Ruptured abdominal aortic aneurysm: the persistent challenge.

Despite improvement in anesthetic and postoperative care, ruptured abdominal aortic aneurysms (AAA) continue to have a high mortality. Thirty-three patients from 1980-1986 underwent surgery at West Virginia University for ruptured AAA, with 12 survivors (36.4 per cent). Age, use of MAST trousers, initial hemoglobin and blood pressure as well as operative time and estimated blood loss were not found to be significantly different between survivors and non-survivors. The blood pressure at the time of induction, during surgery, at the end of surgery, and the final temperature were significantly different. Our results show that the chance of survival is much greater if the patient responds to the initial fluid resuscitation prior to induction, and if blood pressure and temperature are maintained during the operation.

Calcium-accentuated ischemic damage during reperfusion: the time course of the reperfusion injury in the isolated working rat heart model.

The purpose of this study was to determine the time course of calcium-induced postischemic reperfusion injury to the myocardium, using an initial short-term calcium-enriched reperfusion solution. The isolated rat heart model was subjected to 30 min of normothermic potassium cardioplegia-induced ischemic arrest. Control hearts received normal calcium Krebs-Henseliet buffer (KHB) reperfusion. Experimental hearts were challenged with 10 min of calcium-enriched (KHB) reperfusion starting at 0, 1, 2, 5, 15, and 30 min after the beginning of reperfusion. Aortic flow recovery 60 min after reperfusion was used to determine functional recovery. Control hearts recovered 82 +/- 3% of preischemic aortic flow. Hearts which received calcium challenge at 0 and 1 min after the start of reperfusion recovered 43 +/- 4 and 69 +/- 3% of preischemic aortic flow, respectively (P less than 0.01 and P less than 0.05, respectively). Hearts which received calcium challenge 2, 5, 15, and 30 min after reperfusion recovered 75 +/- 2, 80 +/- 2, 85 +/- 2, and 83 +/- 2% of preischemic aortic flow, respectively. Our results indicate that the postischemic myocardium is very susceptible to calcium-accentuated ischemic damage during the initial period of reperfusion. The postischemic heart, however, quickly recovers its ability to withstand a calcium challenge. Five minutes after the start of reperfusion the heart is not influenced by calcium challenge.

Morphine sulfate depression of cardiac function is attenuated by opiate receptor antagonism with naloxone.

In previous work, morphine sulfate was shown to decrease heart rate (HR) and cardiac output (CO) in a dose-related fashion. It was hypothesized that this effect was mediated by opiate receptors located in the myocardium. The present study evaluated the effect of opiate receptor antagonism with naloxone using a modified Langendorff rat heart perfusion apparatus. Sixty-five rat hearts were excised and perfused with Krebs-Henseleit buffer (KHB) solution, to which morphine sulfate and naloxone (NAL) were added in different concentrations. In the initial studies, NAL (10(-5) M) was added to the perfusate prior to the incremental additions of morphine. This resulted in no antagonism of the previously described opiate agonist effects. Norepinephrine (NE; 10(-9) M) was then added to the perfusate prior to the NAL or morphine. The NE did not affect the dose-related decrease in HR and CO when morphine was added but did permit the attenuation of the morphine effect by the addition of increasing concentrations of NAL up to 10(-5) M. These results suggest that the agonist effect can be attenuated by opiate receptor antagonism with NAL; the data also suggest a possible interrelationship between opiate and catecholamine receptor activity in the myocardium.

Cardiac myxomas. Diagnosis, surgical excision, and nursing care.

Diagnosis of cardiac myxoma is rare, but one that prompts expeditious action by the cardiac surgical service. It is one form of acquired heart disease for which surgical intervention can result in a cure. Perioperative nursing care plays an important part in helping the patient and family cope with this urgent situation.

Opiate agonist depression of myocardial function is dose related and independent of pentobarbital or chloral hydrate anesthesia.

Previous work has demonstrated that a common opiate agonist, morphine sulfate (MS), causes significant depression of myocardial performance when added to the perfusate of a modified Langendorff isolated rat heart preparation. The same model has been used in this study with the addition of higher concentrations of MS to demonstrate that the aforementioned effects occur in a dose-related fashion. In addition, different anesthetics, sodium pentobarbital (P) or chloral hydrate (CH), were compared and demonstrated that there was no significant difference in results. This implies that there is not an anesthetic-morphine interaction occurring. These results suggest opiate agonist depression of myocardial function acts on opiate receptors, causing primarily a chronotropic effect.

Morphine depression of myocardial function.

A modified Langendorff rat heart preparation with an isolated working rat heart was used to establish the presence of opiate receptors in the myocardium and to demonstrate the effects of an opiate agonist on myocardial function in the absence of neuronal and humoral factors. Twenty-five Sprague-Dawley rats weighing 400-500 gm were anesthetized and had their hearts excised and attached to the Langendorff perfusion apparatus. After a 30 min control period, the Krebs-Henseleit Buffer (KHB) perfusion solution was altered by the addition of 0.9% NaCl (S) or morphine sulfate (MS), which resulted in a final concentration of 2 X 10(-4) M or 3 X 10(-4) M MS in the KHB. Temperature, preload, and afterload were kept constant while heart rate (HR), cardiac output (CO), and aortic dP/dtmax were measured. Significant dose-related depression of HR, CO, and less significantly, aortic dP/dtmax were demonstrated. The data suggest that opiate receptors are present in the myocardium and that morphine sulfate directly effects the myocardium causing a significant decrease in HR, CO, and aortic dP/dtmax. These changes are a result of opiate receptor agonism, which seems to be primarily a negative chronotropic effect and might explain the mechanism for the role of endogenous opiates during shock.

