B., DEN-Is BLOOMFIELD, M.B., AN'D AScG1AR DAVxACnII, MI1). W JT:[II the widespread use of wire guidesand catheters inserted into the leart and blood vessels (Iiiring cardiac catleterizationi and other diaginostic pirocedur-es, l()ss of a part of sulch instru-ments should 1c) considered as a poSsible) complication. The pu.trpose of this paper is to report the loss anfl sulbse(Iuent retriexal withouit suirgery of a portion of stainless steel guide in. the riglht atriu.m and inferior vena cava duiring a rouitine cardiac catlheterizatioi.Case Report A 48 ear 0(1 Negro \vomain xas adImitted to the hospital becauise of increasing (lx/spuea,te su.ltinig froIn rhl-eumticl,heart disease. Exatminiationi revealed rmaiked cardiomegalv, a loud blox wing holosystollc and a slight early diastolic mulr1Mur11 at the apex. There were rales in both luIng fields and moderate hepatomegaly. She responided well to treatment with digitalis and diuretics. An anatomic diagnosis of mitral insufficiency xas made anid cardiac catheterization was planned.Duiring preparation for a tran-sseptal entrance inito the left atriuim, a 110-cm. stainlless-steel spring guide was pass.ed bv conventional clutdowii anld exposuire, through the sapheniotus x eim inlto the right atriuim unider cinefluor-oscopic ot) servationl. The guidle ( fig. 1) was 0.045) inch in diameter with an 0.014-inch, internal steel core that xxwas not movable and fixed 3 em. short of thle clistal tip. A Brockenbrouigh transseptal left lhearit Tefloni catheter was passed ovex the gu.i(le into the right ati-inii wxithlouit difficuilty. After approximnately 150 cin. of the guidle was xitdaxthrough the catheter, slight resistaicie to ftirthei vxitiadrxx A xxal s experieniced. Thlius, the catheter From the Cardiovascular Disease Clinical Research

A B S T R A C T The effect of glucagon (50 ng/kg/min) on arterial glycerol concentration and net splanchnic production of total ketones and glucose was studied after an overnight fast in four normal and five insulin-dependent diabetic men. Brachial artery and hepatic vein catheters were inserted and splanchnic blood flow determined using indocyanine green. The glucagon infusion resulted in a mean circulating plasma level of 4,420 pg/mI.In the normal subjects, the glucagon infusion resulted in stimulation of insulin secretion indicated by rising levels of immunoreactive insulin and C-peptide immunoreactivity. Arterial glycerol concentration (an index of lipolysis) declined markedly and net splanchnic total ketone production was virtually abolished. In contrast, the diabetic subjects secreted no insulin (no rise in C-peptide immunoreactivity) in response to glucagon. Arterial glycerol and net splanchnic total ketone production in these subjects rose significantly (P = < 0.05) when compared with the results in four diabetics who received a saline infusion after undergoing the same catheterization procedure.Net splanchnic glucose production rose markedly during glucagon stimulation in the normals and diabetics despite the marked rise in insulin in the normals. Thus, the same level of circulating insulin which markedly suppressed lipolysis and ketogenesis in the normals failed to inhibit the glucagon-mediated increase in net splanchnic glucose production. It is concluded (a) that glucagon at high concentration is capable of stimulating lipolysis and ketogenesis in insulin-deficient diabetic man; (b) that insulin, mole for mole, has more antilipolytic activity in man than glucagon has lipolytic activity; and (c) that glucagon, on a molar basis, has greater stimulatory activity than insulin has inhibitory activity on hepatic glucose release.

No abstract

It is well established that the liver is a major site of metabolic inactivation of aldosterone. In 1962 Coppage, Island, Cooner, and Liddle (2) reported that the human liver was capable of converting aldosterone both to its acid-hydrolyzable conjugate (AHC) 1 and to tetrahydroaldosterone. The same study also demonstrated that aldosterone was almost completely inactivated during a single passage through the normal liver. More recent studies by Luetscher and associates (4) have indicated that the normal liver extracts about 97%o of the aldosterone delivered to it by the arterial circulation, and the studies of Bougas and co-workers (5, 6) have indicated that in subjects with minimal cardiac dysfunction the rate of splanchnic clearance of aldosterone amounts to about 89%o of the hepatic blood flow.The fact that the liver metabolizes almost all of the aldosterone presented to it does not imply that the liver is the only site of metabolism of aldosterone. Sandor and Lanthier (7) observed that kidney slices could convert aldosterone to AHC. From their analyses of hepatic and peripheral venous plasma after the continuous infusion of tritiated aldosterone into human subjects, Bougas and co-workers (5,6)

A B S T R A C T Glucagon activates hepatic adenylate cyclase, thereby increasing acutely the liver content of cyclic AMP (cAMP) as well as the release of cAMP into the hepatic vein. Insulin, on the other hand, antagonizes this glucagon-mediated cAMP production, thus providing a hypothetical mechanism through which insulin might correct some of the metabolic abnormalities of diabetes.To study this hormonal interaction in man, net splanchnic cAMP production (NScAMPP) was investigated in normal and insulin-dependent diabetic men under basal conditions and in response to intravenous glucagon, 50 ng/kg/nmin for 2 h.In normals (n = 19), basal hepatic vein cAMP concentration was 23.6±1.1 nM and NScAMPP was 1.7±0.6 nmol/min. Glucagon stimulated NScAMPP in four normal subjects to a peak of 99.6±43 nmol/min at 25 min with a subsequent fall to 12.4±5.1 nmol/min by 90 min despite continuing glucagon infusion. Endogenous insulin secretion was stimulated as indicated by rising levels of immunoreactive insulin and C-peptide (connecting peptide) immunoreactivity, raising the possibility that endogenous insulin might be responsible for the fall in NScAMPP that followed the initial spike.In the diabetics (n = 8), basal hepatic vein cAMP concentration was 24.7±1.2 nM and NScAMPP was undetectable. Glucagon stimulated NScAMPP in five diabetics to a peak of 169.9±42.6 with a subsequent fall to 17.4±3.9 nmol/min by 90 min even though endogenous