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Biomedical subjects

K L Goetz

Publications and source records attributed to K L Goetz.

At least 55 records · Page 3Linked to original sources
PubMed1985

Aortic baroreceptor discharge during nonhypotensive hemorrhage in anesthetized dogs.

We tested the hypothesis that arterial baroreceptor discharge remains constant during nonhypotensive hemorrhage. Aortic baroreceptor activity was recorded from anesthetized dogs during slow, continuous hemorrhage until 24 ml blood/kg body wt had been removed. The relationship between simultaneously recorded hemodynamic variables and single-unit aortic baroreceptor activity was evaluated by a unique computer program that sampled all variables 500 times/s and analyzed data from each consecutive cardiac cycle throughout the entire experiment. In three hemorrhages performed on three dogs, aortic blood pressure did not decrease during the experiment (nonhypotensive hemorrhage), but aortic nerve activity decreased progressively when data from individual cardiac cycles having identical mean aortic pressures were compared. Reduced baroreceptor activity correlated closely with progressive reductions in pulse pressure. In other hemorrhages, mean aortic pressure decreased by a variable amount; decreases in recorded single-unit baroreceptor activity occurred during each of these hemorrhages also. In summary, hemorrhage consistently caused decreases in the activity of aortic baroreceptors regardless of whether mean aortic pressure decreased or remained constant during hemorrhage. We conclude that experimental techniques employing nonhypotensive hemorrhage do not provide an effective method for selectively studying reflexes from cardiopulmonary receptors in the absence of changes in arterial baroreceptor input.

Action Potentials↗
PubMed1985

Factors influencing the secretion of vasopressin into cerebrospinal fluid.

Vasopressin (VP) has been found in the cerebrospinal fluid (CSF) of several species of animals. Although it is known that hemorrhage, hypertonicity of body fluid, hypoxia, and hypercapnia all increase VP in plasma, little is known regarding the stimuli that cause the secretion of VP into the CSF. We therefore performed several studies to examine whether stimuli capable of increasing plasma levels of VP can also increase VP in the CSF of anesthetized dogs. We found that hemorrhage, intracerebroventricular infusion of hypertonic artificial CSF, hypoxia, and hypercapnia all produced increases in the concentration of VP in plasma and in CSF, but the time courses and the magnitude of the increases in the two compartments were different. In addition, an i.v. infusion of hypertonic saline or of hydrochloric acid produced an increase in plasma VP without significantly changing CSF VP. Thus, although the secretion of VP into plasma and CSF may be influenced by the same stimuli, changes in one compartment do not necessarily correlate with changes in the other. Taken together, our results are consistent with the hypothesis that the plasma and CSF VP may derive from different sources.

Acidosis↗
PubMed1984

Vasopressin in plasma and cerebrospinal fluid of dogs during hypoxia or acidosis.

Hypoxia and hypercapnia have been shown to cause an increase in the concentration of vasopressin in plasma, but their effects on vasopressin in cerebrospinal fluid (CSF) are not known. In addition, the effect of metabolic acidosis on plasma and CSF vasopressin has not been reported. In this study, plasma and CSF vasopressin levels were measured in anesthetized dogs subjected to either hypoxia, hypercapnia, or metabolic acidosis. Rate and depth of respiration were closely regulated with the aid of muscle paralysis and mechanical ventilation. Vasopressin increased markedly in both plasma and CSF during severe hypoxia (10% O2) and during hypercapnia (10% CO2) but did not change during either mild (15% O2) or moderate (12.5% O2) hypoxia. Although mild hypoxia by itself did not affect either plasma or CSF vasopressin, it did potentiate the increase in plasma and CSF vasopressin that was induced by severe hypercapnia, thus suggesting that hypoxia and hypercapnia may exert synergistic effects on vasopressin secretion. Metabolic acidosis produced by slow intravenous infusion of 1 N hydrochloric acid decreased arterial pH to values comparable to those induced by hypercapnia and increased vasopressin in plasma; CSF vasopressin was unchanged. These results are consistent with the concept that the source of vasopressin secreted into plasma may be different from that secreted into CSF.

Acidosis↗
PubMed1984

Cardiac receptor influences on the plasma osmolality-plasma vasopressin relationship.

