occlusion. This increase was ascribed to splenic contraction evoked by carotid occlusion, since no comparable augmentation was observed when the splenic circulation was temporarily interrupted.

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