Developmental changes in the neutral alpha-amino acid transport systems of rat brain over the first three weeks after birth.

Transport of seven different amino acids into brain slices increased as donor rats aged from 1 to 6 days. Uptakes of 2-aminoisobutyric acid, 2-(methyl-amino)isobutyric acid, and L-alanine then decreased by day 14, while uptakes of other amino acids continued to increase or remained fairly constant. Neutral alpha-amino acid transport systems were characterized by measuring inhibition of uptakes and kinetics for representative amino acids at different ages. Results indicate that 2-aminoisobutyrate and 2-(methylamino)isobutyrate used only one (and the same) system in brain slices from 6-day-old rats, with characteristics of system A (the major sodium-dependent system in most mammalian cells). They used at least two systems at ages 1, 14, and 23 days, but, of these, only at 1 day did they use the same systems in the same proportions. Alanine and leucine used more than one system at all four ages, and somewhat different combinations than used by each other or by 2-aminoisobutyrate or 2-(methylamino)isobutyrate. Their transport characteristics showed they used mostly system ASC (a sodium-dependent system distinguished from A) and/or system L (sodium-independent). We conclude that system A increases as the brain ages from 1 to 6 days and declines thereafter. System L probably increases with aging from 1 to 23 days.

Thyroxine-induced changes in the development of neutral alpha-amino acid transport systems of rat brain.

Transport of representative neutral alpha-amino acids was measured in brain slices after injecting thyroxine into donor rats of various ages from 1 to 23 days old. The hormone did not alter uptake in slices from 1-day-old rats even when treatment was begun on pregnant rats as much as 10 days before delivery. Injecting thyroxine until age 6 days, however, decreased the activity of transport system A (the major sodium-dependent system in most mammalian cells) and caused appearance of a new transport system used by the model amino acids, 2-aminoisobutyric acid and 2-(methylamino)isobutyric acid. Uptake at 6 days was similar to that found in slices from older, untreated rats (e.g., those 14 days old). These results strongly suggest that one action of thyroxine is to accelerate the development of neutral alpha-amino acid transport systems of brain over the first six days after birth. Thyroxine treatment of rats from birth to age 14 days also appears to increase the activities of both system A and the second transport system used by the two model amino acids in brains from 14-day-old rats.

Amino acid transport in diaphragms from newborn rats: evidence for insulin resistance.

Diaphragms from rats under 24-h-old did not show the well-known increased transport of alpha-aminoisobutyrate found in older tissues in respone to insulin in vitro. A small effect was apparent by 3 days, and stimulation increased as donor rats aged (up to 4--5 wk). One-day diaphragms also had greater uptake than older tissues, due to both decreased Km and elevated Vmax. The change in insulin sensitivity did not result from alteration in the transport system used by alpha-aminoisobutyrate because uptake showed characteristics of the A system at both 1 day and older. Results suggest instead that the 1-day tissues had been made insulin-resistant by high insulin levels in donor animals. Plasma insulin levels of 1-day-old rats were 5 times those of 5-day animals. Elevating the plasma insulin levels of 5-day or 25- to 35-day rats led to a decreased effectiveness of insulin in vitro in stimulating alpha-aminoisobutyrate transport into their diaphragms. In the older animals, the stimulation was inversely proportional to the plasma insulin level 2 h after insulin injection.

Transport of amino acids into the oestrogen-primed uterus. Enchancement of the uptake by a preliminary incubation.

1. Preincubation of the immature rat uterus under physiological conditions was found to increase its subsequent ability to transport alpha-aminoisobutyric acid, l-proline, l-alanine and 1-aminocyclopentanecarboxylic acid. Uptakes of l-valine, l-phenylalanine and l-leucine were not affected. With alpha-aminoisobutyric acid, a doubling of the uptake could be obtained after a 3-5h preincubation period. Uteri from oestradiol-primed rats gave increases similar to those found in tissues from untreated animals. In both cases the preincubation increased the V(max.) of alpha-aminoisobutyric acid uptake but did not affect the K(m). 2. The conditions during the preincubation period determined the increase in subsequent uptake of alpha-aminoisobutyric acid. No increase in uptake was found if the preincubation was carried out at 1 degrees C, in the presence of cyanide or dinitrophenol, under anaerobiosis or with a concentration of puromycin that depressed incorporation of l-leucine into protein by 95%. The puromycin was also shown to prevent the increase in V(max.) normally found after the preincubation period. In addition, no increase was found if Na(+) was omitted from the preincubation medium. Other inorganic ions had smaller effects. 3. The uptake of alpha-aminoisobutyric acid by uteri before and after a preincubation period showed the same general patterns of sensitivity to competitive inhibitors, K(+), pH, temperature and 2,4-dinitrophenol. 4. The results suggest that the preincubation leads to an increase in a protein component of the ;A system' for amino acid transport in the uterus, and that metabolic energy is required for the reactions involved.