Changes in blood volume are capable of altering the relationship between plasma osmolality (Posmol) and plasma arginine vasopressin (PAVP), presumably via a reflex elicited from cardiovascular receptors, but the precise location of the receptors involved in this response has not been established. Because cardiac receptors are capable of influencing AVP secretion, their specific effect was examined by producing volume changes in cardiac-denervated (CD) dogs and comparing the Posmol-PAVP relationship in these dogs with data from comparable experiments on sham-operated control dogs (cardiac-sham, CS). Posmol was increased by water deprivation for 96 h (volume depletion) and also by administration of hypertonic saline for 2 h (volume expansion). The slope of the regression line describing the Posmol-PAVP relationship in CS control dogs was steeper (P less than 0.01) during volume depletion (0.390) than it was during volume expansion (0.228), thus suggesting that volume depletion had enhanced and volume expansion had inhibited the secretion of AVP. In contrast, the slope of the regression line delineating the Posmol-PAVP relationship in CD dogs was essentially the same during volume depletion (0.288) as it was during volume expansion (0.291). It would seem that most, if not all, of the volume influences on the Posmol-PAVP relationship are mediated via reflex effects elicited by cardiac receptors.

Animals↗
PubMed1984

Cardiovascular and renin responses to vanadate in the conscious dog: attenuation after calcium channel blockade.

The effects of vanadate on cardiovascular function and on the secretion of renin and vasopressin were investigated by infusing sodium orthovanadate (0.32 mu mole/kg X min) intravenously into five conscious dogs. Vanadate caused significant increases in mean arterial pressure, total peripheral resistance, pulmonary arterial pressure, and cardiac output. These data illustrate that the hemodynamic effects of vanadate in the conscious dog are similar to those of the anesthetized dog but that minor differences do exist. Vanadate significantly suppressed plasma renin activity, but plasma vasopressin was unchanged. The effects of vanadate also were investigated in the same dogs on another day after administration of the calcium channel blocker, verapamil (0.3 mg/kg bolus + 0.01 mg/kg X min). After calcium channel blockade, the increases in arterial pressure and pulmonary arterial pressure induced by vanadate were attenuated, and cardiac output did not increase. Calcium channel blockade also prevented the vanadate-induced decrease in plasma renin activity. These data suggest that the cardiovascular and humoral alterations produced by vanadate in the conscious dog are at least partially mediated by changes in intracellular calcium.

Animals↗
PubMed1984

Comparative effects of cardiac receptors and sinoaortic baroreceptors on elevations of plasma vasopressin and renin activity elicited by haemorrhage.

Increases in plasma vasopressin and renin activity that occur in response to haemorrhage have been attributed in part to reflex effects from cardiac receptors and sinoaortic baroreceptors, but the relative importance of these different receptors in causing humoral changes during haemorrhage in conscious dogs has not been reported. We investigated this question by hemorrhaging 6 sham-operated (SO), 6 cardiac-denervated (CD), 4 sinoaortic-denervated (SAD), and 4 combined sinoaortic and cardiac-denervated (SACD), conscious dogs. Blood was removed at a rate of 0.9 ml/kg X min. Plasma vasopressin and renin samples were taken during a control period and after 10, 20, and 30 ml/kg of blood had been removed. Results (mean +/- SE) are shown in the tables below. (table; see text) These experiments illustrate that: resting plasma levels of vasopressin and renin in conscious dogs are unaffected by the denervation procedures used in these experiments, the increase in plasma vasopressin that occurs during haemorrhage is mediated largely via cardiac receptors, with a considerably smaller contribution from the sinoaortic baroreceptors, during moderately severe haemorrhage (30 ml/kg) vasopressin secretion can be increased by a mechanism independent of sinoaortic and cardiac reflexes, the increase in plasma renin activity that occurs during haemorrhage is not dependent upon either cardiac or sinoaortic reflexes.

Animals↗
PubMed1983

Arterial baroreceptors have minimal physiological effects on adrenal medullary secretion.

