Rapid brain cooling in exercising dogs.

In alert, resting dogs, the brain is warmer than arterial blood in the common carotid artery. When dogs run, brain temperature drops, despite a sharp rise in carotid blood temperature, and is maintained 1.3 degrees C below carotid temperature during exercise. This brain cooling apparently results from countercurrent heat exchange between warm arterial blood supplying the brain and cool venous blood draining the nose and mouth. The heat exchange occurs in the arteries at the base of the brain, which form a rudimentary carotid rete in the dog, and is greatest during exercise, when respiratory evaporation is at a peak. In animals with a carotid rete, the brain is protected against overheating during the severe thermal stress of exercise.

Epinephrine enhancement of potassium-stimulated immunoreactive insulin secretion. Role of beta-adrenergic receptors.

Although epinephrine stimulates insulin release by activation of beta-adrenergic receptors, its dominant effect (mediated by stimulation of alpha-adrenergic receptors) is an inhibition of insulin secretion that is powerful enough to suppress the secretory activity of insulin's most potent stimulants. The insulin-secretory response to potassium chloride (KCl) infusion, however, is not suppressed; in fact, in ureter-ligated dogs simultaneously infused with 360 microgram. epinephrine per hour and 2 mEq. KCl per kilogram per hour, insulin release is actually increased about threefold (over controls). Propranolol blockade of beta-adrenergic receptors essentially abolishes the insulin response to KCl infusion, with and without epinephrine. It is unlikely that KCl, like epinephrine, provokes insulin release by direct stimulation of the beta-adrenergic receptors of the beta cells of the pancreatic islets. However, potassium in some way enhances the beta adrenergic (secretory) activity of epinephrine and blunts its usually dominant alpha-adrenergic (inhibitory) effect.

Cardiac output of dogs exercising in the heat.

We measured cardiac output and central blood temperature in five large dogs (27 kg mean body wt) running at 7.5 km/h for 30 min at two work loads and at low and high ambient temperature (Ta). Each animal ran on a level treadmill (O2 cost about 4 times that of resting) at 25 and 35 degrees C Ta and at a 20% slope (O2 cost about 10 times that of resting) at 25 and 35 degrees C Ta. Cardiac output (CO) was the same at 15 and 30 min of exercise at both work loads and both TaS. CO was higher at 35 degrees C Ta at both work loads. Blood temperature rose 0.6 degrees C during exercise on the level treadmill at 25 degrees C and stabilized after the 15th min of exercise. On the level treadmill at 35 degrees C, blood temperature increased by 1.9 degrees C after 30 min. During 30 min of running at 20% slope, blood temperature increased by 3.2 degrees C at 25 degrees C and by 4.6 degrees C at 35 degrees C. At these work loads the dog is able to increase CO during exercise in the heat. This response is similar to that of humans doing moderate exercise in the heat but is in contrast to that of humans doing heavy exercise in the heat, in whom CO shows a drop or no change compared with cool conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

An exchangable intra-atrial balloon device.

An exchangeable atrial balloon device is described. It consists of an outer guide and a latex Foley urinary retention catheter. The guide is sutured into the atrial appendage and brought out through the chest wall. The advantages of the device are discussed.

K transfer in ureter ligated dogs loaded with KCl.

In control ureter ligated dogs infused with 2 mEq KCl/kg.h until prelethal electrocardiographic changes of hyperkalemic cardiotoxicity appear, a kaluresis independent K homeostatic mechanism delays the development of hyperkalemia by transferring some 55% of administered K to intracellular fluid. In preparations with cervical trunk vagotomy the proportion increases to about 70%; but not if the adrenals are simultaneously removed or denervated. A dosage of atropine that crosses the blood-brain barrier is an exact substitute for cervical vagotomy. Our findings suggest that ureter ligated K loaded dogs, ureteral and/or renal afferent vagal fibres to the brain release a "muscarinic" neurotransmitter(s) that modulated neural traffic in rami of splanchnic nerves to the adrenal medulla.

