Left ventricular inotropic responses to stimulation of carotid body chemoreceptors in anaesthetized dogs.

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SUMMARY1. Dogs were anaesthetized with thiopentone sodium and a-chloralose and artificially ventilated. The carotid sinus regions were vascularly isolated and perfused with arterial or venous blood to stimulate the chemoreceptors. Left atrial receptors were stimulated by distending four balloons, three in the left pulmonary vein-atrial junctions and one in the left atrial appendage. Mean aortic pressure was held constant by means of a pressure control device. Atenolol and atropine (2-0 and 0(5 mg kg-', respectively), and gallamine triethiodide (3 0 mg kg-' h-1) were given I.v. Renal blood flow was measured by an electromagnetic flowmeter, glomerular filtration rate by creatinine clearance, urinary sodium by flame photometry and solute excretion by osmometry.2. In fifteen tests in eight dogs (in one dog responses of both left and right kidneys were determined), at a constant aortic pressure (AoP) of 92-0 + 32 mmHg, and carotid sinus pressure (CSP) of 95 0 + 2-0 mmHg, stimulation of left atrial receptors with balloon inflation resulted in significant increases in renal blood flow (RBF) by 8-3 + 0 9 from 255-0 + 14-6 ml min-(100 g kidney weight)-' (n = 9), in glomerular filtration rate (GFR) by 4-1 +0-6 from 21-2+ 19 ml min-' (100 g)-1, in filtration fraction (FF) by 0 04 + 0 003 from 0-20 + 0-01, in urine flow rate (V) by 0-08 + 0-02 from 0-33+0-05 ml min-1 (100 g)-1, in sodium excretion (UNaV) by 44+0-9 from 27-7 + 4-2,mol min-1 (100 g)-1, in osmolar excretion (UosmV) by 62-0+5-6 from 303 0+ 28-3 /tosmol min-(100 g)-1, and in a decrease in free water clearance (CH20) by 0 13+0-03 from -0-63+0-04 ml min-(100 g)-1. Left atrial pressure (LAP) and heart rate (HR) did not change significantly from 6-9 + 0-3 cmH2O, and 133-0 + 3-4 beats min-respectively.3. In fifteen tests in the same dogs, at a constant AoP of 95 0 + 3-3 mmHg and CSP of 96-0 + 2-2 mmHg, changing the carotid perfusate from arterial to venous blood to stimulate the carotid chemoreceptors resulted in significant decreases in RBF by 26*4+2X7 from 2580+ 14-9 ml mind (100 g)-1, in GFR by 5 4+0 9 from 20-8+ 1-7 ml min' (100 g)-', in FF by 0-03+0-001 from 0-12+0-01, in V by 0'15+0-02 from 0 35+0-06 ml min' (100 g)-', in UNaV by 15-5+ 1-9 from 28-7 + 4 8 /tmol min-(100 g)-1, in UosmV by 68 + 6-9 from 312-0 + 2941 aosmol min-(100 g)-1, and in an increase in CH20 by 0 17+0-03 from -0-65+0-04 ml min-' MS 9770 F. KARIM AND M. AL-OBAIDI (100 g)-'. LAP and HR did not change significantly from 67 +03 cmH2O and 130-0 + 3-3 beats min-respectively.4. In twelve tests in the same eight dogs, at a constant AoP of 95-0 + 3-1 mmHg and CSP of 97-0 + 25 mmHg, stimulation of left atrial receptors during venous perfusion of the carotid sinus regions (chemoreceptor stimulation) resulted in significant increases in RBF by 14-0+ 1 1 from 228-0+ 16-2 ml min-(100 g)-1, in GFR by 7-8+0 8 from 14-4+22 ml min-(100 g)-', in FF by 0-07+0{002 from 0-11+0'01, in V by 0-11+0-01 from 018+0'03mlmin-1 (100g)-', in UNaV by 7-2+1P0 from 10-7+±13/itmolmin1 (100 g)-1, in UosmV by 810+6-2 from 20...

Section: Discussionmentioning

confidence: 96%

Effects of left atrial receptor stimulation on carotid chemoreceptor‐induced renal responses in dogs.

Karim

Al-Obaidi

1992

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“…The responses were also unlikely to be the result of any inhibition by the venous blood of the carotid baroreceptor activity, because the heart rate response was a bradycardia and not a baroreceptor-induced tachycardia. The details of this method of stimulation of the carotid bodies have been described elsewhere (Hainsworth, Karim & Sofola, 1979;Karim, Hainsworth, Sofola & Wood, 1980). That the reflex originated in the carotid bodies was indicated by the fact that it was abolished by crushing them.…”

Section: Discussionmentioning

confidence: 99%

The effects of stimulating carotid chemoreceptors on renal haemodynamics and function in dogs.