The influence of arterial baroreceptors on secretion of catecholamines from the adrenal medulla was evaluated by several methods. Conscious mongrel dogs with surgically denervated hearts were hemorrhaged until an estimated 16% of their blood volume had been removed. On a separate day they were anesthetized and their blood pressure was lowered with intravenous nitroglycerin. Neither of these maneuvers produced appreciable increases in heart rate in these dogs. In contrast, in a group of sham-operated control dogs, hemorrhage induced a mean increase in heart rate of 20 beats/min (P less than 0.05), and nitroglycerin-induced hypotension induced an increase of 50 beats/min (P less than 0.05). In a separate group of conscious dogs with aortic arch denervation but intact cardiac nerves, occlusion of the common carotid arteries for 5 min increased blood pressure and heart rate significantly but elicited only small, insignificant increases in plasma epinephrine and norepinephrine; the peak concentration of epinephrine achieved was considerably less than the amount necessary to cause appreciable effects on blood pressure and heart rate as determined in another experiment by infusing varying amounts of epinephrine into conscious, cardiac-denervated dogs. We conclude that the arterial baroreceptor reflex, within the range of activity likely to occur during most physiological and pathophysiological adjustments in the conscious dog, exerts only minimal effects on the secretion of catecholamines from the adrenal medulla.

Adrenal Medulla↗
PubMed1983

Vasopressin and renin responses to hemorrhage in conscious, cardiac-denervated dogs.

We measured plasma arginine vasopressin (AVP) and plasma renin activity (PRA) during continuous hemorrhage in cardiac-denervated and sham-operated conscious dogs. Hemorrhage produced comparable decreases in aortic pressure, cardiac output, stroke volume, pulmonary arterial pressure, and left and right atrial pressures in each group of dogs. After 10 ml blood/kg body wt had been removed, AVP was increased in sham-operated dogs (P less than 0.05) but not in cardiac-denervated dogs. After 20 and 30 ml blood/kg body wt had been removed, AVP was increased in all dogs, but the response was markedly attenuated in cardiac-denervated dogs. Hemorrhage at 10 and 20 ml/kg caused comparable increases in PRA in each group of dogs. However, at 30 ml/kg hemorrhage the increase in PRA was significantly higher in cardiac-denervated dogs than in sham-operated dogs. Our results suggest that cardiac receptors play a dominant role in mediating the release of AVP during hemorrhage in conscious dogs. In contrast, we found no evidence for a dominant role of cardiac receptors in mediating renin secretion during hemorrhage.

Animals↗
PubMed1983

Arterial baroreceptor reflex control of heart rate in two species of turtle.

Attempts were made to stimulate an arterial baroreceptor reflex in anesthetized and conscious pond turtles. In turtles anesthetized with either alpha-chloralose or pentobarbital, occlusion of the ascending or descending aortas produced no reflex heart rate (HR) changes. In pentobarbital-anesthetized turtles, direct electrical or mechanical stimulation of potential baroreceptor sites along the central aortic arches and carotid arteries produced no significant changes in either HR or blood pressure (BP). Occlusion of the common carotid arteries also produced no HR or BP changes. Intravenously administered nitroglycerin lowered BP but caused no reflex tachycardia in anesthetized turtles. Phenylephrine and angiotensin elevated BP in the anesthetized turtle but caused no reflex bradycardia. In conscious turtles phenylephrine increased BP and nitroglycerin decreased BP. Neither response produced a statistically significant HR change, although HR tended to decrease transiently with phenylephrine and increase with nitroglycerin. These HR changes were abolished by atropine. Rapid intra-arterial infusion of 6% dextran transiently raised BP but caused no reflex bradycardia. These experiments suggest that cardiovascular regulation in the turtle is accomplished without a major contribution from arterial baroreceptor reflexes.

Anesthesia, General↗
PubMed1982

Effects of left atrial stretch in cardiac-denervated and intact conscious dogs.