Left atrial receptor inhibition of cardiac efferent vagal activity in the dog.

1. The tachycardia produced by atrial receptor stimulation has been reported to be 'solely' due to an increased sympathetic activity, but not inhibitable by propranolol. We examined the effect of left atrial balloon inflation in chloralose-anaesthetized dogs on heart rate with and without propranolol (1.0 mg/kg) and on the activity in single cardiac efferent fibres of the vagus nerve. 2. Propranolol reduced the cardiac response to balloon inflation by one-third, but did not abolish the tachycardia. Efferent cardiac vagal activity was 3.8 +/- 0.4 spikes/s and 2.3 +/- 0.7 spikes/s prior to and during balloon inflation respectively. 3. It was concluded that the left atrial receptors produce a tachycardia by decreasing cardiac parasympathetic and increasing sympathetic efferent activities.

Enhancement of K transfer to intracellular fluid by cerebral artery K-loading.

Intact, UL, and pancreatectomized UL dogs were loaded with K by administration of 2 mEq KCl/kg/hr through a cerebral (vertebral) artery. K transfer to ICF was calculated and compared with that computed in control animals K-loaded through a PV. At the same rate of K administration, the change of route from PV to VA markedly increased transmembrane K transfer, even in the absence of insulin; the increase seems a specific response to K. KCl administration via a VA, with a resulting abrupt rise in the serum K concentration of cerebral blood, activates a K transfer mechanism (possibly by stimulation of a K-sensitive CNS receptor) that is strikingly unlike the insulin-mediated one stimulated by intravenous KCl. Hyperkalemic dogs may have more than one mechanism for maintaining K homeostasis, depending on the rate at which K enters the circulation.

Influence of epinephrine and propranolol on transmembrane K transfer in anuric dogs with hyperkalemia.

In anuric dogs K loaded by infusion of 2 mEq of KCl per kg per hr the quantity of K transferred to intracellular fluid in ureter-ligated animals is considerably less than in nephrectomized ones; the combination of ureter ligation and hyperkalemia seems to suppress transmembrane K transfer. In the present investigation we found that treatment of K loaded ureter-ligated dogs with epinephrine markedly increased the animals' ability to transfer K to intracellular fluid, and that administration of propranolol (with and without epinephrine) reduced K transfer capacity below the control level. Further, we found that propranolol treatment of K-loaded nephrectomized dogs produced a striking diminution of K transfer ability. The data suggest that beta adrenergic receptors are importantly involved in the transmembrane K transfer of K-loaded anuric dogs, and that ureter ligation and hyperkalemia suppress K transfer capacity by blocking beta receptors.

Transmembrane K transfer in hyperkalemic dogs.

In a dog K loaded by infusion of 2 mEq KCl/kg/hr, kaluresis plays a relatively small part in slowing the development of hyperkalemia and cardiotoxicity. These are largely retarded by a non-renal mechanism that transfer most of the infused K from extracellular to intracellular fluid. Treatment with beta receptor blocking dosages of propranolol significantly reduces K transfer capacity, but it also markedly diminishes the KCl stimulated secretory response of insulin, a powerful mediator of K transfer. In dogs in which diminution of the insulin response is prevented by administration of exogenous hormone, beta receptor blockade has no effect on K transfer capacity. Thus, it appears that decreased insulin secretion is responsible for the observed fall of K transfer capacity in dogs with beta receptor blockade. However, other evidence suggests that our results can also mean that a K load elicits the secretion of enough insulin to mediate K transfer in the presence of beta receptor blockade; if the hormone response is absent or deficient, beta receptors may be importantly involved in mediation of K transfer to intracellular fluid.

Kaluresis independent K homeostasis in dogs: activity after ureter ligation and pancreatectomy.