Karim

Poucher

Summerill

1987

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SUMMARY1. Dogs were anaesthetized with chloralose and artificially ventilated. The carotid chemoreceptors were stimulated by changing the perfusion ofvascularly isolated carotid sinus regions from arterial to venous blood. The mean carotid sinus pressure and the mean arterial blood pressure were held constant at 124 + 3 and 122 + 3 mmHg, respectively. Both vagosympathetic trunks were sectioned in the neck and propranolol (17 ,tg kg-' min-' i.v.) and gallamine triethiodide (0-2-2 0 mg kg-' 30 min-' i.v.) were infused. Renal blood flow was measured by an electromagnetic flow probe, glomerular filtration rate by creatinine clearance, sodium excretion by flame photometry and solute excretion by osmometry.2. In sixteen tests in thirteen dogs perfusion of the carotid sinus regions with venous blood resulted in significant decreases in renal blood flow from 271+24 to 198 + 21 ml min-1 100 g-1 renal mass; glomerular filtration rate from 41-0 + 4-8 to 22-1 + 3-1 ml min-' 100 g-; filtration fraction from 0-25 + 0-02 to 0 19 + 0-02; urine flow from 0-48 + 1-0 to 0-21 + 0-03 ml min-1 100 g-'; sodium excretion from 18-1 + 4-1 to 12-9 + 4-2 #smol min-' 100 g-; and osmolar excretion 327 + 42 to 171 + 26 posmol min-1 100 g-'. The right atrial pressure did not change significantly from 4-6 + 1P2 cmH20.3. In seven dogs, tying renal sympathetic nerves abolished all the responses except that of sodium excretion which was now reversed; sodium excretion increased from 68+19 to 116 + 38 /tmol min-1 00 g-1 without significant change in right atrial pressure from 7-4 + 1-9 cmH2O. Crushing the carotid bodies, however, abolished all the responses.4. The results show that carotid chemoreceptor stimulation can cause significant reflex effects on renal haemodynamics and function which are mediated via renal sympathetic nerves. They also show that the chemoreceptor stimulation can cause natriuresis in the absence of haemodynamic changes, in the denervated kidney, presumably via a humoral factor.

“…The distal ends of both common carotid arteries were cannulated and both carotid bifurcations which had been isolated vascularly, were perfused with blood from the arterial reservoir (R2) or from the inferior vena cava as described by Hainsworth, Karim & Sofola (1979) and Karim, Hainsworth, Sofola & Wood (1980b Figure. Arterial blood is drawn out from the left femoral artery and passed into R2 which controls and maintains constant the pressure (c.p.) in the systemic circuit.…”

Section: Methodsmentioning

confidence: 99%

Effects of combined carotid chemoreceptor and atrial receptor stimulation on renal blood flow in anaesthetized dogs.

Kappagoda¹,

Karim²,

MacKay³

1983

Self Cite

SUMMARY1. In dogs anaesthetized with chloralose and artificially ventilated, carotid chemoreceptors were stimulated by changing the perfusate of the vascularly isolated carotid bifurcations from arterial to venous blood. Left atrial receptors were stimulated by distending balloons in two pulmonary vein-left atrial junctions and in this left atrial appendage.2. The left renal blood flow was measured by an electromagnetic flow meter at a constant systemic (renal) arterial pressure in preparations in which heart rate changes were prevented by administration of propranolol hydrochloride (0-5 mg kg-') and atropine sulphate (0-4 mg kg-'). Muscular movement was prevented by gallamine triethiodide (0-2 mg kg-').3. Stimulation of left atrial receptors resulted in a significant increase (P < 0-001)in renal blood flow of 5-6 + 0'88 ml min' 100 g-renal mass from a control of 223 ml min' 100 g-' renal mass. The responses were abolished by cooling the cervical vagus nerves to 6-8 'C. 4. Stimulation of carotid chemoreceptors, by perfusion of the carotid bifurcations by venous blood, caused a decrease in renal blood flow of 20+ 6-9 ml min' 100 g-' renal mass from 224 ml min' 100 g-' renal mass. Stimulation of left atrial receptors during venous perfusion of carotid chemoreceptors resulted in an increase in renal blood flow of 10-9 + 1-82 ml min' 100 g-1 renal mass from 208 ml min' 100 g-1 renal mass.5. These results show that atrial receptors and chemoreceptors can interact in their effects on renal blood flow.