We monitored cardiovascular and renal function in conscious dogs with surgically denervated hearts during two experimental procedures: 1) inflation of a balloon in the left atrium and 2) intravascular volume expansion. The results obtained were compared with results from identical experiments on sham-operated control dogs. Left atrial balloon inflation in the sham-operated dogs produced an increase in left atrial pressure, heart rate, urine flow, and sodium excretion; central venous pressure decreased. These changes were absent in the cardiac-denervated dogs. Infusion of 6% dextran in isotonic saline (16% of estimated blood volume) increased the heart rate significantly in the control dogs but not in the cardiac-denervated dogs; other hemodynamic measurements were comparable in the two groups. Urine flow and sodium excretion increased significantly in both the cardiac-denervated and control dogs; the responses did not differ significantly between the two groups. These experiments demonstrate that inflation of a balloon in the left atrium of a conscious dog elicits diuretic and natriuretic responses that are dependent on intact cardiac neural pathways, presumably specifically dependent on afferent neural impulses from left atrial receptors. On the other hand, an increase in circulating blood volume induced by the intravenous infusion of an isotonic, isoncotic solution elicits diuretic and natriuretic responses in the cardiac-denervated dog that are similar to the renal responses produced in a control dog. Thus, although cardiac receptors are capable of eliciting reflex changes in both hemodynamics and renal function, it is not clear what role they play in mediating the renal responses evoked by increases in blood volume.

Animals↗
PubMed1982

Reflexes elicited by acute stretch of atrial vs. pulmonary receptors in conscious dogs.

We measured hemodynamics and renal function in conscious dogs while partially obstructing blood flow at various sites within the thorax. Inflation of a balloon in the left atrium increased left atrial pressure (LAP) by 9 mmHg and caused a parallel increase in pulmonary arterial pressure (PAP); heart rate, arterial pressure, and total peripheral resistance increased; stroke volume and right atrial pressure decreased; and cardiac output remained unchanged. The increase in LAP was accompanied by a fourfold increase in urine flow and a threefold increase in sodium excretion. Plasma vasopressin (AVP) and renin activity (PRA) decreased. On the other hand, partial occlusion of the pulmonary veins or the main pulmonary artery produced similar increases in PAP without affecting LAP, systemic hemodynamics, renal function, or plasma AVP. Similarly, inflation of a balloon in the right atrium failed to alter renal function, plasma AVP, or PRA. Finally, constriction of the thoracic inferior vena cava decreased LAP and increased PRA. In summary, these data emphasize that inflation of a balloon in the left atrium of the conscious dog produces a composite response consisting of alterations in cardiovascular function, renal function, and circulating hormones. Moreover, our data indicate that the response is mediated by a reflex initiated from receptors located in the left atrium; we detected no evidence that receptors located in the pulmonary vasculature or right heart contribute to this response.

Animals↗
PubMed1977

Circuit for automatically zeroing aortic flow base line from electromagnetic flowmeter.

We describe an inexpensive circuit designed to correct base-line drift of electromagnetic flowmeters automatically when cardiac output is being measured. The circuit measures the flowmeter output voltage during a portion of each diastole when blood flow in the aorta is assumed to be zero. Any deviation of the flowmeter output voltage from zero during this time represents either base-line offset or drift. The output voltage obtained during zero flow conditions is stored throughout the next cardiac cycle and subtracted continuously from the flowmeter output during each beat, thus giving a beat-by-beat correction of any base-line drift.

Animals↗
PubMed1977

Effect of dipivalyl derivatives of catecholamines on cardiovascular function in the conscious dog.

Dipivalyl derivatives of epinephrine, norepinephrine and isoproterenol were injected intravenously into conscious dogs while cardiovascular variables were monitored. The dipivalyl compounds produced cardiovascular effects that were comparable to those produced by their respective parent catecholamines except that the responses had a delayed onset and a prolonged duration. The catecholamines were more potent than their derivatives; norepinephrine was 28 times, epinephrine 15 times and isoproterenol 1.7 times as effective as their respective dipivalyl derivatives. Alpha or beta adrenergic responses to the dipivalyl compounds were attenuated or abolished after alpha adrenergic blockade (phenoxybenzamine or phentolamine), or beta adrenergic blockade (propranolol), respectively, or combined alpha and beta blockade. Since other evidence indicates that the dipivalyl derivatives themselves are inactive, our results suggest that these compounds act as prodrugs that exert their cardiovascular effects only after they are biotransformed to catecholamines.

Adrenergic alpha-Antagonists↗