Neuropeptide Y-like immunoreactivity (NPY-LI) in dog plasma was characterized and quantified using three extraction methods (Sep-Pak:acetonitrile, HCl:ethanol, and ethanol). Sep-Pak extraction yields the best recovery and preserves the integrity of the peptide. Oxidized NPY is not generated during blood collection. Using two antisera of different specificities, at least three peptide forms in normal dog arterial and venous plasma were detected. A peptide with retention times similar to oxidized NPY or peptide YY is the major component of plasma NPY-LI under basal conditions, but NPY(1-36) predominates during sympathetic stimulation. The mature peptide in dog plasma is similar to human NPY. The antiserum ABII provides a more accurate measure of circulating NPY(1-36) and its oxidized form. The antiserum ABI is useful for detecting NPY-like fragments.

Animals↗

PubMedDate not supplied

Modulation of coronary vascular resistance in female rabbits by estrogen and progesterone.

OBJECTIVE: To study the roles of estradiol and various progestins on the regulation of coronary flow in female rabbits. METHODS: Ovariectomized adult female rabbits were treated with estradiol, with progesterone (or one of the following synthetic progestins: megace, norethindrone, or medroxyprogesterone acetate), or with both an estradiol and a progestin. Hearts were isolated and perfused at constant pressure by a modified Langendorff technique. Changes in coronary flow were determined at baseline and in response to direct infusion into the coronary circulation of NG-nitro-L-arginine (L-NNA), an inhibitor of nitric oxide (NO) synthase. RESULTS: Coronary flow rates were 40-50% greater in hearts of animals treated with estradiol than in control hearts of animals not treated with the hormone. Treatment of the animals with progestin alone had little effect on coronary flow. However, when administered with estradiol, it abrogated the estradiol-related increase in coronary flow. The increments in coronary flow evoked by estradiol were virtually abolished by L-NNA, an inhibitor of NO synthase. In hearts of animals treated with estradiol plus progesterone, L-NNA had no additional inhibitory effect on coronary flow to that of progesterone. CONCLUSION: Estradiol decreases coronary vascular resistance (CVR) and hence increases coronary flow. Progestins attenuate this effect of estradiol.

Animals↗

PubMedDate not supplied

Beneficial effects of estrogen on cardiac stunning in female rabbits.

OBJECTIVE: To determine the effect of estrogen treatment on the contractile, relaxation, and chronotropic responses of hearts of female rabbits to cessation of perfusion. METHODS: Adult female rabbits were treated either with estradiol or with the vehicle (control). The hearts were then isolated and perfused at constant pressure by the Langendorff technique. A saline-filled balloon connected to a pressure transducer was inserted in the left ventricle in order to assess the mechanical function of the isolated heart. Cardiac stunning was induced by halting the perfusion of the coronary vasculature for four successive periods of 1, 3, 5, and 5 minutes, followed by reperfusion between nonperfusion periods. Changes in cardiac function induced by the cessation of perfusion were assessed by monitoring the changes in heart rate and in left ventricular pressure ([dP/dt]max as an index of ventricular contractility and [dP/dt]min as an index of ventricular relaxation). Changes in coronary flow were determined at baseline and following reperfusion. RESULTS: Halting coronary perfusion decreased (dP/dt)max, and (dP/dt)min and slowed left ventricular contractions both in control and in estrogen-treated hearts. The depressant effects of flow cessation on left ventricular (dP/dt)max and (dP/dt)min were smaller in estrogen-treated hearts than in control hearts. Treatment with estrogen had no effect on the changes on the heart rate in responses to cessation of flow and to reperfusion. Treatment with estrogen increased coronary flow by 40%. Coronary reperfusion increased coronary flow transiently, but the effects did not differ significantly between control and estrogen-treated hearts. CONCLUSION: Short-term treatment of adult female rabbits with doses of estrogen that are physiologic for the rabbit exerts a protective effect on cardiac contractility from repetitive periods without perfusion.

Animals↗

PubMedDate not supplied

Effects of angiotensin II on the cardiac responses to sympathetic nerve stimulation in dogs.

In anesthetized dogs with the left cardiac sympathetic nerves and both vagal nerves intact, angiotensin II (AII) induced a substantial, dose-dependent increase in arterial blood pressure and small increments in cardiac cycle length and ventricular contractile force. In dogs in which the cardiac sympathetic and vagal nerves had been interrupted, AII produced similar increases in blood pressure and larger increases in contractile force, but it decreased the cardiac cycle length. In both groups of dogs, AII augmented substantially the positive inotropic responses to sympathetic nerve stimulation, but it enhanced the positive chronotropic responses only slightly. However, AII did not appreciably prolong the cardiac responses to sympathetic nerve stimulation, nor did it alter significantly the cardiac responses to norepinephrine infusions. Hence, at the dosage levels used, AII probably did not inhibit the neuronal uptake of norepinephrine appreciably nor did it enhance the responsiveness of the cardiac effector sites to norepinephrine. Therefore, the potentiation of the cardiac responses to sympathetic nerve stimulation by AII in these experiments was probably achieved principally by facilitating norepinephrine release from the adrenergic nerve terminals in the heart.

Angiotensin II↗

PubMedDate not supplied

Gas embolism death after laparoscopy delayed by "trapping" in portal circulation.

A young woman died suddenly about 1 hour after instillation of CO2 for diagnostic larparoscopy. Post-mortem x-rays revealed large volumes of gas in the portal system, the heart, and the brain. In addition, autopsy revealed gas bubbles in the coronary arteries, pulmonary hemorrhage and edema, and a probe-patent foramen ovale. We postulated the "trapping" of gas in the portal circulation and affirmed this by experiments in 6 dogs. We further postulate the delayed and intermittent release of this gas and of platelet aggregates into the systemic circulation would occur in volumes which would be insufficient to produce hemodynamic signs yet sufficient to produce serious pulmonary insult.

Adult↗

PubMedDate not supplied

Complexity of the neural regulation of the cardiovascular system.

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Autonomic Nervous System↗