In ureter ligated dogs intravenous administration of KCl stimulates both insulin secretion and activity of a kaluresis independent K homeostatic mechanism (K transfer capacity) that retards the development of hyperkalemia by transferring K to intracellular fluid. If the preparation is K loaded by infusion with 2 mEq KCl/kg/hr until prelethal ECG changes of hyperkalemic cardiotoxicity appear, about 50% of administered K is transferred. An increased proportion--70%--is transferred if the animal is K loaded 70 minutes after pancreatectomy--when serum immunoreactive insulin is fixed at less than 4 uU/ml. That proportion (70%) is unchanged by simultaneous adrenalectomy, but is reduced to less than 40% by propranolol blockade of B receptors. Increased post pancreatectomy K transfer capacity apparently involves K transfer mediated by B receptors that are activated by an extra-adrenomedullary B agonist(s). Findings also indicate that residual post pancreatectomy insulin biological activity mediates K transfer.

Kaluresis independent K-homeostasis: glucagon and B receptor blockade in pancreatectomized dogs.

Seventy minutes post pancreatectomy, in dogs that are K loaded - made abruptly hyperkalemic and "life threatened" - by infusion with 2 mEgKC1/kg-/hr until prelethal ECG changes of hyperkalemic cardiotoxicity appear, a kaluresis independent K homeostatic mechanism transfers about 2/3 of administered K to intracellular fluid. Treatment of K loaded pancreatectomized dogs with glucagon or a B receptor blockading dosage of propranolol does not alter the proportion transferred, but treatment with glucagon and propranolol reduces it. It appears that in pancx dogs there is a reciprocal relation between insulin and B receptor mediated K transfer and that glucagon is involved in activity of the kaluresis independent K homeostatic mechanism.

Inhibition of transmembrane K transfer in ureter-ligated dogs infused with KCl.

In anuric dogs loaded with K by infusion with 2 meq KCl/kg per h until prelethal hyperkalemic cardiotoxicity appears, the extent of transmembrane K transfer depends on the origin of the anuria. Animals with bilateral ureter ligation transfer a mean of 1.2 meq/kg to intracellular fluid, while those with bilateral nephrectomy transfer more than 2.5 times as much (3.1 meq/kg). Further, if dogs with functioning kidneys are ureter ligated or nephrectomized after approximately 45 min of K loading, K transfer ultimately falls as infusion continues. The fall is precipitate and over 90% in ligated animals; but it is gradual, and only 10% in those that are nephrectomized. Finally, K transfer, because of the absence of insulin, is negligible in K-loaded pancreatectomized dogs with bilateral ureter ligation, but fairly substantial in pancreatectomized animals with bilateral nephrectomy. The data suggest that ureter ligation and hyperkalemia activate a renal mechanism that interferes with the transfer of infused K to intracellular fluid. The mechanism may involve the renin-angiotensin II-aldosterone system to a limited degree.

Insulin and beta receptor modulation of K homeostasis in nephrectomized dogs with hyperkalemia.

In nephrectomized dogs infused with 2 mEq KCl/kg/hr a homeostatic mechanism retards the development of hyperkalemia by transferring about 70% of the K load to intracellular fluid. beta Adrenergic receptor activity is importantly involved in the transfer process; halting it with propranolol reduces the proportion transferred to less than 35%. The addition of pancreatectomy increases the involvement of beta receptor activity; propranolol treatment now reduces the proportion transferred to less than 20%. Insulin treatment, on the other hand, not only improves transfer of a K load, it also alters the response to propranolol. Nephrectomized dogs treated with 2 U insulin/kg/hr deposit some 80% of the infused K in intracellular fluid. After beta receptor blockade, nearly 90% is transferred. The results suggest that in the K homeostatic mechanism of nephrectomized dogs, insulin and beta receptors may be reciprocally related. K transfer mediated by beta receptors improves after pancreatectomy, and insulin mediated K transfer improves after beta receptors are inactivated.